Pub Date : 1990-02-01DOI: 10.1016/0735-1097(90)92543-B
N. C. Edwards, A. Sinusas, J. Bergin, D. Watson, M. Ruiz, G. Beller
{"title":"Influence of subendocardial ischemia on transmural myocardial function.","authors":"N. C. Edwards, A. Sinusas, J. Bergin, D. Watson, M. Ruiz, G. Beller","doi":"10.1016/0735-1097(90)92543-B","DOIUrl":"https://doi.org/10.1016/0735-1097(90)92543-B","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"42 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1990-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133208509","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 : 1990-02-01DOI: 10.1016/0735-1097(90)91754-I
J. Lucke, J. Elbeery, T. Koutlas, S. Gall, T. D’amico, G. Maier, J. Rankin, D. Glower
{"title":"Effects of cardiac glycosides on myocardial function and energetics in conscious dogs.","authors":"J. Lucke, J. Elbeery, T. Koutlas, S. Gall, T. D’amico, G. Maier, J. Rankin, D. Glower","doi":"10.1016/0735-1097(90)91754-I","DOIUrl":"https://doi.org/10.1016/0735-1097(90)91754-I","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"38 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1990-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126082410","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 : 1989-07-01DOI: 10.1097/00132586-199004000-00004
J. Levasseur, H. Kontos
We evaluated the effect of general anesthesia induced by 45 mg/kg iv pentobarbital sodium or by 75 mg/kg iv alpha-chloralose plus 500 mg/kg iv urethan on the response of cerebral arterioles to hypercapnia in rabbits equipped with chronically implanted cranial windows for the observation of the cerebral microcirculation. Both types of anesthetic induced approximately comparable anesthesia and depressed the responsiveness to CO2 to an equal extent. There were no changes in resting vessel diameter or in mean arterial blood pressure induced by either anesthetic, but both anesthetics increased end-expiratory PCO2 during room air breathing. The findings show that anesthetics depress the responsiveness of cerebral arterioles to hypercapnia. A decrease in cerebral metabolism and/or direct effects of the anesthetics on cerebral vessels may be involved.
{"title":"Effects of anesthesia on cerebral arteriolar responses to hypercapnia.","authors":"J. Levasseur, H. Kontos","doi":"10.1097/00132586-199004000-00004","DOIUrl":"https://doi.org/10.1097/00132586-199004000-00004","url":null,"abstract":"We evaluated the effect of general anesthesia induced by 45 mg/kg iv pentobarbital sodium or by 75 mg/kg iv alpha-chloralose plus 500 mg/kg iv urethan on the response of cerebral arterioles to hypercapnia in rabbits equipped with chronically implanted cranial windows for the observation of the cerebral microcirculation. Both types of anesthetic induced approximately comparable anesthesia and depressed the responsiveness to CO2 to an equal extent. There were no changes in resting vessel diameter or in mean arterial blood pressure induced by either anesthetic, but both anesthetics increased end-expiratory PCO2 during room air breathing. The findings show that anesthetics depress the responsiveness of cerebral arterioles to hypercapnia. A decrease in cerebral metabolism and/or direct effects of the anesthetics on cerebral vessels may be involved.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"25 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1989-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128901748","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 vitro binding of aldosterone to mineralocorticoid receptors on human mononuclear leukocytes (HML) and its effects on the intracellular sodium and potassium concentrations of HML have already been described. In the present paper this easily accessible human cell model was investigated with regard to the regulation of the cell volume by aldosterone, since the concordant changes of sodium and potassium were expected to be accompanied by water and volume shifts. As determined by the measurement of cell diameter and the planimetric estimation of cell area in photographs, cell volume decreased by approximately 16% when cells were incubated in RPMI-1640 medium without aldosterone added for 1 h at 37 degrees C, a decrease not seen when 1.4 nM aldosterone was added to the incubation medium; the effect was half maximal at a concentration between 0.07 and 0.14 nM. One hundred forty nanomoles canrenone antagonized the action of aldosterone, but cortisol was ineffective. The results indicate concordant changes of intracellular sodium and potassium and cell volume, if studied under the same conditions. These data are the first to demonstrate that aldosterone is a major physiological determinant of lymphocyte volume in isotonic media.
