Hypertension: Journal of the American Heart Association最新文献

Hypertension: Journal of the American Heart Association Pub Date : 2003-01-01 DOI: 10.1097/00005768-200305001-02223

M. Miyachi, A. Donato, Kenta Yamamoto, Kouki Takahashi, P. Gates, K. Moreau, Hirofumi Tanaka

{"title":"Greater Age-Related Reductions in Central Arterial Compliance in Resistance-Trained Men","authors":"M. Miyachi, A. Donato, Kenta Yamamoto, Kouki Takahashi, P. Gates, K. Moreau, Hirofumi Tanaka","doi":"10.1097/00005768-200305001-02223","DOIUrl":"https://doi.org/10.1097/00005768-200305001-02223","url":null,"abstract":"Abstract—Reductions in the compliance of central arteries exert a number of adverse effects on systemic cardiovascular function and disease risk. Using the cross-sectional study design, we determined the relation between chronic resistance training and carotid arterial compliance. A total of 62 healthy normotensive men, 20 to 39 years of age (young) and 40 to 60 years of age (middle-aged), who were either sedentary or resistance-trained, were studied. In both activity groups, carotid arterial compliance (simultaneous ultrasound and applanation tonometry) was lower (P <0.05) in the middle-aged compared with the young men. There was no significant difference between young sedentary and resistance-trained men. In the middle-aged group, carotid arterial compliance in the resistance-trained men was ≈30% lower (P <0.01) than their sedentary peers. Femoral artery compliance and arm pulse wave velocity (measures of peripheral artery stiffness) were not different among any groups. Left ventricular hypertrophy index (echocardiography) was greater (P <0.05) in resistance-trained compared with sedentary men and was associated with carotid arterial compliance (r =−0.35;P <0.01). We concluded that (1) resistance training is associated with the smaller central arterial compliance in healthy middle-aged men; (2) age-related reductions in arterial compliance was greater in resistance-trained men than in sedentary men; and (3) the lower arterial compliance in the resistance-trained men is associated with left ventricular hypertrophy. In marked contrast to the beneficial effect of regular aerobic exercise, the present findings are not consistent with the idea that resistance training exerts beneficial influences on arterial wall buffering functions.","PeriodicalId":13233,"journal":{"name":"Hypertension: Journal of the American Heart Association","volume":"525 ","pages":"130-135"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91459599","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}

引用次数: 225

Drug Effects on Aldosterone/Plasma Renin Activity Ratio in Primary Aldosteronism 药物对原发性醛固酮增多症患者醛固酮/血浆肾素活性比的影响

Hypertension: Journal of the American Heart Association Pub Date : 2002-12-01 DOI: 10.1016/S0895-7061(03)00766-0

P. Mulatero, F. Rabbia, A. Milan, C. Paglieri, F. Morello, L. Chiandussi, F. Veglio

引用次数: 373

Mineralocorticoid and Angiotensin Receptor Antagonism During Hyperaldosteronemia 高醛固酮血症时矿化皮质激素和血管紧张素受体的拮抗作用

Hypertension: Journal of the American Heart Association Pub Date : 2002-08-01 DOI: 10.1161/01.HYP.0000025904.23047.27

A. Mihailidou, M. Mardini, J. Funder, Matthew J. Raison

{"title":"Mineralocorticoid and Angiotensin Receptor Antagonism During Hyperaldosteronemia","authors":"A. Mihailidou, M. Mardini, J. Funder, Matthew J. Raison","doi":"10.1161/01.HYP.0000025904.23047.27","DOIUrl":"https://doi.org/10.1161/01.HYP.0000025904.23047.27","url":null,"abstract":"Elevated aldosterone levels induce a spironolactone-inhibitable decrease in cardiac sarcolemmal Na+-K+ pump function. Because pump inhibition has been shown to contribute to myocyte hypertrophy, restoration of Na+-K+ pump function may represent a possible mechanism for the cardioprotective action of mineralocorticoid receptor (MR) blockade. The present study examines whether treatment with the angiotensin type 1 receptor antagonist losartan, with either spironolactone or eplerenone, has additive effects on sarcolemmal Na+-K+ pump activity in hyperaldosteronemia. New Zealand White rabbits were divided into 7 different groups: controls, aldosterone alone, aldosterone plus spironolactone, aldosterone plus eplerenone, aldosterone plus losartan, aldosterone plus losartan and spironolactone, and aldosterone plus losartan and eplerenone. After 7 days, myocytes were isolated by enzymatic digestion. Electrogenic Na+-K+ pump current (Ip), arising from the 3:2 Na+:K+ exchange ratio, was measured by the whole-cell patch clamp technique. Elevated aldosterone levels lowered Ip; treatment with losartan reversed aldosterone-induced reduced pump function, as did MR blockade. Coadministration of spironolactone or eplerenone with losartan enhanced the losartan effect on pump function to a level similar to that measured in rabbits given losartan alone in the absence of hyperaldosteronemia. In conclusion, hyperaldosteronemia induces a decrease in Ip at near physiological levels of intracellular Na+ concentration. Treatment with losartan reverses this aldosterone-induced decrease in pump function, and coadministration with MR antagonists produces an additive effect on pump function, consistent with a beneficial effect of MR blockade in patients with hypertension and congestive heart failure treated with angiotensin type 1 receptor antagonists.","PeriodicalId":13233,"journal":{"name":"Hypertension: Journal of the American Heart Association","volume":"8 1","pages":"124-129"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79179886","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}

