Pub Date : 1982-08-01DOI: 10.7600/JSPFSM1949.31.258
H. Tanaka, M. Yanase, K. Kanosue, T. Nakayama
Rats exercised on a treadmill at daytime lows and nighttime highs of circadian change in body temperature at two different work intensities [40 and 60% of maximal oxygen uptake (VO2max)] with the ambient temperature (Ta) at 24 degrees C. Immediately before exercise at 60% VO2max, rectal temperature (Tre) was 0.7 degrees C higher at night than during the day. During the exercise, Tre rose more during the day than at night, and Tre at the end of exercise was the same in the day as at night. Threshold Tre for tail vasodilation did not differ between day and night. Similar tendencies of Tre change and tail vasomotor response were observed at a work intensity of 40% VO2max, except that the rise in Tre was smaller than at the higher work intensity. On the other hand, threshold Tre for tail vasodilation spontaneously occurring in resting rats in a warm environment (Ta of 28 degrees C) was 0.7 degrees C higher at night than during the day. In conclusion, exercise in rats attenuates the differences in deep body temperature and threshold Tre for tail vasodilation seen between day and night.
{"title":"Circadian variation of thermoregulatory responses during exercise in rats.","authors":"H. Tanaka, M. Yanase, K. Kanosue, T. Nakayama","doi":"10.7600/JSPFSM1949.31.258","DOIUrl":"https://doi.org/10.7600/JSPFSM1949.31.258","url":null,"abstract":"Rats exercised on a treadmill at daytime lows and nighttime highs of circadian change in body temperature at two different work intensities [40 and 60% of maximal oxygen uptake (VO2max)] with the ambient temperature (Ta) at 24 degrees C. Immediately before exercise at 60% VO2max, rectal temperature (Tre) was 0.7 degrees C higher at night than during the day. During the exercise, Tre rose more during the day than at night, and Tre at the end of exercise was the same in the day as at night. Threshold Tre for tail vasodilation did not differ between day and night. Similar tendencies of Tre change and tail vasomotor response were observed at a work intensity of 40% VO2max, except that the rise in Tre was smaller than at the higher work intensity. On the other hand, threshold Tre for tail vasodilation spontaneously occurring in resting rats in a warm environment (Ta of 28 degrees C) was 0.7 degrees C higher at night than during the day. In conclusion, exercise in rats attenuates the differences in deep body temperature and threshold Tre for tail vasodilation seen between day and night.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1982-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125851404","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}
Pub Date : 1982-07-01DOI: 10.1152/AJPCELL.1982.243.1.C1
M. Hayward, Martin L. Brock, David J Shapiro
Administration of estradiol 17 beta [estra-1,3,5(10)-triene-3,17-beta-diol] to male Xenopus laevis induces the massive synthesis by the liver of the egg yolk precursor phospholipoglycoprotein, vitellogenin, and its cognate mRNAs. Restimulation of male X. laevis that have been previously induced to synthesize vitellogenin mRNA but are inactive in vitellogenin mRNA synthesis at the time of restimulation with estrogen results in more rapid accumulation of vitellogenin mRNA and more efficient transcription of the vitellogenin genes than occurs following primary estrogen stimulation. The estrogen receptor system that mediates estrogen action in this organism exhibits several unusual properties. The cytoplasm of unstimulated liver cells contains high levels of a middle-affinity estrogen-specific binding protein and little if any estrogen receptor. The properties of the estrogen binding protein are consistent with a role in protecting estradiol 17 beta against metabolism, as a fraction of cytoplasmic estradiol 17 beta is not subject to rapid metabolism. In addition, similar binding activities are found in all Xenopus tissues surveyed that respond to steroid hormones. The induction of nuclear estrogen receptor is coincident with the onset of vitellogenin mRNA accumulation. However, an increased level of estrogen receptor is not responsible for the elevated rate of vitellogenin gene transcription observed following restimulation with estrogen.