{"title":"Volume regulation of human lymphocytes by aldosterone in isotonic media.","authors":"S. Kuhls, M. Wehling, D. Armanini","doi":"10.1530/acta.0.120s116","DOIUrl":"https://doi.org/10.1530/acta.0.120s116","url":null,"abstract":"In vitro binding of aldosterone to mineralocorticoid receptors on human mononuclear leukocytes (HML) and its effects on the intracellular sodium and potassium concentrations of HML have already been described. In the present paper this easily accessible human cell model was investigated with regard to the regulation of the cell volume by aldosterone, since the concordant changes of sodium and potassium were expected to be accompanied by water and volume shifts. As determined by the measurement of cell diameter and the planimetric estimation of cell area in photographs, cell volume decreased by approximately 16% when cells were incubated in RPMI-1640 medium without aldosterone added for 1 h at 37 degrees C, a decrease not seen when 1.4 nM aldosterone was added to the incubation medium; the effect was half maximal at a concentration between 0.07 and 0.14 nM. One hundred forty nanomoles canrenone antagonized the action of aldosterone, but cortisol was ineffective. The results indicate concordant changes of intracellular sodium and potassium and cell volume, if studied under the same conditions. These data are the first to demonstrate that aldosterone is a major physiological determinant of lymphocyte volume in isotonic media.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"18 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125660511","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 : 1989-05-01DOI: 10.1097/00006254-198905000-00027
P. Boepple, M. Mansfield, K. Link, J. Crawford, J. Crigler, D. Kushner, R. Blizzard, W. Crowley
Forty girls with central precocious puberty (CPP) were studied before and during 1-3 yr of luteinizing hormone-releasing factor (LHRH) agonist (LHRHa) administration to examine the impact of gonadal steroid secretion and its suppression on skeletal growth and maturation. Pubertal growth velocity (GV) was 10.1 +/- 0.7 (SE) cm/yr and, when normalized for chronological age (CA) and bone age (BA), demonstrated that the effects of sex steroids were most profound in patients with the youngest CA and BA. GV decreased significantly to 5.8 +/- 0.3 (n = 40), 4.6 +/- 0.3 (n = 30), and 3.2 +/- 0.6 cm/yr (n = 12) during 3 yr of gonadal suppression and correlated negatively with starting BA. Skeletal maturation was markedly accelerated by premature sex steroid secretion (BA/CA = 1.8 +/- 0.1), was slowed significantly with gonadal suppression (mean delta BA/delta CA less than 1), and also was negatively correlated with the starting BA. Cumulative increases in predicted adult height were observed regardless of starting BA and averaged +2.0 +/- 0.4, +5.2 +/- 0.5, and +6.7 +/- 1.2 cm after 1, 2, and 3 yr of gonadal suppression. The comparable changes in height predictions across all BAs despite highly variable GVs underscore the need for use of developmental (i.e., BA-based) rather than CA-based standards in the analysis of growth during gonadal steroid exposure and suppression in childhood.
