Hypertension: Journal of the American Heart Association最新文献

{"title":"Gender Differences in the Dietary Lard-Induced Increase in Blood Pressure in Rats","authors":"Norika Tamaya-Mori, K. Uemura, A. Iguchi","doi":"10.1161/01.HYP.0000016400.21001.05","DOIUrl":"https://doi.org/10.1161/01.HYP.0000016400.21001.05","url":null,"abstract":"We investigated the difference between male and female rats in the increase in blood pressure (BP) when they were fed a lard-enriched diet. We also investigated the effect of a gonadectomy, with or without testosterone treatment, on the dietary lard-induced increase in BP. Wistar-strain male or female rats were bilaterally castrated or ovariectomized. Some of them were implanted subcutaneously with silicon tubes containing crystalline testosterone. Each group was fed either chow alone or chow in which 50% of the energy content was from substituted lard. Systolic blood pressure (SBP) was determined weekly during each 7- or 11-week feeding period. A steady-state plasma glucose method was used to determine the insulin sensitivity. The dietary lard-induced increase in SBP was observed at 5 weeks after the start of the feeding in the sham-operated male rats. In the sham-operated female rats, SBP did not change from the basal values until 11 weeks into the experimental period. Castration eliminated the dietary lard-induced increase in SBP. Ovariectomy had no effect on SBP throughout the experimental period in both diet groups. In castrated males given testosterone, SBP increased in a dose-dependent manner. In ovariectomized females given testosterone, SBP increased significantly in the lard-enriched diet group. The dietary lard developed an insulin resistance in both the sham-operated and gonadectomized rats. However, SBP increased only in the sham-operated male rats. These results suggest that the dietary lard-induced increase in SBP depends on the presence of testosterone. The development of insulin resistance by dietary lard triggers the increase in SBP.","PeriodicalId":13233,"journal":{"name":"Hypertension: Journal of the American Heart Association","volume":"27 1","pages":"1015-1020"},"PeriodicalIF":0.0,"publicationDate":"2002-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85730867","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":"Serine Protease Activity in M-1 Cortical Collecting Duct Cells","authors":"Lian Liu, K. Hering-Smith, F.R. Schiro, L. Hamm","doi":"10.1161/01.HYP.0000013055.48885.8D","DOIUrl":"https://doi.org/10.1161/01.HYP.0000013055.48885.8D","url":null,"abstract":"An apical serine protease, channel-activating protease 1 (CAP1), augments sodium transport in A6 cells. Prostasin, a novel serine protease originally purified from seminal fluid, has been proposed to be the mammalian ortholog of CAP1. We have recently found functional evidence for a similar protease activity in the M-1 cortical collecting duct cell line. The purposes of the present studies were to determine whether prostasin (or CAP1) is present in collecting duct cells by use of mouse M-1 cells, to sequence mouse prostasin, and to further characterize the identity of the serine protease activity and additional functional features in M-1 cells. Using mouse expressed sequence tag sequences that are highly homologous to the published human prostasin sequence as templates, reverse transcription–polymerase chain reaction and RACE (rapid amplification of cDNA ends) were used to sequence mouse prostasin mRNA, which shows 99% identical to published mouse CAP1 sequence. A single 1800-bp transcript was found by Northern analysis, and this was not altered by aldosterone. Equivalent short-circuit current (Ieq), which represents sodium transport in these cells, dropped to 59±3% of control value within 1 hour of incubation with aprotinin, a serine protease inhibitor. Trypsin increased the Ieq in aprotinin-treated cells to the value of the control group within 5 minutes. Application of aprotinin not only inhibited amiloride sensitive Ieq but also reduced transepithelial resistance (Rte) to 43±2%, an effect not expected with simple inhibition of sodium channels. Trypsin partially reversed the effect of aprotinin on Rte. Another serine protease inhibitor, soybean trypsin inhibitor (STI), decreased Ieq in M-1 cells. STI inhibited Ieq gradually over 6 hours, and the inhibition of Ieq by 2 inhibitors was additive. STI decreased transepithelial resistance much less than did aprotinin. Neither aldosterone nor dexamethasone significantly augmented protease activity or prostasin mRNA levels, and in fact, dexamethasone decreased prostasin mRNA expression. In conclusion, although prostasin is present in M-1 cells and probably augments sodium transport in these cells, serine proteases probably have other effects (eg, resistance) in the collecting duct in addition to effects on sodium channels. Steroids do not alter these effects in M-1 cells. Additional proteases are likely also present in mouse collecting duct cells.","PeriodicalId":13233,"journal":{"name":"Hypertension: Journal of the American Heart Association","volume":"32 1","pages":"860-864"},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74106748","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":"Catecholamines Block 2-Hydroxyestradiol-Induced Antimitogenesis in Mesangial Cells","authors":"L. Zacharia, E. Jackson, Delbert G. Gillespie, R. Dubey","doi":"10.1161/01.HYP.0000014502.44988.39","DOIUrl":"https://doi.org/10.1161/01.HYP.0000014502.44988.39","url":null,"abstract":"Methylation of 2-hydroxyestradiol to 2-methoxyestradiol by catechol-O-methyl transferase (COMT) mediates the antimitogenic effects of 2-hydroxyestradiol on vascular smooth muscle cells. Moreover, 2-hydroxyestradiol inhibits growth of glomerular mesangial cells (GMCs). Because catecholamines are substrates for COMT, which is expressed in GMCs, we hypothesize that catecholamines may abrogate the antimitogenic effects of 2-hydroxyestradiol on GMCs by competing for COMT and inhibiting 2-methoxyestradiol formation. To test this hypothesis, we investigated the antimitogenic effects of 2-hydroxyestradiol on rat GMCs in the presence and absence of catecholamines. The capability of GMCs to methylate 2-hydroxyestradiol in the presence and absence of catecholamines was also evaluated. GMCs metabolized 2-hydoxyestradiol in a concentration-dependent manner with a Vmax of 12.03±0.32 pmol/106 cells/min and an apparent Km of 0.23±0.04 &mgr;mol/L. Norepinephrine (10 &mgr;mol/L) and epinephrine (10 &mgr;mol/L) significantly inhibited methylation of 0.25 &mgr;mol/L 2-hydroxyestradiol. Norepinephrine concentration-dependently abrogated the ability of 2-hydroxyestradiol to inhibit 3H-thymidine incorporation (index of DNA synthesis). In the presence of 5, 10, and 40 &mgr;mol/L norepinephrine, the inhibitory effect of 0.1 &mgr;mol/L 2-hydroxyestradiol on 3H-thymidine incorporation was reduced from 51±0.7% to 46±0.4%, 39±0.3%, and 25±0.7%, respectively. Similar to DNA synthesis, the inhibitory effects of 2-hydroxyestradiol on cell number and 3H-proline incorporation (index of collagen synthesis) on GMCs were abrogated by catecholamines. Our findings provide evidence that methylation of 2-hydroxyestradiol inhibits GMC proliferation and extracellular matrix synthesis and may in part protect against renal proliferative diseases. Moreover, catecholamines may abrogate the renoprotective effects of 2-hydroxyestradiol in the glomeruli by inhibiting COMT and 2-methoxyestradiol formation.","PeriodicalId":13233,"journal":{"name":"Hypertension: Journal of the American Heart Association","volume":"42 1","pages":"854-859"},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77898209","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":"Low-Density Lipoprotein Subfractions and Cardiovascular Risk in Hypertension: Relationship to Endothelial Dysfunction and Effects of Treatment*","authors":"D. Felmeden, C. C. Spencer, A. Blann, G. Lip, G. Beevers","doi":"10.1016/S0895-7061(02)02866-2","DOIUrl":"https://doi.org/10.1016/S0895-7061(02)02866-2","url":null,"abstract":"","PeriodicalId":13233,"journal":{"name":"Hypertension: Journal of the American Heart Association","volume":"14 1","pages":"528-533"},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81839170","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":"Impaired Stress-Induced Pressure Natriuresis Is Related to Left Ventricle Structure in Blacks","authors":"G. Harshfield, F. Treiber, H. Davis, G. Kapuku","doi":"10.1161/01.HYP.0000013735.85681.74","DOIUrl":"https://doi.org/10.1161/01.HYP.0000013735.85681.74","url":null,"abstract":"The mechanisms through which stress may contribute to the racial difference in the prevalence of essential hypertension and associated target organ damage remain unclear. This study examined differences in stress-induced pressure natriuresis in 69 black and 52 white normotensives age 14 to 27 years, all with a positive family history of hypertension. Urine samples for sodium excretion were collected before and after a series of tasks (video game challenge, forehead cold stimulation). The average blood pressure across the 2 tasks and the average increase in blood pressure to the 2 tasks were calculated. Blacks had higher mean systolic (131±12 versus 126±12 mm Hg, P <0.02) and diastolic (77±8 versus 72±9 mm Hg, P <0.001) blood pressure and a greater average change in systolic blood pressure (15±9 versus 11±7 mm Hg, P <0.04). This was associated with a smaller change in sodium excretion (2±6 versus 7±10 mEq/h, P <0.002). The change in sodium excretion was related to the change in systolic (r =0.31, P <0.03) and diastolic (r =0.27, P <0.05) blood pressure in whites but not in blacks. Relative wall thickness was greater in blacks (0.31±0.04 versus 0.29±0.03, P <0.002). In conclusion, impaired stress-induced pressure natriuresis in blacks may contribute to racial differences in essential hypertension and its sequelae.","PeriodicalId":13233,"journal":{"name":"Hypertension: Journal of the American Heart Association","volume":"54 1","pages":"844-847"},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77627069","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":"Neuronal NO Mediates Cerebral Vasodilator Responses to K+ in Hypertensive Rats","authors":"S. Chrissobolis, J. Ziogas, C. Anderson, Y. Chu, F. Faraci, C. Sobey","doi":"10.1161/01.HYP.0000013056.74554.CE","DOIUrl":"https://doi.org/10.1161/01.HYP.0000013056.74554.CE","url":null,"abstract":"Potassium ion (K+) normally causes cerebral vasodilatation by activating inwardly rectifying K+ (KIR) channels. We tested whether chronic hypertension affects the magnitude and/or mechanism of K+-induced cerebral vasodilatation in vivo. Basilar artery responses were examined in anesthetized Wistar-Kyoto (WKY; mean arterial pressure, 114±4 mm Hg) and spontaneously hypertensive (SHR; 176±3 mm Hg) rats. In WKY, elevating cerebrospinal fluid K+ concentration from 3 mmol/L to 5 and 10 mmol/L caused vasodilatation (percent maximum, 12±1 and 48±7, respectively). The response to 5 mmol/L K+ was greater in SHR (percent maximum, 17±2 [P <0.05 versus WKY] and 49±4). The KIR channel inhibitor, barium ion (Ba2+, 100 &mgr;mol/L) selectively inhibited dilator responses to 5 and 10 mmol/L K+ by ≈75% in WKY. In SHR, Ba2+ had no effect on the response to 5 mmol/L K+, and only partially inhibited (by ≈40%) the response to 10 mmol/L K+. The nonselective NO synthase (NOS) inhibitor N&ohgr;-nitro-l-arginine methyl ester, the neuronal NOS (nNOS) inhibitor 1-(2-trifluromethyl-phenyl)imidazole, and the N-type calcium channel inhibitor &ohgr;-conotoxin GVIA, were all without effect in WKY, but markedly inhibited the response to 5 mmol/L K+ in SHR. When applied together with Ba2+, each of these inhibitors also profoundly reduced responses to 10 mmol/L K+ in SHR. Immunostaining of basilar arteries revealed that the perivascular nNOS-containing nerve plexus was denser in SHR. Thus, K+ dilates the normotensive basilar artery predominantly via KIR channel activation. During chronic hypertension, small physiological elevations in K+ dilate the basilar artery by an nNOS-dependent mechanism that appears to be upregulated in a compensatory manner.","PeriodicalId":13233,"journal":{"name":"Hypertension: Journal of the American Heart Association","volume":"1 1","pages":"880-885"},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86143707","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":"Effects of Chronic Calcium Channel Blockade on Sympathetic Nerve Activity in Hypertension","authors":"C. Binggeli, R. Corti, I. Sudano, T. Luscher, G. Noll","doi":"10.1161/01.HYP.0000013264.41234.24","DOIUrl":"https://doi.org/10.1161/01.HYP.0000013264.41234.24","url":null,"abstract":"The sympathetic nervous system (SNS) is an important regulator of the circulation. Its activity is increased in hypertension and heart failure and adversely affects prognosis. Although certain drugs inhibit SNS, dihydropyridine