{"title":"The role of estrogen receptor in Xenopus laevis vitellogenin gene expression.","authors":"M. Hayward, Martin L. Brock, David J Shapiro","doi":"10.1152/AJPCELL.1982.243.1.C1","DOIUrl":"https://doi.org/10.1152/AJPCELL.1982.243.1.C1","url":null,"abstract":"Administration of estradiol 17 beta [estra-1,3,5(10)-triene-3,17-beta-diol] to male Xenopus laevis induces the massive synthesis by the liver of the egg yolk precursor phospholipoglycoprotein, vitellogenin, and its cognate mRNAs. Restimulation of male X. laevis that have been previously induced to synthesize vitellogenin mRNA but are inactive in vitellogenin mRNA synthesis at the time of restimulation with estrogen results in more rapid accumulation of vitellogenin mRNA and more efficient transcription of the vitellogenin genes than occurs following primary estrogen stimulation. The estrogen receptor system that mediates estrogen action in this organism exhibits several unusual properties. The cytoplasm of unstimulated liver cells contains high levels of a middle-affinity estrogen-specific binding protein and little if any estrogen receptor. The properties of the estrogen binding protein are consistent with a role in protecting estradiol 17 beta against metabolism, as a fraction of cytoplasmic estradiol 17 beta is not subject to rapid metabolism. In addition, similar binding activities are found in all Xenopus tissues surveyed that respond to steroid hormones. The induction of nuclear estrogen receptor is coincident with the onset of vitellogenin mRNA accumulation. However, an increased level of estrogen receptor is not responsible for the elevated rate of vitellogenin gene transcription observed following restimulation with estrogen.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"71 5 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1982-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130709675","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}
Pub Date : 1982-02-01DOI: 10.1249/00005768-198202000-00339
E. Noble, C. Ianuzzo
Muscle homogenates representing slow-twitch oxidative, fast-twitch oxidative-glycolytic, fast-twitch glycolytic, and mixed fiber types were prepared from normal, diabetic, and insulin-treated diabetic rats. Diabetes was induced by injection of 80 mg . kg-1 of streptozotocin. The activities of citrate synthase, succinate dehydrogenase, and 3-hydroxyacyl-CoA dehydrogenase were employed as markers of oxidative potential, whereas phosphorylase, hexokinase, and phosphofructokinase activities were used as an indication of glycolytic capacity. Diabetes was associated with a general decrement in the activity of oxidative marker enzymes for all fiber types except the fast-twitch glycolytic fiber. In contrast, the fast-twitch glycolytic fibers demonstrated the greatest decline in glycolytic enzymatic activity. Insulin-treated animals, either trained or untrained, exhibited enzyme activities similar to their normal counterparts. Exercise training of diabetic rats mimicked the effect of insulin treatment and caused a near normalization of the activity of the marker enzymes. These findings suggest that the enzymatic potential of all skeletal muscle fiber types of diabetic rats may be normalized by exercise training even in the absence of significant amounts of insulin.
{"title":"Influence of training on skeletal muscle enzymatic adaptations in normal and diabetic rats.","authors":"E. Noble, C. Ianuzzo","doi":"10.1249/00005768-198202000-00339","DOIUrl":"https://doi.org/10.1249/00005768-198202000-00339","url":null,"abstract":"Muscle homogenates representing slow-twitch oxidative, fast-twitch oxidative-glycolytic, fast-twitch glycolytic, and mixed fiber types were prepared from normal, diabetic, and insulin-treated diabetic rats. Diabetes was induced by injection of 80 mg . kg-1 of streptozotocin. The activities of citrate synthase, succinate dehydrogenase, and 3-hydroxyacyl-CoA dehydrogenase were employed as markers of oxidative potential, whereas phosphorylase, hexokinase, and phosphofructokinase activities were used as an indication of glycolytic capacity. Diabetes was associated with a general decrement in the activity of oxidative marker enzymes for all fiber types except the fast-twitch glycolytic fiber. In contrast, the fast-twitch glycolytic fibers demonstrated the greatest decline in glycolytic enzymatic activity. Insulin-treated animals, either trained or untrained, exhibited enzyme activities similar to their normal counterparts. Exercise training of diabetic rats mimicked the effect of insulin treatment and caused a near normalization of the activity of the marker enzymes. These findings suggest that the enzymatic potential of all skeletal muscle fiber types of diabetic rats may be normalized by exercise training even in the absence of significant amounts of insulin.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"243 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1982-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132122357","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}