引用次数: 21

N-Acetyl-Ser-Asp-Lys-Pro Inhibits Phosphorylation of Smad2 in Cardiac Fibroblasts N-Acetyl-Ser-Asp-Lys-Pro抑制心肌成纤维细胞Smad2磷酸化

Hypertension: Journal of the American Heart Association Pub Date : 2002-08-01 DOI: 10.1161/01.HYP.0000025880.56816.FA

S. Pokharel, S. Rasoul, A. Roks, R. V. van Leeuwen, M. V. van Luyn, L. Deelman, J. Smits, O. Carretero, W. V. van Gilst, Y. Pinto

{"title":"N-Acetyl-Ser-Asp-Lys-Pro Inhibits Phosphorylation of Smad2 in Cardiac Fibroblasts","authors":"S. Pokharel, S. Rasoul, A. Roks, R. V. van Leeuwen, M. V. van Luyn, L. Deelman, J. Smits, O. Carretero, W. V. van Gilst, Y. Pinto","doi":"10.1161/01.HYP.0000025880.56816.FA","DOIUrl":"https://doi.org/10.1161/01.HYP.0000025880.56816.FA","url":null,"abstract":"N-Acetyl-Ser-Asp-Lys-Pro (AcSDKP) is a specific substrate for the N-terminal site of ACE and increases 5-fold during ACE inhibitor therapy. It is known to inhibit the proliferation of hematopoietic stem cells and has also recently been reported to inhibit the growth of cardiac fibroblasts. We investigated its mode of action in cardiac fibroblasts by assessing its influence on transforming growth factor &bgr;1 (TGF&bgr;1)–mediated Smad signaling. AcSDKP inhibited the proliferation of isolated cardiac fibroblasts (P <0.05) but significantly stimulated the proliferation of vascular smooth muscle cells. Flow cytometry of rat cardiac fibroblasts treated with AcSDKP showed significant inhibition of the progression of cells from G0/G1 phase to S phase of the cell cycle. In cardiac fibroblasts transfected with a Smad-sensitive luciferase reporter construct, AcSDKP decreased luciferase activity by 55±9.7% (P =0.01). Moreover, phosphorylation and nuclear translocation of Smad2 was decreased in cardiac fibroblasts treated with AcSDKP. To conclude, AcSDKP inhibits the growth of cardiac fibroblasts and also inhibits TGF&bgr;1-stimulated phosphorylation of Smad2. Because AcSDKP increases substantially during ACE inhibitor therapy, this suggests a novel pathway independent of angiotensin II, by which ACE inhibitors can inhibit cardiac fibrosis.","PeriodicalId":13233,"journal":{"name":"Hypertension: Journal of the American Heart Association","volume":"19 1","pages":"155-161"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87867400","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}

引用次数: 61

Simvastatin Prevents Angiotensin II–Induced Cardiac Alteration and Oxidative Stress 辛伐他汀预防血管紧张素ii诱导的心脏改变和氧化应激

Hypertension: Journal of the American Heart Association Pub Date : 2002-08-01 DOI: 10.1161/01.HYP.0000024348.87637.6F

