ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The causative mechanisms of hypertension were investigated by studying the renal function (pressure-natriuresis) curve in patients with primary aldosteronism (JI = 6) and renovascular hypertension (n = 6). Before and after radical operation (removal of adenoma in primary aldosteron-ism and percutaneous transluminal angioplasty in renovascular hypertension), dietary NaCl intake was altered from 10 to 13 g/day in Week 1 to 1 to 3 g/day in Week 2. Mean arterial pressure (MAP) and urinary sodium excretion were measured on the last 3 days of each week. By restricting sodium intake before operation, MAP was reduced from 122 ± 7 to 113 ± 7 mm Hg (p< 0.025) in primary aldoste-ronism but not in renovascular hypertension (130 ± 6 to 128 ± 5 mm Hg). The renal function curve was drawn by plotting urinary sodium excretion on the ordinate and MAP on the abscissa before and after operation. The slope of the curve was analyzed between the plotted points, and each curve was extrapolated to zero sodium excretion as an estimate of the degree of shift of the curve along the MAP axis. Before, as compared with after operation, the extrapolated v-intercept of the curve was shifted rightward in both primary aldosteronism (111 ± 7 vs 87 ± 4 mm Hg;p< 0.025) and renovascular hypertension (128 ± 5 vs 95 ± 2 mm Hg;p< 0.025) and the slope was depressed in primary aldoste-ronism (16 ± 1 vs 40 ± 17 [mEq/day]7 mm Hg;p< 0.025) but not in renovascular hypertension (130 ± 75 vs 40 ± 13 [mEq/day]/mm Hg). After operation, the renal function curves in primary aldosteronism and renovascular hypertension were normalized. The rightward shift of the curve in renovascular hypertension probably was due to an increase in renal vascular resistance caused by the stenotic renal vascular lesion as well as to increased resistance caused by stimulation of the renin-angiotensin system. The rightward shift in primary aldosteronism presumably was due to enhance-ment of renal tubular sodium reabsorption by aldosterone; the depressed slope likely resulted from suppression of the renin-angiotensin feedback mechanism by the excess aldosterone and resultant volume expansion. Thus, an abnormal renal function curve seems to have played a major role in the genesis of each of these forms of secondary hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

To assess the potential effect of hypertension on the results of thallium-201 stress imaging in patients with chest pain, 272 thallium-201 stress tests performed in 133 hypertensive patients and 139 normotensive patients over a 1-year period were reviewed. Normotensive and hypertensive patients were similar in age, gender distribution, prevalence of cardiac risk factors (tobacco smoking, hyperlipidemia, and diabetes mellitus), medications, and clinical symptoms of coronary disease. Electrocardiographic criteria for left ventricular hypertrophy were present in 16 hypertensive patients. Stepwise probability analysis was used to determine the likelihood of coronary artery disease for each patient. In patients with mid to high likelihood of coronary disease (>25% probability), abnormal thallium-201 stress images were present in 54 of 60 (90%) hypertensive patients compared with 51 of 64 (80%) normotensive patients. However, in 73 patients with a low likelihood of coronary disease (s 25% probability), abnormal thallium-201 stress images were present in 21 patients (29%) of the hypertensive group compared with only 5 of 75 (7%) of the normotensive patients (p< 0.001). These findings suggest that in patients with a mid to high likelihood of coronary artery disease, coexistent hypertension does not affect the results of thallium-201 exercise stress testing. However, in patients with a low likelihood of coronary artery disease, abnormal thallium-201 stress images are obtained more frequently in hypertensive patients than in normotensive patients.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