Pub Date : 1981-11-01DOI: 10.1152/AJPREGU.1981.241.5.R422-R
M. Sayeed, R. Adler, I. Chaudry, A. Baue
In this study we investigated in vivo changes in hepatic cellular electrolytes and resting transmembrane potentials (Em) during hemorrhagic shock. Hepatic Na-K transport and cell volume regulation were assessed in vitro. Rats were bled and the ensuing hypotension (40 mmHg) was maintained by returning 25-30% (intermediate-shock, IS) or 55-60% (late-shock, LS) of the shed blood. We resuscitated IS rats by reinfusion of all of the remaining shed blood and Ringer's lactate solution. Hepatic cellular Na and Cl increased and K decreased progressively with shock. Resuscitation of IS rats restored cell K and Cl but not Na to preshock levels. Em decreased from the control average value of -40 (mV) to -31 in IS and -19 in LS. Em was partially restored (-36 mV) after resuscitation. We evaluated changes in relative membrane permeability to Na and K (PNa/PK) with shock by assuming Em either to be a Na-K exchange diffusion potential or due to an unequally coupled movement of Na and K. These evaluations show a lack of effect of shock (IS, with or without resuscitation) on PNa/PK. Our observations are compatible with failure of an electrogenic Na pump in shock. This may be related to loss of hepatic cell volume regulation in shock.
{"title":"Effect of hemorrhagic shock on hepatic transmembrane potentials and intracellular electrolytes, in vivo.","authors":"M. Sayeed, R. Adler, I. Chaudry, A. Baue","doi":"10.1152/AJPREGU.1981.241.5.R422-R","DOIUrl":"https://doi.org/10.1152/AJPREGU.1981.241.5.R422-R","url":null,"abstract":"In this study we investigated in vivo changes in hepatic cellular electrolytes and resting transmembrane potentials (Em) during hemorrhagic shock. Hepatic Na-K transport and cell volume regulation were assessed in vitro. Rats were bled and the ensuing hypotension (40 mmHg) was maintained by returning 25-30% (intermediate-shock, IS) or 55-60% (late-shock, LS) of the shed blood. We resuscitated IS rats by reinfusion of all of the remaining shed blood and Ringer's lactate solution. Hepatic cellular Na and Cl increased and K decreased progressively with shock. Resuscitation of IS rats restored cell K and Cl but not Na to preshock levels. Em decreased from the control average value of -40 (mV) to -31 in IS and -19 in LS. Em was partially restored (-36 mV) after resuscitation. We evaluated changes in relative membrane permeability to Na and K (PNa/PK) with shock by assuming Em either to be a Na-K exchange diffusion potential or due to an unequally coupled movement of Na and K. These evaluations show a lack of effect of shock (IS, with or without resuscitation) on PNa/PK. Our observations are compatible with failure of an electrogenic Na pump in shock. This may be related to loss of hepatic cell volume regulation in shock.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"51 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1981-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124596668","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}
Pub Date : 1981-02-01DOI: 10.1007/978-3-642-68147-9_13
B. Rennick
{"title":"Renal tubule transport of organic cations.","authors":"B. Rennick","doi":"10.1007/978-3-642-68147-9_13","DOIUrl":"https://doi.org/10.1007/978-3-642-68147-9_13","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"24 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1981-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129575846","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}
Pub Date : 1980-12-01DOI: 10.1152/AJPGI.1981.240.6.G479-R
U. Gafter, J. Kraut, D. B. Lee, V. Silis, M. Walling, K. Kurokawa, M. Haussler, J. Coburn
To investigate the effect of metabolic acidosis on intestinal calcium (Ca) and phosphorus (P) absorption and vitamin D metabolism, metabolic balance studies and in vitro gut sac uptake of 45Ca and [32P]phosphate were performed in rats maintained on low-Ca and moderately low-P diet and fed NH4Cl for 3 or 9 days and pair-fed controls. Plasma 1,25(OH)2D concentration was measured in the rats fed NH4Cl for 9 days and their controls. Net Ca and P absorption was 87-92% in the acidotic rats and did not differ from control. Moreover, gut sac uptakes of 45Ca and [32P]phosphate were not different from control. Plasma 1,25(OH)2D was higher in the ammonium chloride-fed rats than in controls (213 +/- 44 vs. 110 +/- 12 pg/ml), and serum P was lower in the acidotic animals (4.6 +/- 0.7 vs. 7.6 +/- 0.3 mg/dl). These data indicate that metabolic acidosis does not depress the augmented intestinal absorption of calcium and phosphorus noted during their dietary deprivation nor reduce the plasma level of 1,25(OH)2D.