S. Delbosc, J. Cristol, B. Descomps, A. Mimran, B. Jover

{"title":"Simvastatin Prevents Angiotensin II–Induced Cardiac Alteration and Oxidative Stress","authors":"S. Delbosc, J. Cristol, B. Descomps, A. Mimran, B. Jover","doi":"10.1161/01.HYP.0000024348.87637.6F","DOIUrl":"https://doi.org/10.1161/01.HYP.0000024348.87637.6F","url":null,"abstract":"The influence of the HMG-CoA reductase inhibitor simvastatin was assessed on the cardiovascular alterations and production of free radicals associated with chronic angiotensin II (Ang II) infusion. Simvastatin (60 mg/kg per day PO) or placebo were given concomitantly for 10 days in Sprague-Dawley rats infused with Ang II (200 ng/kg per minute SC, osmotic pump). In addition, simvastatin or placebo was also given in vehicle-infused rats. Tail-cuff pressure and albuminuria were measured before and at the end of the treatment period. Cardiac weight, carotid structure, production of reactive oxygen species (ROS, by chemiluminescence) by polymorphonuclear leukocytes and aortic wall as well as protein and lipid oxidation products were determined at the end of the study. Ang II increased tail-cuff pressure by 56±12 mm Hg and simvastatin blunted the development of hypertension by ≈70% (19±5 mm Hg). Increases in heart weight index and carotid cross-sectional area induced by Ang II were obliterated by simvastatin (3.18±0.09 versus 3.46±0.11 mg/g body wt and 0.125±0.010 versus 0.177±0.010 mm2, respectively). The Ang II–induced increases in leukocyte and aortic production of ROS as well as protein and lipid oxidation products were prevented by simvastatin. No effect of simvastatin was detected in non–Ang II–infused rats. These results indicate that simvastatin prevented the development of hypertension and cardiovascular hypertrophy together with inhibition of the induced angiotensin II production of ROS. Therefore, inhibition of HMG CoA reductase by statins may have a beneficial effect on cardiovascular alterations through its antioxidant action in experimental Ang II–dependent hypertension.","PeriodicalId":13233,"journal":{"name":"Hypertension: Journal of the American Heart Association","volume":"1 1","pages":"142-147"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88272937","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}

引用次数: 153

Ouabain-Binding Protein(s) From Human Plasma 来自人血浆的瓦阿巴因结合蛋白

Hypertension: Journal of the American Heart Association Pub Date : 2002-08-01 DOI: 10.1161/01.HYP.0000027134.14160.1D

B. Parhami-Seren, R. Haberly, M. N. Margolies, G. T. Haupert

{"title":"Ouabain-Binding Protein(s) From Human Plasma","authors":"B. Parhami-Seren, R. Haberly, M. N. Margolies, G. T. Haupert","doi":"10.1161/01.HYP.0000027134.14160.1D","DOIUrl":"https://doi.org/10.1161/01.HYP.0000027134.14160.1D","url":null,"abstract":"Conservation of the binding site on mammalian Na+,K+-ATPase for cardiac glycosides and the importance of the Na+ pump in mammalian cellular physiology has stimulated the search for a mammalian analog of these plant compounds. One candidate, isolated from brain and blood, appears to be ouabain itself or a closely related isomer, the ouabain-like compound. Little is known about the circulating form. Because human steroid hormones circulate with carrier proteins, we produced a ouabain-specific monoclonal antibody (mAb 1-10) and used it to probe normal human plasma for ouabain-protein carrier complex. Ouabain-like biological activity was isolated in association with protein bands of 80, 50, and 25 kDa. These proteins appear to be human immunoglobulins or immunoglobulin-like because they are recognized by anti-human immunoglobulin antibodies, but not by anti-mouse immunoglobulin antibodies. The protein-containing fractions inhibit the binding of mAb 1-10 to immobilized ouabain, and with further purification on protein A, the immunoglobulin-like protein binds radioactive ouabain with an IC50 of 200 to 600 nmol/L, but binds digoxin with 100-fold less affinity, suggesting specificity for ouabain or its isomer. Active protein fractions after purification on C18 inhibit Na+ pump activity in human erythrocytes (IC50≈4 nmol/L, ouabain equivalents), and this chromatography appears to dissociate the ouabain-like compound from the immunoglobulin protein(s). These immunoglobulin-like molecules may represent a subset of immunoglobulins (≤0.5% of total protein A immunoglobulin) that function as a reservoir and delivery system for ouabain-like compounds in the modulation of human Na+, K+-ATPase in vivo.","PeriodicalId":13233,"journal":{"name":"Hypertension: Journal of the American Heart Association","volume":"4 1","pages":"220-228"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89200005","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}

引用次数: 12

ETB Receptor in Renal Medulla Is Enhanced by Local Sodium During Low Salt Intake 低盐摄入时局部钠对肾髓质ETB受体的增强作用

Hypertension: Journal of the American Heart Association Pub Date : 2002-08-01 DOI: 10.1161/01.HYP.0000026809.68674.F9