{"title":"Impact of sex steroids and their suppression on skeletal growth and maturation.","authors":"P. Boepple, M. Mansfield, K. Link, J. Crawford, J. Crigler, D. Kushner, R. Blizzard, W. Crowley","doi":"10.1097/00006254-198905000-00027","DOIUrl":"https://doi.org/10.1097/00006254-198905000-00027","url":null,"abstract":"Forty girls with central precocious puberty (CPP) were studied before and during 1-3 yr of luteinizing hormone-releasing factor (LHRH) agonist (LHRHa) administration to examine the impact of gonadal steroid secretion and its suppression on skeletal growth and maturation. Pubertal growth velocity (GV) was 10.1 +/- 0.7 (SE) cm/yr and, when normalized for chronological age (CA) and bone age (BA), demonstrated that the effects of sex steroids were most profound in patients with the youngest CA and BA. GV decreased significantly to 5.8 +/- 0.3 (n = 40), 4.6 +/- 0.3 (n = 30), and 3.2 +/- 0.6 cm/yr (n = 12) during 3 yr of gonadal suppression and correlated negatively with starting BA. Skeletal maturation was markedly accelerated by premature sex steroid secretion (BA/CA = 1.8 +/- 0.1), was slowed significantly with gonadal suppression (mean delta BA/delta CA less than 1), and also was negatively correlated with the starting BA. Cumulative increases in predicted adult height were observed regardless of starting BA and averaged +2.0 +/- 0.4, +5.2 +/- 0.5, and +6.7 +/- 1.2 cm after 1, 2, and 3 yr of gonadal suppression. The comparable changes in height predictions across all BAs despite highly variable GVs underscore the need for use of developmental (i.e., BA-based) rather than CA-based standards in the analysis of growth during gonadal steroid exposure and suppression in childhood.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"22 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1989-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127224859","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 : 1989-03-01DOI: 10.1016/0883-9441(89)90050-6
Aleksander S. Popel, Roland N. Pittman, M. Ellsworth
{"title":"Rate of oxygen loss from arterioles is an order of magnitude higher than expected.","authors":"Aleksander S. Popel, Roland N. Pittman, M. Ellsworth","doi":"10.1016/0883-9441(89)90050-6","DOIUrl":"https://doi.org/10.1016/0883-9441(89)90050-6","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"2 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1989-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"120211726","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 : 1988-09-01DOI: 10.1152/AJPREGU.1988.255.3.R373
H. Tenenhouse, A. Klugerman, W. Gurd, M. Lapointe, G. Tannenbaum
The present study was undertaken to examine 1) the effect of phosphate restriction on growth hormone (GH) secretory dynamics in freely moving, chronically cannulated rats and 2) the effect of hypophysectomy on the renal adaptive responses to phosphate deprivation. Phosphate restriction led to an increase in renal brush-border membrane Na+-dependent phosphate transport (2,511 +/- 283 vs. 1,006 +/- 122 pmol.mg protein-1.15 s-1, P less than 0.001) and in the plasma concentration of 1 alpha,25-dihydroxyvitamin D [1,25(OH)2D] (127 +/- 10 vs. 63 +/- 4 pg/ml, P less than 0.001). In contrast, phosphate deprivation had no effect on either amplitude or frequency of spontaneous GH secretory bursts and did not alter pituitary GH concentration. Hypophysectomy led to a decrease in brush-border membrane Na+-dependent phosphate transport (669 +/- 78 vs. 1,006 +/- 122 pmol.mg protein-1. 15 s-1, P less than 0.003) and to a fall in plasma 1,25(OH)2D (42 +/- 9 vs. 63 +/- 4 pg/ml, P less than 0.02). Phosphate restriction of hypophysectomized rats elicited a twofold increase in Na+-dependent phosphate transport (1,312 +/- 106 vs. 669 +/- 78 pmol.mg protein-1.15 s-1, P less than 0.001) but no rise in plasma 1,25(OH)2D. We conclude that the renal adaptive responses to phosphate deprivation are not mediated by specific alterations in pulsatile GH secretion. Moreover, we demonstrate that the adaptive increase in brush-border membrane phosphate transport occurs after hypophysectomy, is not dependent on increased vitamin D hormone production, and is most likely subject to a different regulatory mechanism.