为了研究代谢性酸中毒对肠道钙(Ca)、磷(P)吸收和维生素D代谢的影响，研究了低钙、中低磷饲粮饲喂NH4Cl 3天或9天的大鼠和两两饲养的对照组的代谢平衡和体外45Ca和[32P]磷酸盐的肠囊摄取。测定各组大鼠血浆1,25(OH)2D浓度。酸性大鼠净钙、磷吸收率为87% ~ 92%，与对照组无显著差异。此外，肠囊对45Ca和[32P]磷酸盐的吸收与对照组无显著差异。氯化铵喂养大鼠的血浆1,25(OH)2D高于对照组(213 +/- 44 vs 110 +/- 12 pg/ml)，而酸性动物的血清P较低(4.6 +/- 0.7 vs 7.6 +/- 0.3 mg/dl)。这些数据表明，代谢性酸中毒不会抑制饮食剥夺期间肠道钙和磷吸收的增加，也不会降低血浆中125 (OH)2D的水平。
{"title":"Effect of metabolic acidosis in intestinal absorption of calcium and phosphorus.","authors":"U. Gafter, J. Kraut, D. B. Lee, V. Silis, M. Walling, K. Kurokawa, M. Haussler, J. Coburn","doi":"10.1152/AJPGI.1981.240.6.G479-R","DOIUrl":"https://doi.org/10.1152/AJPGI.1981.240.6.G479-R","url":null,"abstract":"To investigate the effect of metabolic acidosis on intestinal calcium (Ca) and phosphorus (P) absorption and vitamin D metabolism, metabolic balance studies and in vitro gut sac uptake of 45Ca and [32P]phosphate were performed in rats maintained on low-Ca and moderately low-P diet and fed NH4Cl for 3 or 9 days and pair-fed controls. Plasma 1,25(OH)2D concentration was measured in the rats fed NH4Cl for 9 days and their controls. Net Ca and P absorption was 87-92% in the acidotic rats and did not differ from control. Moreover, gut sac uptakes of 45Ca and [32P]phosphate were not different from control. Plasma 1,25(OH)2D was higher in the ammonium chloride-fed rats than in controls (213 +/- 44 vs. 110 +/- 12 pg/ml), and serum P was lower in the acidotic animals (4.6 +/- 0.7 vs. 7.6 +/- 0.3 mg/dl). These data indicate that metabolic acidosis does not depress the augmented intestinal absorption of calcium and phosphorus noted during their dietary deprivation nor reduce the plasma level of 1,25(OH)2D.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"160 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1980-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"120851045","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}
Pub Date : 1980-07-01DOI: 10.1097/00006254-198007000-00017
G. W. Molnar
The unpredictability of hot flashes makes their investigation difficult. A method for continuous monitoring of subjective arousals and their objective correlates is here described and illustrated with results from one subject. Temperatures of special interest with respect to hot flashes--toe, cheek, vagina, and air--were recorded on a protable magnetic tape during routine living at home. The subject signaled the "on" and "off" of each perceived flash with a hand switch and also entered information in a notebook. She signaled 63 flashes on 5 days, during which the cheek and toe temperatures showed transient increments. Some of the flashes were labeled uncertain in the notebook. The subject also had 23 episodes of these temperature increments that she did not identify by signals as flashes. In these episodes, therefore, the mechanism of consciousness was not activated. Perceptions that coincided with transient temperature increments thus ranged as follows: subconscious, uncertain, definite but bearable, mildly distressful, and strongly distressful. Hence ambulatory monitoring can provide objective evidence of transient activation of the hypothalamic heat loss mechanism, whether perceived or not.