S. Vanni, G. Polidori, I. Cecioni, S. Serni, M. Carini, P. Modesti

{"title":"ETB Receptor in Renal Medulla Is Enhanced by Local Sodium During Low Salt Intake","authors":"S. Vanni, G. Polidori, I. Cecioni, S. Serni, M. Carini, P. Modesti","doi":"10.1161/01.HYP.0000026809.68674.F9","DOIUrl":"https://doi.org/10.1161/01.HYP.0000026809.68674.F9","url":null,"abstract":"Renal endothelin-1 participates in sodium and water handling, and its urinary excretion is increased in sodium-retentive states. We compared the cortical and medullary renal expression of prepro-endothelin-1, endothelin-converting enzyme-1, and endothelin type A and type B receptors in patients who underwent nephrectomy after normal (108 mmol/d NaCl; n=6) or low (20 mmol/d NaCl; n=6) sodium diet and investigated whether sodium exerts a direct role on endothelin receptor binding in vitro. With normal sodium diet prepro-endothelin-1 mRNA was 3-fold higher in renal medulla than in cortex (P <0.01), whereas endothelin-converting enzyme-1 mRNA was equally distributed. Endothelin-1 receptor density was 2-fold higher in renal medulla than in cortex (P <0.05). Type B was the main receptor subtype in both regions. In the renal cortex, low sodium diet caused a 194% increase in prepro-endothelin-1 mRNA (P <0.05), whereas endothelin-converting enzyme-1 type B and type A receptors remained unchanged. In contrast, in the renal medulla the increase in prepro-endothelin-1 mRNA (+30%, P <0.05) was associated with a selective increase in type B receptor for both mRNA expression (+37%, P <0.05) and binding density (+55%, P <0.05). Increasing in vitro sodium concentrations between 154 and 308 mmol/L significantly enhanced type B receptor density (P <0.05) and affinity (P <0.05). In conclusion, during low sodium diet, renal prepro-endothelin-1 synthesis increases mainly in the renal cortex (where no changes in receptors occur), whereas type B receptor is selectively enhanced in the renal medulla. The range of sodium concentrations that are physiologically present in vivo in the renal medulla selectively modulate type B receptor density and affinity.","PeriodicalId":13233,"journal":{"name":"Hypertension: Journal of the American Heart Association","volume":"210 1","pages":"179-185"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77490966","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}

引用次数: 10

TIMP-1: A Marker of Left Ventricular Diastolic Dysfunction and Fibrosis in Hypertension TIMP-1:高血压左室舒张功能障碍和纤维化的标志物

Hypertension: Journal of the American Heart Association Pub Date : 2002-08-01 DOI: 10.1161/01.HYP.0000024573.17293.23

M. Lindsay, P. Maxwell, F. Dunn

{"title":"TIMP-1: A Marker of Left Ventricular Diastolic Dysfunction and Fibrosis in Hypertension","authors":"M. Lindsay, P. Maxwell, F. Dunn","doi":"10.1161/01.HYP.0000024573.17293.23","DOIUrl":"https://doi.org/10.1161/01.HYP.0000024573.17293.23","url":null,"abstract":"This study was designed to document noninvasively the pathological mechanisms responsible for myocardial fibrosis and to assess the clinical utility of plasma markers of collagen synthesis and degradation as screening tools for the assessment of fibrosis in hypertension. We studied 100 never-treated hypertensive patients and 50 normal subjects. Echocardiographic assessment was made of left ventricular (LV) mass and diastolic filling using measurement of E:A ratio, E wave deceleration time (E dec), and isovolumic relaxation time (IVRT). The presence of diastolic dysfunction was taken as a surrogate marker for the presence of myocardial fibrosis. Plasma carboxy-terminal propeptide of collagen type I (PICP), carboxy-terminal telopeptide of collagen type I (CITP), and tissue inhibitor of matrix metalloproteinases type I (TIMP-1) were measured as markers of collagen synthesis, degradation, and inhibition of degradation, respectively. Plasma TIMP-1 was significantly elevated in the hypertensive cohort (358 ng/mL versus 253 ng/mL, P <0.001) as were CITP (5.2 &mgr;g/L versus 2.9 &mgr;g/L, P <0.001), and PICP (200 &mgr;g/L versus 166 &mgr;g/L, P <0.05). TIMP-1 was significantly elevated in patients with diastolic dysfunction (421 ng/mL versus 283 ng/mL P <0.01) and correlated with markers of diastolic filling, namely E:A ratio (r =0.26, P <0.05) and E Dec (r =0.41, P <0.01). A plasma TIMP-1 level of >500 ng/mL had a specificity of 97% and a positive predictive value of 96% in predicting diastolic dysfunction. In patients with untreated hypertension, there is evidence of increased collagen synthesis, degradation, and inhibition of degradation resulting in fibrosis. Our results demonstrate that plasma TIMP-1 correlates with markers of LV diastolic filling, is predictive of LV dysfunction, and is a potential noninvasive marker of fibrosis.","PeriodicalId":13233,"journal":{"name":"Hypertension: Journal of the American Heart Association","volume":"24 1","pages":"136-141"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77848735","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}

引用次数: 190

High Rate of Ventricular Septal Defects in WKY Rats WKY大鼠室间隔缺损发生率高

Hypertension: Journal of the American Heart Association Pub Date : 2002-08-01 DOI: 10.1161/01.HYP.0000025441.06473.89

M. Slama, D. Sušić, J. Varagić, E. Frohlich

{"title":"High Rate of Ventricular Septal Defects in WKY Rats","authors":"M. Slama, D. Sušić, J. Varagić, E. Frohlich","doi":"10.1161/01.HYP.0000025441.06473.89","DOIUrl":"https://doi.org/10.1161/01.HYP.0000025441.06473.89","url":null,"abstract":"In 1979, we first reported occurrence of biventricular hypertrophy in the original normotensive Wistar-Kyoto (WKY) strain obtained from the National Heart, Lung, and Blood Institute, which was derived directly from the Kyoto laboratory of Okamoto. At that time, we recommended that both ventricles be weighted when WKY are studied so that invalid conclusions are not made. Because no paper confirmed these findings for almost 20 years, heart weights were reported in only a few WKY studies, and the cause of this biventricular hypertrophy remained unknown, we re-evaluated this problem in commercially available rats. We, therefore, investigated WKY rats using transthoracic echocardiography to define the congenital heart defect. Up to 28% of commercially available WKY rats demonstrated severe congenital cardiac abnormalities associated with biventricular hypertrophy. Ventricular septal defect with pulmonary regurgitation was the most commonly encountered cardiac defect; other abnormalities included patent ductus arteriosus, and valvular defects. Pathologic and invasive hemodynamic studies confirmed these echocardiographic findings. Because this defect occurs in a large number of WKY rats obtained commercially from 2 different sources, investigators using this strain must carefully measure both ventricular weights to be certain that inappropriate and invalid conclusions are not derived therefrom.","PeriodicalId":13233,"journal":{"name":"Hypertension: Journal of the American Heart Association","volume":"15 1","pages":"175-178"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76497865","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}

引用次数: 19

Endogenous Endothelin-1 Limits Exercise-Induced Vasodilation in Hypertensive Humans 内源性内皮素-1限制高血压患者运动诱导的血管舒张

Hypertension: Journal of the American Heart Association Pub Date : 2002-08-01 DOI: 10.1161/01.HYP.0000024218.04872.F3

C. McEniery, I. Wilkinson, D. Jenkins, D. Webb

{"title":"Endogenous Endothelin-1 Limits Exercise-Induced Vasodilation in Hypertensive Humans","authors":"C. McEniery, I. Wilkinson, D. Jenkins, D. Webb","doi":"10.1161/01.HYP.0000024218.04872.F3","DOIUrl":"https://doi.org/10.1161/01.HYP.0000024218.04872.F3","url":null,"abstract":"Essential hypertension is a common disorder, associated with increased endothelin-1–mediated vasoconstrictor tone at rest. We hypothesized that increased vasoconstrictor activity of endothelin-1 might explain why the normal decrease in peripheral vascular resistance in response to exercise is attenuated in hypertensive patients. Therefore, we investigated the effect of endothelin A (ETA) receptor blockade on the vasodilator response to handgrip exercise. Forearm blood flow responses to handgrip exercise (15%, 30%, and 45% of maximum voluntary contraction) were assessed in hypertensive patients and matched normotensive subjects, before and after intra-arterial infusions of the ETA receptor antagonist BQ-123; a control dilator, hydralazine; and placebo (saline). Preinfusion (baseline) vasodilation in response to exercise was significantly attenuated at each workload in hypertensive patients compared with normotensive subjects. Intra-arterial infusions of hydralazine and saline did not increase the vasodilator response to exercise in either hypertensives or normotensives at any workload. The vasodilator response to exercise was markedly enhanced after BQ-123 at the 2 higher workloads in hypertensives (157±48%, P <0.01; 203±58%, P <0.01) but not in normotensives. This suggests that the impaired vasodilator response to exercise in hypertensive patients is, at least in part, a functional limitation caused by endogenous ETA receptor–mediated vasoconstriction. Treatment with endothelin receptor antagonists may, therefore, increase exercise capacity in essential hypertension.","PeriodicalId":13233,"journal":{"name":"Hypertension: Journal of the American Heart Association","volume":"39 1","pages":"202-206"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79195358","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}

引用次数: 40