{"title":"Autonomic and Autacoid Pharmacology: Goodbye and thank you","authors":"Peter Penson","doi":"10.1111/aap.12060","DOIUrl":"10.1111/aap.12060","url":null,"abstract":"","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/aap.12060","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35610902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In addition to providing mechanical support for blood vessels, the perivascular adipose tissue (PVAT) secretes a number of vasoactive substances and exerts an anticontractile effect. The main objective of this study was to find out whether the anticontractile effect of cooling in the rat aorta is affected by PVAT. Our hypothesis was that PVAT would enhance the anticontractile effect of cooling in the rat aorta.
Aorta segments, with or without PVAT, were used in this investigation. Cumulative concentration-response curves were established for phenylephrine at 37°C or 24°C. Phenylephrine (10-9M – 10-5M) induced concentration-dependent contractions of aorta segments with or without PVAT at 37°C. The maximum response, but not pD2 value, was reduced in aorta segments with PVAT.
Cooling the tissues to 24 °C resulted in a significant reduction in the maximum response in aorta segments without PVAT with no change in pD2 values. However, the anticontractile effect of cooling was attenuated in the presence of PVAT with no significant (p > 0.05) change in either the maximum response or pD2 value.
L-NAME potentiated PE-induced contractions and this was greater in aorta segments without PVAT at both temperatures.
The expression of eNOS protein and basal tissue level of nitric oxide (NO) were greater in aorta segments with PVAT at both temperatures. However, PE significantly increased tissue levels of NO only in aorta segments without PVAT.
We concluded that PVAT-induced loss of anticontractile effect of cooling against PE-induced contractions could be due to impaired generation of NO in aorta segments with PVAT.
{"title":"Attenuation of the anti-contractile effect of cooling in the rat aorta by perivascular adipose tissue","authors":"Y. Rafique, M. AlBader, M. Oriowo","doi":"10.1111/aap.12058","DOIUrl":"10.1111/aap.12058","url":null,"abstract":"<div>\u0000 \u0000 <p>\u0000 \u0000 </p><ol>\u0000 \u0000 \u0000 <li>In addition to providing mechanical support for blood vessels, the perivascular adipose tissue (PVAT) secretes a number of vasoactive substances and exerts an anticontractile effect. The main objective of this study was to find out whether the anticontractile effect of cooling in the rat aorta is affected by PVAT. Our hypothesis was that PVAT would enhance the anticontractile effect of cooling in the rat aorta.</li>\u0000 \u0000 \u0000 <li>Aorta segments, with or without PVAT, were used in this investigation. Cumulative concentration-response curves were established for phenylephrine at 37°C or 24°C. Phenylephrine (10<sup>-9</sup>M – 10<sup>-5</sup>M) induced concentration-dependent contractions of aorta segments with or without PVAT at 37°C. The maximum response, but not pD<sub>2</sub> value, was reduced in aorta segments with PVAT.</li>\u0000 \u0000 \u0000 <li>Cooling the tissues to 24 °C resulted in a significant reduction in the maximum response in aorta segments without PVAT with no change in pD<sub>2</sub> values. However, the anticontractile effect of cooling was attenuated in the presence of PVAT with no significant (p > 0.05) change in either the maximum response or pD<sub>2</sub> value.</li>\u0000 \u0000 \u0000 <li>L-NAME potentiated PE-induced contractions and this was greater in aorta segments without PVAT at both temperatures.</li>\u0000 \u0000 \u0000 <li>The expression of eNOS protein and basal tissue level of nitric oxide (NO) were greater in aorta segments with PVAT at both temperatures. However, PE significantly increased tissue levels of NO only in aorta segments without PVAT.</li>\u0000 \u0000 \u0000 <li>We concluded that PVAT-induced loss of anticontractile effect of cooling against PE-induced contractions could be due to impaired generation of NO in aorta segments with PVAT.</li>\u0000 </ol>\u0000 \u0000 </div>","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/aap.12058","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35323822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Retraction: F. Mignini, E. Bronzetti, L. Felici, A. Ricci, M. Sabbatini, S. K. Tayebati, F. Amenta (2000), Dopamine receptor immunohistochemistry in the rat choroid plexus. Journal of Autonomic Pharmacology, 20: 325-332. https://doi.org/10.1046/j.1365-2680.2000.00198.x The above article, published online on 09 October 2008, in Wiley Online Library (wileyonlinelibrary.com), has been retracted by the Publisher John Wiley and Sons Ltd. This journal is no longer published by Wiley. Concerns were raised by a third party regarding suspected duplication and fabrication of elements within Figure 1. The Integrity Assurance and Case Resolution team evaluated the paper and found legitimate concerns affecting the reliability of Figure 1. The manuscript was published many years ago, and so the original data was not available for evaluation. As a result, the Integrity Assurance and Case Resolution team considers the conclusions of this manuscript invalid. The authors disagree with the retraction and the team´s evaluation.