A recently presented hypothesis contends that the excess coronary heart disease mor-tality associated with hypertension is more prominent in lean men than in overweight men. This hypothesis was addressed using data collected in the Israeli Ischemic Heart Disease Study (n = 10,059). The ratios of age-adjusted 15-year death rates in hypertensive and normotensive men were 4.7,2.8,2.0, and 1.9 in the Quetelet index groups of <2.29,2.29 to 2.56,2.56 to 2.83 and >2.83 g/cm 2, respectively. The corresponding ratios for all-cause mortality were 2.2,2.1,2.0, and 1.7, respectively. The group with the highest all-cause age-adjusted mortality, at 33.6%, was that of the leanest (<2.29 g/cm, bottom 20% of the Quetelet index distribution) hypertensive subjects. The same group also displayed the highest coronary heart disease mortality (age-adjusted rate, 18.2%). The findings persisted for both smokers and nonsmokers and after exclusion of men with coronary heart disease or diabetics at intake, men on antihypertensive medication, or those who died in the first 2 years of follow-up (1963–1965). A multivariate risk score for developing myocardial infarction was calculated, based on levels of age, systolic blood pressure, total cholesterol, high density lipoprotein cholesterol, cigarette smoking, diabetes mellitus, and Quetelet index. This score varied little across the four Quetelet index groups in hypertensive men: 5-year mean estimated risks of myocardial infarction were between 70 and 74/1000. In normotensive men the scores increased from 19/1000 in the leanest subjects to 29/1000 in the overweight ones. The overall trend of 15-year coronary heart disease mortality is thus in line with the multiple risk of 5-year myocardial infarction incidence, but the source of the risk differences between lean and overweight hypertensive subjects remains unclear. These findings may have important implications in making decisions regarding the mode of treatment, especially in the wide group of mildly hypertensive persons in whom the benefit of treatment is still controversial. The treating physician who wishes to make a therapeutic decision might need to consider low body weight as either inherently representing or associated with an unfavorable progno-sis.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Changes in hemodynamic parameters following 50-degree head-up tilt were studied in a population of 56 men, including 35 subjects with sustained essential hypertension and 21 age-matched normotensive controls. The increase in heart rate following tilt was similar in both groups and exhibited the same reduction in response with age. The increase in vascular resistance following tilt was strongly and positively correlated with both age and baseline vascular resistance. The latter finding was observed mainly in hypertensive subjects. The study provided evidence that differentiated responses of heart rate and vascular resistance may be observed following orthostasis. In both normal and hypertensive subjects, the age dependence of heart rate response possibly reflected differences in baroreceptor reflex control of parasympathetic and sympathetic activity. In hypertensive subjects, the vascular response was amplified with age and baseline vascular resistance, suggesting a role for structural changes of the vessels in the increased vascular response.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The purpose of our study was to determine the effects of treatment with hydrochlorothiazide (n = 10) or diltiazem (n = 8) on reflex humoral, hemodynamic, and vascular responses to graded lower body negative pressure in subjects with mild to moderate hypertension (supine diastolic pressure, 95–114 mm Hg). All subjects received placebo for 2 to 4 weeks followed by either hydrochlorothiazide (25–50 mg b.i.d.) or diltiazem (120–180 mg b.i.d.) to achieve a reduction in supine diastolic pressure of 10 mm Hg or more and a final pressure below 90 mm Hg. Mean arterial pressure, forearm vascular resistance, plasma norepinephrine, and renin responses to graded lower body negative pressure (−10, − 20, − 40 mm Hg) and head-up tilt were examined before and after 12 weeks of treatment with either drug. Pretreatment basal values of mean arterial pressure (114 ± 2 vs 117 ± 2 mm Hg), forearm vascular resistance (29 ± 3 vs 35 ± 7 units), and plasma renin activity (0.7 ± 0.2 vs 0.6 ± 0.2 ng angiotensin I/ml/hr) were not significantly different between groups. There were no significant differences in basal plasma norepinephrine or in the increases of norepinephrine in response to lower body negative pressure before and after treatment in either group. Forearm vascular resistance responses to lower body negative pressure were virtually abolished in the diltiazem-treated group but not in the hydrochlorothiazide-treated group despite similar levels of mean arterial pressure and basal forearm vascular resistance. Plasma renin activity was significantly higher in the hydrochlorothiazide-treated group after therapy, but the change in renin activity in response to lower body negative pressure was similar before and after therapy in either group. These results suggest that the reflex neurogenic vasoconstriction during lower body negative pressure is inhibited by diltiazem through deactivation of calcium-dependent contractile responses of vascular smooth muscle in the forearm.