{"title":"Investigation of hot flashes by ambulatory monitoring.","authors":"G. W. Molnar","doi":"10.1097/00006254-198007000-00017","DOIUrl":"https://doi.org/10.1097/00006254-198007000-00017","url":null,"abstract":"The unpredictability of hot flashes makes their investigation difficult. A method for continuous monitoring of subjective arousals and their objective correlates is here described and illustrated with results from one subject. Temperatures of special interest with respect to hot flashes--toe, cheek, vagina, and air--were recorded on a protable magnetic tape during routine living at home. The subject signaled the \"on\" and \"off\" of each perceived flash with a hand switch and also entered information in a notebook. She signaled 63 flashes on 5 days, during which the cheek and toe temperatures showed transient increments. Some of the flashes were labeled uncertain in the notebook. The subject also had 23 episodes of these temperature increments that she did not identify by signals as flashes. In these episodes, therefore, the mechanism of consciousness was not activated. Perceptions that coincided with transient temperature increments thus ranged as follows: subconscious, uncertain, definite but bearable, mildly distressful, and strongly distressful. Hence ambulatory monitoring can provide objective evidence of transient activation of the hypothalamic heat loss mechanism, whether perceived or not.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"57 11","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1980-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"120925587","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}
Pub Date : 1980-04-01DOI: 10.1097/00003246-198004000-00188
S. Schwartz, R. Frantz, W. Shoemaker
Sequential cardiorespiratory measurements were made in 30 mongrel dogs during controlled hypovolemia, normovolemic anemia, and hypoxia. The responses to each of these three types of O2 deprivation were studied both as a function of time and of the rate of O2 delivery (normalized cardiac output x arterial O2 content). With progressively decreasing O2 delivery, compensations appeared, reached a maximum, and fell before the final circulatory deterioration. O2 extraction increased in each experiment, but there was differences in the hemodynamic responses to the three types of O2 deprivation; e.g., cardiac output increased in the anemic dogs, and there were greater increases in systemic and pulmonary resistances after hemorrhage. The striking finding was that O2 consumption (VO2) remained relatively constant until the preterminal stage. At this time O2 delivery had fallen from about 27 to less than 10 ml . min-1 . kg-1, blood volume was less than 50%, hematocrit was less than 8%, and arterial O2 tension was less than 30 Torr at an average fractional inspired O2 concentration of 8%, for the hypovolemic, anemic, and hypoxic groups, respectively. Then VO2 dropped precipitously and death rapidly occurred. These results suggest that VO2 represents a physiological marker of impending death in the face of progressively diminishing O2 delivery.
{"title":"Sequential hemodynamic and oxygen transport responses in hypovolemia, anemia, and hypoxia.","authors":"S. Schwartz, R. Frantz, W. Shoemaker","doi":"10.1097/00003246-198004000-00188","DOIUrl":"https://doi.org/10.1097/00003246-198004000-00188","url":null,"abstract":"Sequential cardiorespiratory measurements were made in 30 mongrel dogs during controlled hypovolemia, normovolemic anemia, and hypoxia. The responses to each of these three types of O2 deprivation were studied both as a function of time and of the rate of O2 delivery (normalized cardiac output x arterial O2 content). With progressively decreasing O2 delivery, compensations appeared, reached a maximum, and fell before the final circulatory deterioration. O2 extraction increased in each experiment, but there was differences in the hemodynamic responses to the three types of O2 deprivation; e.g., cardiac output increased in the anemic dogs, and there were greater increases in systemic and pulmonary resistances after hemorrhage. The striking finding was that O2 consumption (VO2) remained relatively constant until the preterminal stage. At this time O2 delivery had fallen from about 27 to less than 10 ml . min-1 . kg-1, blood volume was less than 50%, hematocrit was less than 8%, and arterial O2 tension was less than 30 Torr at an average fractional inspired O2 concentration of 8%, for the hypovolemic, anemic, and hypoxic groups, respectively. Then VO2 dropped precipitously and death rapidly occurred. These results suggest that VO2 represents a physiological marker of impending death in the face of progressively diminishing O2 delivery.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"56 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1980-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123474376","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}
Pub Date : 1980-04-01DOI: 10.1016/S0022-5347(17)46112-X
O. Carretero, A. Scicli
{"title":"The renal kallikrein-kinin system.","authors":"O. Carretero, A. Scicli","doi":"10.1016/S0022-5347(17)46112-X","DOIUrl":"https://doi.org/10.1016/S0022-5347(17)46112-X","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"373 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1980-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123409142","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}
Pub Date : 1979-06-01DOI: 10.1097/00006254-198004000-00017
L. Parker, W. Odell
An animal model using dexamethosone-suppressed, castrated dogs was developed to test the hypothesis that a pituitary hormone other than ACTH modulates adrenal androgen (AA) secretion. Plasma samples were obtained every 15 min during infusions of saline, synthetic alpha 1-24 corticotropin, porcine 1-39 corticotropin (ACTH), or bovine pituitary gland extract (PE) in a wide range of doses. Androstenedione (A), dehydroepiandrosterone (DHA), and cortisol (F) were quantified by radioimmunoassay. When the ratio of AA levels was related to those of F, in order to correct for ACTH content in the PE, the slopes of the dose-response curves for corticotropin and PE were different at the 0.01 level. For A the dose-response slope for the PE was 0.18 +/- 0.5 SE, whereas that of ACTH was 0.02 +/- 0.01. For the DHA response the slopes were 0.17 +/- 0.04 for the PE and 0.04 +/- 0.03 for ACTH. Related studies showed no increase in AA levels in response to luteinizing hormone-releasing hormone, bovine growth hormone (GH), bovine prolactin, ovine thyroid-stimulating hormone (TSH), or synthetic aqueous arginine vasopressin (AVP). We conclude that a pituitary factor other than ACTH, prolactin, GH, luteinizing hormone, follicle-stimulating hormone, TSH, or AVP may be responsible for the observed increase in AA concentrations.
{"title":"Evidence for existence of cortical androgen-stimulating hormone.","authors":"L. Parker, W. Odell","doi":"10.1097/00006254-198004000-00017","DOIUrl":"https://doi.org/10.1097/00006254-198004000-00017","url":null,"abstract":"An animal model using dexamethosone-suppressed, castrated dogs was developed to test the hypothesis that a pituitary hormone other than ACTH modulates adrenal androgen (AA) secretion. Plasma samples were obtained every 15 min during infusions of saline, synthetic alpha 1-24 corticotropin, porcine 1-39 corticotropin (ACTH), or bovine pituitary gland extract (PE) in a wide range of doses. Androstenedione (A), dehydroepiandrosterone (DHA), and cortisol (F) were quantified by radioimmunoassay. When the ratio of AA levels was related to those of F, in order to correct for ACTH content in the PE, the slopes of the dose-response curves for corticotropin and PE were different at the 0.01 level. For A the dose-response slope for the PE was 0.18 +/- 0.5 SE, whereas that of ACTH was 0.02 +/- 0.01. For the DHA response the slopes were 0.17 +/- 0.04 for the PE and 0.04 +/- 0.03 for ACTH. Related studies showed no increase in AA levels in response to luteinizing hormone-releasing hormone, bovine growth hormone (GH), bovine prolactin, ovine thyroid-stimulating hormone (TSH), or synthetic aqueous arginine vasopressin (AVP). We conclude that a pituitary factor other than ACTH, prolactin, GH, luteinizing hormone, follicle-stimulating hormone, TSH, or AVP may be responsible for the observed increase in AA concentrations.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"8 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1979-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129010106","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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