撤回：F. Mignini、E. Bronzetti、L. Felici、A. Ricci、M. Sabbatini、S. K. Tayebati、F. Amenta（2000 年），《大鼠脉络丛中的多巴胺受体免疫组织化学》。自律神经药理学杂志》（Journal of Autonomic Pharmacology），20: 325-332。https://doi.org/10.1046/j.1365-2680.2000.00198.x 上述文章于 2008 年 10 月 9 日在线发表于 Wiley Online Library (wileyonlinelibrary.com)，已被出版商 John Wiley and Sons Ltd 撤回。该期刊已不再由 Wiley 出版。第三方对图 1 中的元素涉嫌重复和捏造提出了质疑。诚信保证与案件解决小组对论文进行了评估，发现影响图 1 可靠性的问题是合理的。该手稿发表于多年前，因此没有原始数据可供评估。因此，诚信保证与个案解决小组认为该手稿的结论无效。作者不同意撤稿和团队的评价。
{"title":"Retraction: Dopamine receptor immunohistochemistry in the rat choroid plexus.","authors":"","doi":"10.1002/aap.12061","DOIUrl":"https://doi.org/10.1002/aap.12061","url":null,"abstract":"<p><p>Retraction: F. Mignini, E. Bronzetti, L. Felici, A. Ricci, M. Sabbatini, S. K. Tayebati, F. Amenta (2000), Dopamine receptor immunohistochemistry in the rat choroid plexus. Journal of Autonomic Pharmacology, 20: 325-332. https://doi.org/10.1046/j.1365-2680.2000.00198.x The above article, published online on 09 October 2008, in Wiley Online Library (wileyonlinelibrary.com), has been retracted by the Publisher John Wiley and Sons Ltd. This journal is no longer published by Wiley. Concerns were raised by a third party regarding suspected duplication and fabrication of elements within Figure 1. The Integrity Assurance and Case Resolution team evaluated the paper and found legitimate concerns affecting the reliability of Figure 1. The manuscript was published many years ago, and so the original data was not available for evaluation. As a result, the Integrity Assurance and Case Resolution team considers the conclusions of this manuscript invalid. The authors disagree with the retraction and the team´s evaluation.</p>","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140961432","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The effect of nicotine on heart rate variability (HRV) is controversial. Autonomic nervous system is the main regulator of heart rhythm, and heart rate variability is an appropriate index to assessment of the effects of the autonomic system on heart.
In this study, the combination effect of nicotine and black tea consumption on sympatho-vagal balance and heart rate variability was investigated in rats.
Male Wistar rats were randomized into four groups as control, tea (2.5 g/100 cc, daily), nicotine (2 mg/kg/d) and tea plus nicotine groups which treated for 28 days, and in the 29th day, their electrocardiograms (lead II) were recorded.
The mean of high-frequency power (HF) in tea, nicotine and tea plus nicotine groups was significantly more than control group (P < .05), and low-frequency power/high-frequency power (LF/HF) ratio in the nicotine and tea + nicotine groups was significantly less than control group (P < .05). LF values did not differ significantly among groups. Mean of standard deviation of normal RR intervals (SDNN) and square root of the mean squared differences of successive RR intervals (RMSSD) increased significantly in tea, nicotine and tea + nicotine groups in comparison with control group (P < .05)
Overall, 4-week administration of black tea, nicotine or their combination with dosages used in this study can increase the heart rate variability and improve the sympatho-vagal balance in rat.