本研究旨在探讨1)限制磷酸盐对自由运动慢性插管大鼠生长激素(GH)分泌动力学的影响，以及2)垂体切除术对肾对磷酸盐剥夺的适应性反应的影响。磷酸盐限制导致肾刷边膜Na+依赖的磷酸盐转运增加(2,511 +/- 283比1,006 +/- 122 pmol)。血浆中1 α，25-二羟基维生素D [1,25(OH)2D]的浓度(127 +/- 10比63 +/- 4 pg/ml, P < 0.001)。相比之下，磷酸盐剥夺对自发性生长激素分泌爆发的幅度和频率没有影响，也没有改变垂体生长激素浓度。垂体切除术导致刷边膜Na+依赖的磷酸盐运输减少(669 +/- 78比1,006 +/- 122 pmol)。毫克蛋白1。15 s-1, P < 0.003)，血浆中1,25(OH)2D下降(42 +/- 9 vs. 63 +/- 4 pg/ml, P < 0.02)。去垂体的大鼠的磷酸盐限制引起Na+依赖的磷酸盐运输增加两倍(1,312 +/- 106 vs. 669 +/- 78 pmol)。1.15 s-1, P < 0.001)，血浆1.25 (OH)2D无升高。我们得出结论，肾脏对磷酸盐剥夺的适应性反应不是由搏动GH分泌的特异性改变介导的。此外，我们证明，在垂体切除后，刷边膜磷酸盐转运的适应性增加并不依赖于维生素D激素产生的增加，而且很可能受到不同的调节机制的影响。
{"title":"Pituitary involvement in renal adaptation to phosphate deprivation.","authors":"H. Tenenhouse, A. Klugerman, W. Gurd, M. Lapointe, G. Tannenbaum","doi":"10.1152/AJPREGU.1988.255.3.R373","DOIUrl":"https://doi.org/10.1152/AJPREGU.1988.255.3.R373","url":null,"abstract":"The present study was undertaken to examine 1) the effect of phosphate restriction on growth hormone (GH) secretory dynamics in freely moving, chronically cannulated rats and 2) the effect of hypophysectomy on the renal adaptive responses to phosphate deprivation. Phosphate restriction led to an increase in renal brush-border membrane Na+-dependent phosphate transport (2,511 +/- 283 vs. 1,006 +/- 122 pmol.mg protein-1.15 s-1, P less than 0.001) and in the plasma concentration of 1 alpha,25-dihydroxyvitamin D [1,25(OH)2D] (127 +/- 10 vs. 63 +/- 4 pg/ml, P less than 0.001). In contrast, phosphate deprivation had no effect on either amplitude or frequency of spontaneous GH secretory bursts and did not alter pituitary GH concentration. Hypophysectomy led to a decrease in brush-border membrane Na+-dependent phosphate transport (669 +/- 78 vs. 1,006 +/- 122 pmol.mg protein-1. 15 s-1, P less than 0.003) and to a fall in plasma 1,25(OH)2D (42 +/- 9 vs. 63 +/- 4 pg/ml, P less than 0.02). Phosphate restriction of hypophysectomized rats elicited a twofold increase in Na+-dependent phosphate transport (1,312 +/- 106 vs. 669 +/- 78 pmol.mg protein-1.15 s-1, P less than 0.001) but no rise in plasma 1,25(OH)2D. We conclude that the renal adaptive responses to phosphate deprivation are not mediated by specific alterations in pulsatile GH secretion. Moreover, we demonstrate that the adaptive increase in brush-border membrane phosphate transport occurs after hypophysectomy, is not dependent on increased vitamin D hormone production, and is most likely subject to a different regulatory mechanism.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"51 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1988-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115973900","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 : 1988-09-01DOI: 10.1016/0300-9572(89)90123-8
M. Mazzoni, P. Borgstrom, K. Arfors, Marcos Intaglietta
{"title":"Dynamic fluid redistribution in hyperosmotic resuscitation of hypovolemic hemorrhage.","authors":"M. Mazzoni, P. Borgstrom, K. Arfors, Marcos Intaglietta","doi":"10.1016/0300-9572(89)90123-8","DOIUrl":"https://doi.org/10.1016/0300-9572(89)90123-8","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"72 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1988-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127476252","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 : 1988-06-01DOI: 10.1016/S0022-5347(17)40957-8
F. Tajima, S. Sagawa, J. Iwamoto, K. Miki, J. Claybaugh, K. Shiraki
{"title":"Renal and endocrine responses in the elderly during head-out water immersion.","authors":"F. Tajima, S. Sagawa, J. Iwamoto, K. Miki, J. Claybaugh, K. Shiraki","doi":"10.1016/S0022-5347(17)40957-8","DOIUrl":"https://doi.org/10.1016/S0022-5347(17)40957-8","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"8 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1988-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128680656","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 : 1987-04-01DOI: 10.1097/00132586-198704000-00041
V. Addonizio, C. Fisher, J. Strauss, Y. Wachtfogel, R. Colman, M. Josephson
In this study the antiplatelet properties of two calcium channel blockers, verapamil and diltiazem, were evaluated. In 20 random aspirin-abstaining donors, both diltiazem and verapamil (0.01-10 microM) reduced epinephrine-induced aggregation [46 +/- 6% (SE) inhibition] and demonstrated a dose-dependent inhibition of epinephrine-induced [14C]serotonin release (43 +/- 3% reduction). However, at equimolar concentrations, verapamil was twice as effective. Neither drug altered ADP, collagen, thrombin, or calcium ionophore-induced platelet aggregation or platelet granule secretion. Neither drug prevented formation of thromboxane B2 during secondary aggregation. Verapamil, but not diltiazem, increased the Kd of [3H]yohimbine binding from 2.03 to 46.99 nM without altering the calculated number of binding sites per platelet (124 sites/platelet). Supplemental calcium added to citrated platelet-rich plasma reversed both verapamil and diltiazem-induced inhibition of platelet aggregation. We conclude that, at the concentrations tested, both verapamil and diltiazem are specific inhibitors of epinephrine-induced platelet activation. Clearly, both agents may be acting by preventing epinephrine-induced increases in plasma membrane permeability to calcium. However, the greater potency of verapamil compared with diltiazem with only verapamil binding to alpha2-adrenergic receptors suggests that alpha-blockade represents a significant component of verapamil-induced platelet inhibition.
{"title":"Effects of verapamil and diltiazem on human platelet function.","authors":"V. Addonizio, C. Fisher, J. Strauss, Y. Wachtfogel, R. Colman, M. Josephson","doi":"10.1097/00132586-198704000-00041","DOIUrl":"https://doi.org/10.1097/00132586-198704000-00041","url":null,"abstract":"In this study the antiplatelet properties of two calcium channel blockers, verapamil and diltiazem, were evaluated. In 20 random aspirin-abstaining donors, both diltiazem and verapamil (0.01-10 microM) reduced epinephrine-induced aggregation [46 +/- 6% (SE) inhibition] and demonstrated a dose-dependent inhibition of epinephrine-induced [14C]serotonin release (43 +/- 3% reduction). However, at equimolar concentrations, verapamil was twice as effective. Neither drug altered ADP, collagen, thrombin, or calcium ionophore-induced platelet aggregation or platelet granule secretion. Neither drug prevented formation of thromboxane B2 during secondary aggregation. Verapamil, but not diltiazem, increased the Kd of [3H]yohimbine binding from 2.03 to 46.99 nM without altering the calculated number of binding sites per platelet (124 sites/platelet). Supplemental calcium added to citrated platelet-rich plasma reversed both verapamil and diltiazem-induced inhibition of platelet aggregation. We conclude that, at the concentrations tested, both verapamil and diltiazem are specific inhibitors of epinephrine-induced platelet activation. Clearly, both agents may be acting by preventing epinephrine-induced increases in plasma membrane permeability to calcium. However, the greater potency of verapamil compared with diltiazem with only verapamil binding to alpha2-adrenergic receptors suggests that alpha-blockade represents a significant component of verapamil-induced platelet inhibition.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"26 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1987-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132491254","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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