calcium antagonists may stimulate the system. Phenylalkylamine calcium antagonists such as verapamil have a different pharmacological profile. We therefore tested the hypothesis of whether amlodipine, nifedipine, or verapamil differs in the effects on muscle sympathetic nerve activity (MSA). Forty-three patients (31 men, 12 women) with mild to moderate hypertension were randomly assigned to 1 drug for 8 weeks. Blood pressure, heart rate, and MSA (by microneurography) were measured at baseline and after 8 weeks of treatment. All calcium antagonists led to a similar decrease in blood pressure of 5.0±1.5 to 6.4±1.4 mm Hg at 8 weeks (P <0.001 versus baseline). There were no significant differences in MSA between groups. With amlodipine, MSA averaged 49±3 bursts/min (3 versus baseline); with nifedipine, 48±3 bursts/min (2 versus baseline); and with verapamil, 49±2 bursts/min (all, P =NS). With verapamil, norepinephrine decreased by 4% but tended to increase by about one third with amlodipine or nifedipine (P =NS). Thus, in hypertension slow release forms of verapamil, nifedipine, and amlodipine exert comparable antihypertensive effects and do not change MSA, although there was a trend toward decreased MSA and plasma norepinephrine with verapamil.","PeriodicalId":13233,"journal":{"name":"Hypertension: Journal of the American Heart Association","volume":"321 1","pages":"892-896"},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86772816","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":"Diagnostic Value of the Post-Captopril Test in Primary Aldosteronism","authors":"O. L. Castro, Xichun Yu, D. Kem","doi":"10.1161/01.HYP.0000014324.68506.CA","DOIUrl":"https://doi.org/10.1161/01.HYP.0000014324.68506.CA","url":null,"abstract":"Primary aldosteronism is a disorder with hypertension, hypokalemia, increased plasma aldosterone, and suppressed renin activity. A random plasma aldosterone/renin activity (PA/PRA) >65 (conventional units ratio [CUR] >30) has been proposed as a screening test. We have retrospectively determined the value of the post-captopril plasma aldosterone/renin activity (CAPT PA/PRA) test for the diagnosis of patients with primary aldosteronism whose PA/PRA was <65. We considered the CAPT PA/PRA test to be positive for primary aldosteronism if either the plasma aldosterone concentration did not drop below 0.33 nmol/L (12 ng/dL) or the ratio was >26 (CUR >12). We found 6 patients with a random PA/PRA of 21 to 60 (CUR 10 to 28), yet with an abnormal post-captopril test criteria for primary aldosteronism. Five had an abnormal saline suppression test, and all 6 were confirmed by a combination of diagnostic localization with computerized axial tomography, iodocholesterol scan, adrenal venous sampling, and/or surgery. Four had idiopathic adrenal hyperplasia, and 2 had an aldosterone-producing adenoma. One other patient had an abnormal random plasma aldosterone/renin activity ratio of 99 (CUR 46), a negative saline infusion study, and was determined to have essential hypertension. In summary, the CAPT PA/PRA, but not the random PA/PRA, correctly diagnosed 6 patients with primary aldosteronism in our institution. An additional patient with essential hypertension was incorrectly diagnosed as having primary aldosteronism by the PA/PRA test. We conclude that the simple addition of 25 mg of captopril, taken orally 2 hours before sampling, enhances the accuracy for diagnosing patients with primary aldosteronism.","PeriodicalId":13233,"journal":{"name":"Hypertension: Journal of the American Heart Association","volume":"30 1","pages":"935-938"},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86808830","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":"In Vivo klotho Gene Transfer Ameliorates Angiotensin II-Induced Renal Damage","authors":"H. Mitani, N. Ishizaka, T. Aizawa, M. Ohno, S. Usui, Toru Suzuki, T. Amaki, I. Mori, Yasushi Nakamura, Misako Sato, M. Nangaku, Y. Hirata, R. Nagai","doi":"10.1161/01.HYP.0000013734.33441.EA","DOIUrl":"https://doi.org/10.1161/01.HYP.0000013734.33441.EA","url":null,"abstract":"The klotho gene, originally identified by insertional mutagenesis in mice, suppresses the expression of multiple aging-associated phenotypes. This gene is predominantly expressed in the kidney. Recent studies have shown that expression of renal klotho gene is regulated in animal models of metabolic diseases and in humans with chronic renal failure. However, little is known about the mechanisms and the physiological relevance of the regulation of the expression of the klotho gene in the kidney in some diseased conditions. In the present study, we first investigated the role of angiotensin II in the regulation of renal klotho gene expression. Long-term infusion of angiotensin II downregulated renal klotho gene expression at both the mRNA and protein levels. This angiotensin II-induced renal klotho downregulation was an angiotensin type 1 receptor-dependent but pressor-independent event. Adenovirus harboring mouse klotho gene (ad-klotho, 3.3×1010 plaque forming units) was also intravenously administered immediately before starting angiotensin II infusion in some rats. This resulted in a robust induction of Klotho protein in the liver at day 4, which was still detectable 14 days after the gene transfer. Ad-klotho gene transfer, but not ad-lacZ gene transfer, caused an improvement of creatinine clearance, decrease in urinary protein excretion, and amelioration of histologically demonstrated tubulointerstitial damage induced by angiotensin II administration. Our data suggest that downregulation of the renal klotho gene may have an aggravative role in the development of renal damage induced by angiotensin II, and that induction of the klotho gene may have therapeutic possibilities in treating angiotensin II-induced end organ damage.","PeriodicalId":13233,"journal":{"name":"Hypertension: Journal of the American Heart Association","volume":"16 1","pages":"838-843"},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79866060","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":"Sympathetic Response to Ventricular Extrasystolic Beats in Hypertension and Heart Failure","authors":"G. Grassi, G. Seravalle, G. Bertinieri, M. Stella, C. Turri, G. Mancia","doi":"10.1161/01.HYP.0000013265.48954.A5","DOIUrl":"https://doi.org/10.1161/01.HYP.0000013265.48954.A5","url":null,"abstract":"Provoked premature ventricular contractions (PVCs) evoke, in concomitance with an early and late blood pressure fall and overshoot, an early sympathoexcitation and a later period of sympathoinhibition, respectively. The present study was designed to examine whether in healthy subjects this is the case for spontaneous PVCs. Because of their pathophysiological relevance for arrhythmogenesis, it was also designed to determine whether the sympathetic responses are different from those seen in essential hypertension and congestive heart failure. In 14 untreated mild essential hypertensives (EH; age, 53.8±2.6 years; mean±SEM), 20 untreated congestive heart failure patients (CHF; age, 56.7±2.5 years; New York Heart Association class, II or III), and 16 age-matched healthy subjects (control) in Lown class <II, we evaluated the blood pressure (Finapres), heart rate (ECG), and muscle sympathetic nerve traffic (MSNA; by microneurography) responses to isolated monofocal PVCs. MSNA, quantified as bursts/100 heart beats, was significantly increased in EH (57.8±3.8, P <0.05) and CHF patients (77.7±4.0, P <0.01) compared with controls (44.6±4.4). In controls, the PVC-induced blood pressure fall and overshoot were accompanied by a sympathoexcitation (144.2±14%), followed by a period of sympathoinhibition (average duration, 12043±985 ms). The responses were similar in EH but not in CHF, in whom the magnitude of the sympathoexcitation and particularly the duration of the subsequent sympathoinhibition were strikingly reduced (average reduction, −46.1 and −72.8%, respectively). The most important factor accounting for this reduction appeared to be an altered baroreflex response to the PVC-induced BP changes. These data demonstrate that the MSNA responses to spontaneous PVCs are similar in controls and EH but markedly impaired in CHF, presumably because of the baroreflex alteration. This may represent an important factor for the genesis of the life-threatening ventricular arrhythmias that characterize CHF.","PeriodicalId":13233,"journal":{"name":"Hypertension: Journal of the American Heart Association","volume":"9 1","pages":"886-891"},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91271393","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}