{"title":"Combinatorial effect of nicotine and black tea on heart rate variability: Useful or harmful?","authors":"S. Joukar, M. Sheibani","doi":"10.1111/aap.12059","DOIUrl":"10.1111/aap.12059","url":null,"abstract":"<div>\u0000 \u0000 <p>\u0000 \u0000 </p><ol>\u0000 \u0000 \u0000 <li>The effect of nicotine on heart rate variability (HRV) is controversial. Autonomic nervous system is the main regulator of heart rhythm, and heart rate variability is an appropriate index to assessment of the effects of the autonomic system on heart.</li>\u0000 \u0000 \u0000 <li>In this study, the combination effect of nicotine and black tea consumption on sympatho-vagal balance and heart rate variability was investigated in rats.</li>\u0000 \u0000 \u0000 <li>Male Wistar rats were randomized into four groups as control, tea (2.5 g/100 cc, daily), nicotine (2 mg/kg/d) and tea plus nicotine groups which treated for 28 days, and in the 29th day, their electrocardiograms (lead II) were recorded.</li>\u0000 \u0000 \u0000 <li>The mean of high-frequency power (HF) in tea, nicotine and tea plus nicotine groups was significantly more than control group (<i>P</i> < .05), and low-frequency power/high-frequency power (LF/HF) ratio in the nicotine and tea + nicotine groups was significantly less than control group (<i>P</i> < .05). LF values did not differ significantly among groups. Mean of standard deviation of normal RR intervals (SDNN) and square root of the mean squared differences of successive RR intervals (RMSSD) increased significantly in tea, nicotine and tea + nicotine groups in comparison with control group (<i>P</i> < .05)</li>\u0000 \u0000 \u0000 <li>Overall, 4-week administration of black tea, nicotine or their combination with dosages used in this study can increase the heart rate variability and improve the sympatho-vagal balance in rat.</li>\u0000 </ol>\u0000 \u0000 </div>","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/aap.12059","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35420877","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
H. J. Lee, S. M. Cantú, A. S. Donoso, M. R. Choi, H. A. Peredo, A. M. Puyó
Perivascular adipose tissue dysfunction induced by high-fat feeding leads to alterations in the modulation of inflammation, contractile activity of the vascular smooth muscle and endothelial function, all risk factors in the development of hypertension. Metformin, an activator of AMP-activated protein kinase (AMPK), is currently the first-line drug treatment for type 2 diabetes (T2DM) and metabolic syndrome. Besides its glucose-lowering effect, there is an interest in actions of this drug with potential relevance in cardiovascular diseases.
The high-fat (HF) diet is an experimental model that resembles human metabolic syndrome. We have previously reported an altered pattern of prostanoid release in mesenteric vessels in this model.
The aim of this study was to analyse the effects of metformin on mesenteric vascular bed prostanoid release, adiposity index and its relation to blood pressure in Sprague-Dawley rats fed a HF diet for 8 and 12 weeks. Eight groups were used: control (C8, C1), HF diet (HF8, HF12, 50% w/w bovine fat), metformin-treated (CMf8, CMf12, 500 mg/kg/day) and metformin-treated HF diet (HFMf8, HFMf12, both treatments).
HF diet increased mesenteric vascular bed adiposity index (%, HF8: 1.7±0.1 vs C8: 0.9±0.04 and HF12: 1.8±0.1 vs C12: 0.8±0.1, P<.001); systolic blood pressure (SBP, mm Hg, HF8: 145±6 vs C8: 118±4, P<.01 and HF12: 151±1 vs C12: 121±3, P<.001). We found a positive correlation between these two parameters. Moreover HF diet increased the release of vasoconstrictor prostanoids such as thromboxane (TX) B2 (ng PR/mg of tissue, HF8: 117±6 vs C8: 66±2 and HF12: 123±6 vs C12: 62±5, P<.001) and prostaglandin (PG) F2α (ng/mg, HF8: 153±9 vs C8: 88±3 and HF12: 160±11 vs C12: 83±5, P<.001). We also found that this increase in the release of vasoconstrictor prostanoids positively correlates with the elevation of SBP. In addition, HF diet increases the release of PGE2 and decreases the prostacyclin (PGI2)/TXA2 release ratio at 8 and 12 weeks of treatment compared to control groups.
In the HFMf group, metformin treatment prevented all these increases in mesenteric vascular bed adiposity index (%, HFMf8: 1.3±0.2 vs HF8 and HFMf12: 1.3±0.1 vs HF12, P<.05); SBP (mm Hg, HFMf8: 127±2 vs HF8 and HFMf12: 132±1 vs HF12, P<.001); TXB2 release (ng PR/mg of tissue, HFMf8: 65±12 vs HF8, P<.05 and HFMf12: 53±3 vs HF12, P<.001) and PGF2α (ng PR/mg of tissue, HFMf8: 99±13 vs HF8, P<.01 and HFMf12: 77±8 vs HF12, P<.001). Meanwhile metformin prevented the increment in PGE2 r
高脂肪喂养引起的血管周围脂肪组织功能障碍导致炎症调节、血管平滑肌收缩活动和内皮功能的改变，这些都是高血压发生的危险因素。二甲双胍是一种amp活化蛋白激酶(AMPK)的激活剂，目前是治疗2型糖尿病(T2DM)和代谢综合征的一线药物。除了降糖作用外，人们对该药在心血管疾病中的潜在作用也很感兴趣。高脂肪饮食是一种类似于人类代谢综合征的实验模型。我们之前曾报道过该模型中前列腺素在肠系膜血管中释放的改变模式。本研究的目的是分析二甲双胍对饲喂HF饮食8周和12周的Sprague-Dawley大鼠肠系膜血管床前列腺素释放、肥胖指数及其与血压的关系。采用8组:对照组(C8、C1)、HF饲粮(HF8、HF12，牛脂肪比为50%)、二甲双胍处理(CMf8、CMf12, 500 mg/kg/d)和二甲双胍处理HF饲粮(HFMf8、HFMf12，两种处理)。HF日粮增加肠系膜血管床肥胖指数(%，HF8: 1.7±0.1 vs C8: 0.9±0.04;HF12: 1.8±0.1 vs C12: 0.8±0.1,p < 0.01);收缩压(SBP, mm Hg, HF8: 145±6 vs C8: 118±4,P<01和HF12: 151±1 vs C12: 121±3,p < 0.01)。我们发现这两个参数之间呈正相关关系。此外，HF饮食增加了血管收缩剂前列腺素的释放，如血栓素(TX) B2 (ng PR/mg, HF8: 117±6 vs C8: 66±2,HF12: 123±6 vs C12: 62±5,p < 0.01)和前列腺素(PG) F2α (ng/mg, HF8: 153±9 vs C8: 88±3,HF12: 160±11 vs C12: 83±5,p < 0.01)。我们还发现血管收缩剂前列腺素释放的增加与收缩压升高呈正相关。此外，与对照组相比，HF饮食在治疗8周和12周时增加了PGE2的释放，降低了前列环素(PGI2)/TXA2的释放比。在HFMf组，二甲双胍治疗阻止了所有这些肠系膜血管床肥胖指数的增加(%，HFMf8: 1.3±0.2 vs HF8, HFMf12: 1.3±0.1 vs HF12, P< 0.05);收缩压(mmhg, HFMf8: 127±2 vs HF8, HFMf12: 132±1 vs HF12, p < 0.01);TXB2释放量(ng PR/mg组织，HFMf8: 65±12 vs HF8, P<HFMf12: 53±3 vs HF12, p < 0.01)和PGF2α (ng PR/mg)， HFMf8: 99±13 vs HF8, p < 0.01;01和HFMf12: 77±8 vs HF12, p < 0.01)。二甲双胍仅在12周时阻止PGE2释放增加。另一方面，二甲双胍在研究的两个时期都改善了PGI2/TXA2比率。综上所述，二甲双胍可能通过改善该模型肠系膜血管周围脂肪组织血管活性物质失衡引起的内皮功能障碍，对脂肪组织和血管系统发挥有益作用。
{"title":"Metformin prevents vascular prostanoid release alterations induced by a high-fat diet in rats","authors":"H. J. Lee, S. M. Cantú, A. S. Donoso, M. R. Choi, H. A. Peredo, A. M. Puyó","doi":"10.1111/aap.12057","DOIUrl":"10.1111/aap.12057","url":null,"abstract":"<div>\u0000 \u0000 <p>\u0000 \u0000 </p><ol>\u0000 \u0000 \u0000 <li>Perivascular adipose tissue dysfunction induced by high-fat feeding leads to alterations in the modulation of inflammation, contractile activity of the vascular smooth muscle and endothelial function, all risk factors in the development of hypertension. Metformin, an activator of AMP-activated protein kinase (AMPK), is currently the first-line drug treatment for type 2 diabetes (T2DM) and metabolic syndrome. Besides its glucose-lowering effect, there is an interest in actions of this drug with potential relevance in cardiovascular diseases.</li>\u0000 \u0000 \u0000 <li>The high-fat (HF) diet is an experimental model that resembles human metabolic syndrome. We have previously reported an altered pattern of prostanoid release in mesenteric vessels in this model.</li>\u0000 \u0000 \u0000 <li>The aim of this study was to analyse the effects of metformin on mesenteric vascular bed prostanoid release, adiposity index and its relation to blood pressure in Sprague-Dawley rats fed a HF diet for 8 and 12 weeks. Eight groups were used: control (C8, C1), HF diet (HF8, HF12, 50% w/w bovine fat), metformin-treated (CMf8, CMf12, 500 mg/kg/day) and metformin-treated HF diet (HFMf8, HFMf12, both treatments).</li>\u0000 \u0000 \u0000 <li>HF diet increased mesenteric vascular bed adiposity index (%, HF8: 1.7±0.1 vs C8: 0.9±0.04 and HF12: 1.8±0.1 vs C12: 0.8±0.1, <i>P</i><.001); systolic blood pressure (SBP, mm Hg, HF8: 145±6 vs C8: 118±4, <i>P</i><.01 and HF12: 151±1 vs C12: 121±3, <i>P</i><.001). We found a positive correlation between these two parameters. Moreover HF diet increased the release of vasoconstrictor prostanoids such as thromboxane (TX) B<sub>2</sub> (ng PR/mg of tissue, HF8: 117±6 vs C8: 66±2 and HF12: 123±6 vs C12: 62±5, <i>P</i><.001) and prostaglandin (PG) F<sub>2α</sub> (ng/mg, HF8: 153±9 vs C8: 88±3 and HF12: 160±11 vs C12: 83±5, <i>P</i><.001). We also found that this increase in the release of vasoconstrictor prostanoids positively correlates with the elevation of SBP. In addition, HF diet increases the release of PGE<sub>2</sub> and decreases the prostacyclin (PGI<sub>2</sub>)/TXA<sub>2</sub> release ratio at 8 and 12 weeks of treatment compared to control groups.</li>\u0000 \u0000 \u0000 <li>In the HFMf group, metformin treatment prevented all these increases in mesenteric vascular bed adiposity index (%, HFMf8: 1.3±0.2 vs HF8 and HFMf12: 1.3±0.1 vs HF12, <i>P</i><.05); SBP (mm Hg, HFMf8: 127±2 vs HF8 and HFMf12: 132±1 vs HF12, <i>P</i><.001); TXB<sub>2</sub> release (ng PR/mg of tissue, HFMf8: 65±12 vs HF8, <i>P</i><.05 and HFMf12: 53±3 vs HF12, <i>P</i><.001) and PGF<sub>2</sub>α (ng PR/mg of tissue, HFMf8: 99±13 vs HF8, <i>P</i><.01 and HFMf12: 77±8 vs HF12, <i>P</i><.001). Meanwhile metformin prevented the increment in PGE<sub>2</sub> r","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/aap.12057","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35094716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Epoxyeicosatrienoic acids (EETs) are endogenous ligands that undergo hydrolysis by soluble epoxide hydrolase (sEH). The responses of 11, 12-EET in comparison with other vasodilator agonists including carbachol and sodium nitroprusside (SNP) were investigated. The effect of 1-cyclohexyl-3-dodecyl urea (CDU), a sEH, was tested on the vasodilator effect induced by 11, 12-EET in the perfused mesenteric beds isolated from normo-glycaemic and type-1 STZ-diabetic rats.
In the perfused mesenteric beds of control and diabetic animals, 11, 12-EET produced vasodilation in a dose-dependent manner. The vasodilator response induced by 11, 12-EET was significantly decreased in tissues obtained from diabetic animals, but this was significantly corrected through inhibition of sEH.
The effects of nitric oxide synthase inhibitor, cyclo-oxygenase inhibitor, specific potassium channel inhibitors, soluble guanylyl cyclase inhibitor and transient receptor potential channel V4 inhibitor, on vasodilator response to 11, 12-EET were investigated.
In tissues isolated from control animals, vasodilator responses to 11, 12-EET were not inhibited by acute incubation with l-NAME, l-NAME with indomethacin, glibenclamide, iberiotoxin, charybdotoxin, apamin or ODQ.
Incubation with the transient receptor potential channel V4 inhibitor ruthenium red caused significantly reduced vasodilator responses induced by 11, 12-EET.
In conclusion, results from this study indicate that 11, 12-EET has a vasodilator effect in the perfused mesenteric bed, partly through activation of vanilloid receptor. A strategy to elevate the levels of EETs may have a significant impact in correcting microvascular abnormality associated with diabetes.
{"title":"11,12-Epoxyeicosatrienoic acid induces vasodilator response in the rat perfused mesenteric vasculature","authors":"S. M. Bihzad, M. H. M. Yousif","doi":"10.1111/aap.12052","DOIUrl":"10.1111/aap.12052","url":null,"abstract":"<div>\u0000 \u0000 <p>\u0000 \u0000 </p><ol>\u0000 \u0000 \u0000 <li>Epoxyeicosatrienoic acids (EETs) are endogenous ligands that undergo hydrolysis by soluble epoxide hydrolase (sEH). The responses of 11, 12-EET in comparison with other vasodilator agonists including carbachol and sodium nitroprusside (SNP) were investigated. The effect of 1-cyclohexyl-3-dodecyl urea (CDU), a sEH, was tested on the vasodilator effect induced by 11, 12-EET in the perfused mesenteric beds isolated from normo-glycaemic and type-1 STZ-diabetic rats.</li>\u0000 \u0000 \u0000 <li>In the perfused mesenteric beds of control and diabetic animals, 11, 12-EET produced vasodilation in a dose-dependent manner. The vasodilator response induced by 11, 12-EET was significantly decreased in tissues obtained from diabetic animals, but this was significantly corrected through inhibition of sEH.</li>\u0000 \u0000 \u0000 <li>The effects of nitric oxide synthase inhibitor, cyclo-oxygenase inhibitor, specific potassium channel inhibitors, soluble guanylyl cyclase inhibitor and transient receptor potential channel V4 inhibitor, on vasodilator response to 11, 12-EET were investigated.</li>\u0000 \u0000 \u0000 <li>In tissues isolated from control animals, vasodilator responses to 11, 12-EET were not inhibited by acute incubation with <span>l</span>-NAME, <span>l</span>-NAME with indomethacin, glibenclamide, iberiotoxin, charybdotoxin, apamin or ODQ.</li>\u0000 \u0000 \u0000 <li>Incubation with the transient receptor potential channel V4 inhibitor ruthenium red caused significantly reduced vasodilator responses induced by 11, 12-EET.</li>\u0000 \u0000 \u0000 <li>In conclusion, results from this study indicate that 11, 12-EET has a vasodilator effect in the perfused mesenteric bed, partly through activation of vanilloid receptor. A strategy to elevate the levels of EETs may have a significant impact in correcting microvascular abnormality associated with diabetes.</li>\u0000 </ol>\u0000 \u0000 </div>","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/aap.12052","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34846119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Altered renal adrenergic responses have been recognized as pathophysiological responses to high salt intake. This study aims to investigate the influence of 6 weeks of high salt diet on α1A-adrenoceptor regulation of renal tubular antinatriuretic and antidiuretic response in normal Wistar Kyoto rats.
To achieve the above objective, antinatriuretic and antidiuretic response to phenylephrine was measured in the absence and presence of 5-methylurapidil (5-MeU) using the inulin clearance method. Systemic mean arterial blood pressure and renal haemodynamics were also measured simultaneously.
Six weeks of high salt intake in Wistar-Kyoto (WKY) rats did not bring any significant increase in mean arterial blood pressure. WKY rat on high salt diet (WKYHNa) showed an exaggerated increase in absolute and fractional sodium excretion. There was a significant involvement of α1A-adrenoceptor in carrying out renal tubular antinatriuretic and antidiuretic response in Wistar Kyoto rats on normal sodium diet (WKYNNa). However, α1A-adrenoceptor played a minimal role in handling the tubular reabsorptive response in WKY rats on high salt diet.
{"title":"Antidiuretic and antinatriuretic response to high salt load in normotensive Wistar-Kyoto rats: Role of alpha-1A-adrenoreceptors","authors":"R. N. Kazi, M. A. Sattar, E. J. Johns","doi":"10.1111/aap.12053","DOIUrl":"10.1111/aap.12053","url":null,"abstract":"<div>\u0000 \u0000 <p>\u0000 \u0000 </p><ol>\u0000 \u0000 \u0000 <li>Altered renal adrenergic responses have been recognized as pathophysiological responses to high salt intake. This study aims to investigate the influence of 6 weeks of high salt diet on α<sub>1A</sub>-adrenoceptor regulation of renal tubular antinatriuretic and antidiuretic response in normal Wistar Kyoto rats.</li>\u0000 \u0000 \u0000 <li>To achieve the above objective, antinatriuretic and antidiuretic response to phenylephrine was measured in the absence and presence of 5-methylurapidil (5-MeU) using the inulin clearance method. Systemic mean arterial blood pressure and renal haemodynamics were also measured simultaneously.</li>\u0000 \u0000 \u0000 <li>Six weeks of high salt intake in Wistar-Kyoto (WKY) rats did not bring any significant increase in mean arterial blood pressure. WKY rat on high salt diet (WKYHNa) showed an exaggerated increase in absolute and fractional sodium excretion. There was a significant involvement of α<sub>1A</sub>-adrenoceptor in carrying out renal tubular antinatriuretic and antidiuretic response in Wistar Kyoto rats on normal sodium diet (WKYNNa). However, α<sub>1A</sub>-adrenoceptor played a minimal role in handling the tubular reabsorptive response in WKY rats on high salt diet.</li>\u0000 </ol>\u0000 \u0000 </div>","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/aap.12053","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34846118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Autonomic & Autacoid Pharmacology 2016: The year in review","authors":"P. E. Penson","doi":"10.1111/aap.12051","DOIUrl":"10.1111/aap.12051","url":null,"abstract":"","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/aap.12051","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85509230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
J.Y. Al-Hashel, D. Youssry, H.M. Rashaed, T. Shamov, R.T. Rousseff
Objective assessment of the effect of botulinum toxin A (BT) treatment in primary palmar hyperhidrosis (PH) is attempted by different methods.
We decided to use for this purpose sympathetic skin responses evoked by train of stimuli (TSSR).
Twenty patients with severe PH (five female, median age 24, range 18-36) were examined regularly over 3 months after receiving 50 UI BT in each palm. TSSR were recorded from the palms after sensory stimulation by a train of three supramaximal electric pulses 3 millisecond apart. Results were compared to longitudinally studied TSSR of 20 healthy sex- and age-matched control subjects.
All hyperhidrosis patients reported excellent improvement. TSSR amplitudes decreased at week 1 (mean 54% range 48%-67%) and over the following months in a clinically significant trend (slope R=−.82, P<.0001). TSSR in controls changed insignificantly (±13% from the baseline). The difference between patients and controls was highly significant at any time point (P<.001).
This study suggests that TSSR may help in assessment of treatments in PH. It confirms objectively the efficacy of BT in PH.
{"title":"Botulinum toxin A for palmar hyperhidrosis: assessment with sympathetic skin responses evoked by train of stimuli","authors":"J.Y. Al-Hashel, D. Youssry, H.M. Rashaed, T. Shamov, R.T. Rousseff","doi":"10.1111/aap.12050","DOIUrl":"10.1111/aap.12050","url":null,"abstract":"<div>\u0000 \u0000 <p>\u0000 \u0000 </p><ol>\u0000 \u0000 \u0000 <li>Objective assessment of the effect of botulinum toxin A (BT) treatment in primary palmar hyperhidrosis (PH) is attempted by different methods.</li>\u0000 \u0000 \u0000 <li>We decided to use for this purpose sympathetic skin responses evoked by train of stimuli (TSSR).</li>\u0000 \u0000 \u0000 <li>Twenty patients with severe PH (five female, median age 24, range 18-36) were examined regularly over 3 months after receiving 50 UI BT in each palm. TSSR were recorded from the palms after sensory stimulation by a train of three supramaximal electric pulses 3 millisecond apart. Results were compared to longitudinally studied TSSR of 20 healthy sex- and age-matched control subjects.</li>\u0000 \u0000 \u0000 <li>All hyperhidrosis patients reported excellent improvement. TSSR amplitudes decreased at week 1 (mean 54% range 48%-67%) and over the following months in a clinically significant trend (slope <i>R</i>=−.82, <i>P</i><.0001). TSSR in controls changed insignificantly (±13% from the baseline). The difference between patients and controls was highly significant at any time point (<i>P</i><.001).</li>\u0000 \u0000 \u0000 <li>This study suggests that TSSR may help in assessment of treatments in PH. It confirms objectively the efficacy of BT in PH.</li>\u0000 </ol>\u0000 \u0000 </div>","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/aap.12050","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85862923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In a rat model, the baroreceptor reflex can be assessed by graded infusions of either phenylephrine or sodium nitroprusside with continuous hemodynamic monitoring.
Microinjection of the cholinergic agonist carbachol (CCh) into the posterior hypothalamic nucleus (PHN) evokes an increase in mean arterial pressure and a change in heart rate. Lower doses of CCh evoke only tachycardia, whereas middle and higher doses evoke a biphasic change in heart rate of tachycardia followed by bradycardia.
The bradycardia following the microinjection of CCh into the PHN can be attenuated by the previous administration of the vasopressin V1 receptor antagonist [d(CH2)5Tyr(Me)] arginine vasopressin (AVPX).
Circulating arginine vasopressin (AVP) has been shown to increase the sensitivity of the baroreceptor reflex by stimulating vasopressin V1 receptors in the area postrema.
The attenuation by AVPX of the bradycardia that results following the high doses of CCh suggests that AVP is released into the circulation following stimulation of cholinergic systems within the PHN.
Thus, microinjection of a high dose of CCh (11 nmol) into the PHN alters the sensitivity of the baroreceptor reflex by increasing peripheral levels of AVP.
{"title":"Increase in sensitivity of the baroreceptor reflex following microinjection of carbachol into the posterior hypothalamic nucleus of awake rats","authors":"C. R. Newey, J. R. Martin","doi":"10.1111/aap.12041","DOIUrl":"10.1111/aap.12041","url":null,"abstract":"<div>\u0000 \u0000 <p>\u0000 \u0000 </p><ol>\u0000 \u0000 \u0000 <li>In a rat model, the baroreceptor reflex can be assessed by graded infusions of either phenylephrine or sodium nitroprusside with continuous hemodynamic monitoring.</li>\u0000 \u0000 \u0000 <li>Microinjection of the cholinergic agonist carbachol (CCh) into the posterior hypothalamic nucleus (PHN) evokes an increase in mean arterial pressure and a change in heart rate. Lower doses of CCh evoke only tachycardia, whereas middle and higher doses evoke a biphasic change in heart rate of tachycardia followed by bradycardia.</li>\u0000 \u0000 \u0000 <li>The bradycardia following the microinjection of CCh into the PHN can be attenuated by the previous administration of the vasopressin V<sub>1</sub> receptor antagonist [d(CH<sub>2</sub>)<sub>5</sub>Tyr(Me)] arginine vasopressin (AVPX).</li>\u0000 \u0000 \u0000 <li>Circulating arginine vasopressin (AVP) has been shown to increase the sensitivity of the baroreceptor reflex by stimulating vasopressin V<sub>1</sub> receptors in the area postrema.</li>\u0000 \u0000 \u0000 <li>The attenuation by AVPX of the bradycardia that results following the high doses of CCh suggests that AVP is released into the circulation following stimulation of cholinergic systems within the PHN.</li>\u0000 \u0000 \u0000 <li>Thus, microinjection of a high dose of CCh (11 nmol) into the PHN alters the sensitivity of the baroreceptor reflex by increasing peripheral levels of AVP.</li>\u0000 </ol>\u0000 \u0000 </div>","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/aap.12041","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34331042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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