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Whether the dopaminergic system may be involved in essential hypertension is of pathogenetic as well as therapeutic interest. Therefore, we investigated in eight hypertensive and 12 normal subjects cardiovascular, endocrine, and renal responses to fenoldopam, which has been characterized experimentally as an agonist of peripheral postsynaptic dopamine, receptors. A single oral dose of fenoldopam, 100 mg, changed blood pressure (BP) in hypertensive subjects (from 163/103 to 147/76 mm Hg;p< 0.01 for systolic andp< 0.001 for diastolic BP) and normal subjects (from 121/81 to 123/65 mm Hg;p< 0.001 for diastolic BP); percentage decreases in diastolic BP averaged −20 ± 6 and −1 6 ± 7%, respectively. Fenoldopam-induced effects on other variables were similar in the two groups. Heart rate rose (p< 0.001) on average from 69 to 92 beats/min in hypertensive and from 64 to 84 beats/min in normal subjects. Effective renal plasma flow increased (from 552 to 765 and 634 to 937 ml/min/1.73 m2;p< 0.01), while glomerular nitration rate tended to decrease (from 121 to 99 ml/min/1.73 m2in the hypertensive and from 119 to 97 ml/min/1.73 m2;p< 0.001 in the normal group). Fractional sodium clearance was elevated (from 2.8 to 5.2 and 1.7 to 3.8%;p< 0.01), as was free water clearance (from −1.7 to 0.6 and −1.7 to 0.1 ml/min/1.73 m2;p< 0.01). Potassium clearance was largely unchanged. Plasma renin activity increased about twofold (p< 0.01 in normal subjects), and plasma aldosterone by 40% (NS). Plasma norepinephrine levels increased twofold to 2.5-fold (p< 0.001), and urinary norepinephrine excretion fivefold to 10-fold (p< 0.01). Fenoldopam-induced changes were not significantly modified by intravenous and/or oral pretreatment with the dopamine-receptor antagonist metoclopramide or the cyclooxygenase inhibitor indomethacin. These findings suggest that in humans, fenoldopam may acutely override the dopaminergic antagonism of metoclopramide given in clinical dosage and that its cardiovascular and renal effects are not prostaglandin-mediated. Although acute sympathetic stimulation may be partially antagonistic, the concomitant BP-lowering, renal vasodilating, and natriuretic actions of fenoldopam represent a desirable profile of a potential antihypertensive agent.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

High salt diet alters neural cardiovascular control. This influence has been attributed to central neural or efferent mechanisms. To test the hypothesis that a high salt diet might alter afferent baroreceptor function, Dahl salt-resistant (DR) and salt-sensitive rats (DS) were fed a high or a low salt diet. Blood pressure was measured intra-arterially in unanesthetized animals. Aortic baroreceptor function was then evaluated during urethane anesthesia by recording multifiber aortic depressor nerve activity during a phenylephrine-induced blood pressure ramp. Mean arterial pressure in the conscious state was elevated (155 ± 5 [SE] mm Hg) in DS fed a high salt diet but was normal in DS fed a low salt diet and in DR. Slopes of linear regressions relating aortic nerve discharge to mean arterial pressure were 71 % higher in DR fed a high salt diet than in DR fed a low salt diet (p< 0.025), indicating that high salt potentiated baroreceptor function in DR. In contrast, high salt diet produced no significant effects on baroreceptor function in DS. No salt-induced changes in dynamic or static aortic distensibility (assessed from pressure-volume curves of the in situ isolated arch) were detectable in either rat strain. Absence of salt-induced baroreceptor sensitization in DS was not due to the hypertensive state because the sensitization also failed to occur in separate groups of DS in which saltinduced hypertension had been prevented by chemical sympathectomy with 6-OH-dopamine. Thus, high dietary salt 1) potentiates afferent arterial baroreceptor function in DR, a phenomenon unrelated to aortic distensibility and probably resulting from sensitization of baroreceptors by high salt diet, and 2) fails to sensitize baroreceptors in DS, probably because of a primary abnormality in baroreceptor function in DS.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID