ISSN:0194-911X    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Angiotensin II (Ang II) plays an important role in regulating cardiovascular hemodynamics and structure. Multiple lines of evidence have suggested the existence of Ang II receptor subtypes, and at least 2 distinct receptor subtypes have been defined on the basis of their differential pharmacological and biochemical properties and designated as type 1 (AT1) and type 2 (AT2) receptors. To date, most of the known effects of Ang II in adult tissues are attributable to the AT1receptor. Recent cloning of the AT2receptor contributes to reveal its physiological functions, but many functions of the AT2receptor are still an enigma. AT1and AT2receptors belong to the 7-transmembrane, G protein-coupled receptor family. However, accumulating evidence demonstrates that the function and signaling mechanisms of these receptor subtypes are quite different, and these receptors may exert opposite effects in terms of cell growth and blood pressure regulation. We will review the role of the AT2receptor in the cardiovascular system and the molecular and cellular mechanisms of AT2receptor action. (Hypertension. 1999;33:613-621.)

ISSN:0194-911X    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Although the angiotensin II subtype 2 receptor (AT2-R) is expressed abundantly in the adrenal medulla, its physiological significance has not yet been determined. To obtain fundamental knowledge of the regulation of AT2-Rexpression in the adrenal medulla, we investigated the effects of modulating several ion channels on AT2-Rexpression in PC12W cells. Experiments were performed after 24 hours of serum depletion under subconfluent conditions. After 48 hours of treatment with various agonists or antagonists, the receptor density and mRNA level of AT2-Rswere quantified by125I-[Sar1,Ile8]angiotensin II binding and Northern blot analysis. Ouabain (10 to 100 nmol/L) and insulin (10 to 100 nmol/L) dose-dependently increased receptor density and mRNA level. Analysis of the binding characteristics revealed that the ouabain-dependent increase in AT2-Rlevels was due to an increase in binding capacity without a change in the Kdvalue. These increases were blocked by lowering the Na+concentration in the medium. A low concentration of the sodium ionophore monensin (10 nmol/L), the K+-channelblocker quinidine (10 [micro sign]mol/L), and the ATP-sensitive K+-channelblockers tolbutamide (100 [micro sign]mol/L) and glybenclamide (10 [micro sign]mol/L) also significantly increased receptor density, but the ATP-sensitive K+-channelagonist cromakalim (100 [micro sign]mol/L) decreased receptor density significantly (P<0.01). Nifedipine (10 [micro sign]mol/L) decreased basal receptor density and completely blocked the increase in receptor density caused by these agents. The increase in receptor density caused by an increase in intracellular Na+was accompanied by an increase in mRNA level, whereas the ATP-sensitive K+-channelblockers did not change mRNA level. Nifedipine slightly decreased mRNA level. These results suggest that AT2-Rexpression is sensitively regulated by intracellular cation levels. The change in intracellular Na+level transcriptionally regulates AT2-Rexpression, whereas the K+-channelblocker-dependent upregulation appears to be at least in part posttranslational. (Hypertension. 1999;33:626-632.)

ISSN:0194-911X    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

In 16 African Americans (blacks, 14 men, 2 women) with average admission mean arterial pressure (MAP, mm Hg) 99.9 +/- 3.5 (mean +/- SEM), we investigated whether NaCl-induced renal vasoconstriction attends salt sensitivity and, if so, whether supplemental KHCO3ameliorates both conditions. Throughout a 3-week period under controlled metabolic conditions, all subjects ate diets containing 15 mmol NaCl and 30 mmol potassium (K+) (per 70 kg body wt [BW] per day). Throughout weeks 2 and 3, NaCl was loaded to 250 mmol/d; throughout week 3, dietary K+was supplemented to 170 mmol/d (KHCO3+5%) and 6 salt resistant (SR). In NaCl-loaded SS but not SR subjects, RBF (mL/min/1.73 m2) decreased from 920 +/- 75 to 828 +/- 46 (P<0.05); filtration fraction (FF, %) increased from 19.4 +/- to 21.4 (P<0.001); and renal vascular resistance (RVR) (103x mm Hg/[mL/min]) increased from 101 +/- 8 to 131 +/- 10 (P<0.001). In all subjects combined, Delta MAP varied inversely with Delta RBF (r = -0.57, P=0.02) and directly with Delta RVR (r = 0.65, P=0.006) and Delta FF (r = 0.59, P=0.03), but not with MAP before NaCl loading. When supplemental KHCO3abolished the pressor effect of NaCl in SS subjects, RBF was unaffected but GFR and FF decreased. The results show that in marginally K+-deficientblacks (1) NaCl-induced renal vasoconstrictive dysfunction attends salt sensitivity; (2) the dysfunction varies in extent directly with the NaCl-induced increase in blood pressure (BP); and (3) is complexly affected by supplemented KHCO3, GFR and FF decreasing but RBF not changing. In blacks, NaCl-induced renal vasoconstriction may be a pathogenetic event in salt sensitivity. (Hypertension. 1999;33:633-639.)

ISSN:0194-911X    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

The objective of the present study was to examine the hypothesis that baseline heart rate (HR) predicts subsequent blood pressure (BP) independently of baseline BP. In the multicenter longitudinal Coronary Artery Risk Development in Young Adults study of black and white men and women initially aged 18 to 30 years, we studied 4762 participants who were not current users of antihypertensive drugs and had no history of heart problems at the baseline examination (1985-1986). In each race-sex subgroup, we estimated the effect of baseline HR on BP 2, 5, 7, and 10 years later by use of repeated measures regression analysis, adjusting for baseline BP, age, education, body fatness, physical fitness, fasting insulin, parental hypertension, cigarette smoking, alcohol consumption, oral contraceptive use, and change of body mass index from baseline. The association between baseline HR and subsequent systolic BP (SBP) was explained by multivariable adjustment. However, HR was an independent predictor of subsequent diastolic BP (DBP) regardless of initial BP and other confounders in white men, white women, and black men (0.7 mm Hg increase per 10 bpm). We incorporated the part of the association that was already present at baseline by not adjusting for baseline DBP: the mean increase in subsequent DBP was 1.3 mm Hg per 10 bpm in white men, white women, and black men. A high HR may be considered a risk factor for subsequent high DBP in young persons. (Hypertension. 1999;33:640-646.)

ISSN:0194-911X    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

24 hours. Of 36 studies initially identified, 11 (522 participants) met these inclusion criteria. Information on sample size, study design, participant characteristics (gender, race, age, baseline blood pressure, and antihypertensive medications), and treatment results were abstracted by 3 reviewers using a standardized protocol. Treatment effect of coffee consumption on blood pressure was estimated with the use of a random-effects model. In the 11 trials, median duration was 56 days (range, 14 to 79 days), and median dose of coffee was 5 cups/d. Systolic and diastolic blood pressure increased by 2.4 (range, 1.0 to 3.7) mm Hg and 1.2 (range, 0.4 to 2.1) mm Hg, respectively, with coffee treatment compared with control. Multiple linear regression analysis identified an independent, positive relationship between cups of coffee consumed and subsequent change in systolic blood pressure, independent of age of study participants and study design characteristics. The effect of coffee drinking on systolic and diastolic blood pressure was greater in trials with younger participants. Our findings provide support for a relationship between coffee consumption and higher blood pressure. Trials of coffee cessation of longer duration and in persons with hypertension should be performed. (Hypertension. 1999;33:647-652.)

ISSN:0194-911X    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

or=to85 mm Hg) fell from 42% during alcohol drinking to 12% after 1 month of complete abstinence. Abstinence did not modify either the long-term BP variability, assessed by SD of 24-hour BP, or its circadian profile. We conclude that abstinence in heavy alcohol drinkers significantly reduces BP assessed by 24-hour ABPM and that this reduction is clinically relevant. These results show that heavy alcohol consumption has an important effect on BP, and thus cessation of alcohol consumption must be recommended as a priority for hypertensive alcohol drinkers. (Hypertension. 1999;33:653-657.)

ISSN:0194-911X    

出版商:OVID    

年代:1999

数据来源: OVID