ISSN:0194-911X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

To characterize the hemodynamlc response to exercise and the effects of calcium channel antagonism in hypertensive subjects, invasive exercise hemodynamics were performed in the baseline state after intravenous infusion of verapamil and after 5 to 7 days of oral verapamil in 10 subjects with moderate to severe hypertension. We also assessed oxygen delivery and use and the response of the sympathetic nervous system by measuring plasma norepinephrine levels at rest and during exercise. Both routes of administration were associated with significant reductions of mean arterial pressure and systemic vascular resistance at rest and peak exercise (p< 0.05). Changes in heart rate were not statistically significant. Following oral administration of verapamil, stroke volume increased significantly in both tbe resting and exercise states. Pulmonary wedge pressure did not increase; in fact, the Frank-Starling relationship of cardiac performance actually was improved. Oxygen delivery and use were unchanged with both routes of administration. There was no significant difference in rest and exercise plasma norepinephrine levels following verapamil therapy. Thus, verapamil resulted in a significant reduction of mean arterial pressure, mediated by a significant reduction of systemic vascular resistance, following both intravenous and short-term oral administration. This reduction occurred without expression of left ventricular dysfunction and was not at the expense of increased oxygen use or enhanced sympathetic nervous systemic activity.

ISSN:0194-911X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Concentrations of serum total calcium and serum calcium fractions were compared between 28 hypertensive subjects and 28 race-sex-age-matched normotensive controls. Mean levels of serum total calcium were not different between the two groups. Hypertensive subjects had lower mean serum levels of ultrafilterable calcium (−0.32 mg/dl; p = 0.01), ionized calcium (−0.07 mg/dl; p = 0.09), and complexed calcium (−0.23 mg/dl; p = 0.04) and higher levels of protein-bound calcium (+ 0.36 mg/dl; p = 0.07). Estimated dietary calcium intake was similar in the two groups. These findings add to the evidence that essential hypertension is associated with perturbations in calcium metabolism.

ISSN:0194-911X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

We examined the time course and extent to which central and peripheral mechanisms contribute to the short-term effects of a 500-mg oral dose of α-methyldopa on supine mean arterial pressure, cardiac output, and total peripheral resistance, as well as its effects on total urinary excretion of norepinephrine and its metabolites, in five subjects with essential hypertension. Total peripheral resistance was reduced significantly 1 hour after α-methyldopa administration and remained so for the ensuing 7 hours of the study (p< 0.05). A small but significant reduction in mean arterial pressure occurred 7 hours after the dose (p< 0.05), while cardiac output did not change significantly. Total 24-hour urinary norepinephrine and metabolite excretion was reduced by 8.1 fimol (35% compared with placebo). The relative distribution of urinary norepinephrine metabolites was unaffected by α-methyldopa, and the catecholamine metabolites of α-methyldopa, α-methy lnorepinephrine and α-methylnormetanephrine did not account for this reduction. Competitive inhibition of methyldopa transport across the blood-brain barrier and into the central nervous system by large oral doses of isoleucine antagonized most of the effect of α-methyldopa. The effects on total peripheral resistance were completely abolished, and small, insignificant changes during the 7-hour study were similar to those observed after placebo. Changes in mean arterial pressure were not significant; however, 24-hour total urinary norepinephrine and metabolite excretion increased by 6.1 μ.mol to 22.7 fimol (24.7 fimol excreted after placebo). Adding benserazide to the α-methyldopa-isoleucine dose regimen in an attempt to inhibit any residual, presumably peripheral, effects of α-methyldopa caused little, if any, further antagonism. Our results suggest that short-term oral administration of amethyldopa inhibits norepinephrine release from sympathetic nerves by central mechanisms, and the responses in mean arterial pressure, although small, are consistent with this hypothesis. The reductions in total peripheral resistance also appear to be centrally mediated.

ISSN:0194-911X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Relationships between initial anthropometric variables and subsequent diastolic blood pressure (fourth phase) were examined in children identified as being in the upper quintile for diastolic blood pressure at Year 1. Of 156 white children, aged 10 to 14 years, with diastolic blood pressure levels in the upper age-race-sex-specific quintile at Year 1, 38% remained in the upper quintile at Year 4. However, there was a definite trend for leaner children, defined by ponderosity (weight/height3) to remain in the highest diastolic blood pressure quintile (p< 0.001). Of white children originally identified in the highest quintile for diastolic blood pressure and the lowest quintile for ponderosity (lean group), 67% (18 of 27) remained in the upper quintile at Year 4. In contrast, only 21% (11 of 52) of white children identified as being in the highest quintile for both diastolic blood pressure and ponderosity (obese group) at Year 1 were in the upper diastolic blood pressure quintile at Year 4. Similar results were seen in children examined 5 years later. Pearson correlation coefficients and linear regression analyses confirmed the negative relationship between initial ponderosity and subsequent diastolic blood pressure, especially in older children. A similar relationship was noted in black children. Potential differences in the etiological process of obesity-related and non-obesityrelated high blood pressure were examined. These observations indicate that characteristics other than obesity can contribute to high blood pressure in late childhood.

ISSN:0194-911X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

To investigate the pathophysiology of essential hypertension, detailed biochemical and clinical variables were collected and analyzed for 2091 Utah subjects aged 3 to 83 years. Three different measurements of erythrocyte cation transport were obtained: Na+-Li+countertransport, Li+-K+cotransport, and furosemide-insensitive Li+efflux into MgCI2. Total plasma cholesterol, triglycerides, and high density lipoprotein cholesterol levels were obtained from fasting subjects. Levels of high density lipoprotein subfractions 2 and 3 were also obtained from 350 subjects. Standardized data collection also included blood pressure, height, weight, and presence or absence of a diagnosis or treatment of essential hypertension. In univariate analyses of all 1420 adults, each of the three transport systems showed the same significant correlations with triglyceride levels (r = 0.33–0.35,p< 0.0001), high density lipoprotein concentration (r = — 0.19 to — 0.21,p< 0.001), and weight (r = 0.22–0.28,p< 0.0001). In multivariate regression analyses, values for each transport system were significantly higher in hypertensive subjects; values for triglycerides, high density lipoprotein, and usually, the high density lipoprotein subfractions continued to have strong significant independent associations with all three transport systems; and weight remained significantly related only to Na+-Li+countertransport. In separate logistic regressions, plasma triglyceride levels (positively,p< 0.001) and high density lipoprotein subfraction 3 levels (inversely,p< 0.03) were associated with hypertension itself. In multivariate analyses among 671 children, high density lipoprotein and high density lipoprotein subfraction 3 levels showed significant (p< 0.05) inverse correlations with Na+-Li+countertransport and furosemide-insensitive Li+efflux. These associations of all three cation transport systems with several blood lipids as well as with weight and hypertension suggest that a general relationship exists between blood lipids and membrane cation transport in the pathophysiology of essential hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Experiments were designed to investigate the importance of vascular endothelium in the vasomotor response to increases in flow as observed in conduit arteries (flow-dependent dilation). The diameter changes of femoral arteries (sonomicrometry) in response to increases in flow before and after endothelial damage procedures were studied in 23 dogs anesthetized with sodium pentobarbital. The functional integrity of the endothelial cells underneath the diameter sensors was tested by intraarterial acetylcholine (local acetylcholine dilation) applied proximally to the sensors while a constant flow was maintained. Unilateral augmentation of femoral arterial flow (4.6 ± 1.9-fold) induced by peripheral vasodilation or by arteriovenous shunt, elicited dilation (increase in diameter, 116 ± 91 fim) in 18 of 23 dogs, whereas the diameter of the contralateral control artery was not affected. Mechanical removal of the endothelial cells by means of a balloon catheter abolished both the flowdependent dilation and the local acetylcholine dilation, whereas the vasomotor responses to norepinephrine and nitroglycerin were not affected. Brief perfusions (1 minute) of the arteries with cell-free hydrogen peroxide solution (90 mM) also abolished the flow-dependent dilation and attenuated the local acetylcholine dilation (by 27 ± 19%;p< 0.02), while the responses to norepinephrine and nitroglycerin were not altered. These results suggest that endothelial cells act as mediators of flowdependent dilation.

ISSN:0194-911X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Epidemiological studies suggest an association between reduced calcium uptake and hypertension, while clinical trials and rat experiments indicate a small but significant hypotensive effect with oral calcium supplements. These data imply that calcium deficiency has a role in genetic hypertension. We reasoned that if the hypothesis is correct, the hypertension should be aggravated by further reducing calcium balance but attenuated by augmenting calcium balance. We tested this hypothesis by evaluating the blood pressure response in spontaneously hypertensive rats (SHR) as calcium balance was decreased by dietary restriction of calcium or increased by supplementation with magnesium or la,25-dihydroxycholecalciferol (calcitriol). A low calcium diet within the physiological range did not accentuate the hypertension in SHR during the 11 weeks of treatment, even though calcium balance was reduced by half. Similar results were obtained with dietary calcium restriction in parathyroidectomized SHR, which excludes any offsetting effects of changes in parathyroid hormone levels. Conversely, 7 weeks of a high magnesium diet, which increased calcium balance without reducing PO4 balance, did not correct the hypertension of SHR. Similarly, long-term administration of calcitriol failed to reduce the blood pressure of parathyroidectomized SHR and normotensive Wistar-Kyoto (WKY) controls, despite the presence of increased serum calcium levels comparable to those produced by oral calcium loading. Finally, external calcium balance was measured directly in 25-day-old, prehypertensive SHR. As a result of the increased calcium absorption and reduced calcium excretion, SHR retained more calcium than did the normotensive WKY, which directly refutes the existence of calcium deficiency at this normotensive stage. These data do not support the role of calcium deficiency in genetic hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The influence of β-adrenergic receptor blockade on the impulse activity of 21 cardiovascular sympathetic afferent nerve fibers (11 from the thoracic aorta, 10 from the pulmonary veins), isolated from the left sympathetic rami communicantes T-3 and T-4 was studied in anesthetized, vagotomized cats. Aortic pressure, heart rate, and neural discharge were recorded during control conditions and during brief aortic occlusions of comparable amplitude and duration. Administration of (μ-propranolol (0.2–0–4 mg/kg) did not modify aortic pressure or neural discharge of the fibers during control conditions, although, as expected, heart rate was diminished. (μ-Propranolol administration did change the response of cardiovascular sympathetic afferents to similar aortic pressure increases. Before drug administration, aortic occlusion caused a significant increase in neural discharge of both aortic and pulmonary vein sympathetic afferent fibers, from 0.52 ± 0.12 to 1.64 ± 0.31 and from 0.67 ± 0.10 to 2.08 ± 0.25 impulses/sec, respectively (p< 0.05). After (μ-propranolol administration, comparable increases in aortic pressure resulted in slight but not significant increases in neural discharge of aortic and pulmonary vein fibers. Administration of d-propranolol (0.4–0.6 mg/kg), which possesses only membrane-stabilizing properties, did not modify the firing rate of four pulmonary sympathetic afferents, which subsequently decreased their response to pressure rises after administration of (μ-propranolol. These results indicate that β-adrenergic receptor blockade reduces the responsiveness to hemodynamic stimuli of sympathetic cardiovascular afferent fibers that are capable of mediating excitatory pressor reflexes.

ISSN:0194-911X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

We have previously reported that 1) selective dietary sodium loading (without chloride) does not produce hypertension in rats of the Dahl salt-sensitive strain (DS) and 2) selective chloride loading (without sodium) lowers plasma renin activity in the intact Sprague-Dawley rat maintained on a low NaCI diet. The present study examined the effect of selective dietary chloride loading on two models of hypertension: the DS and the renin-dependent one-kidney, one clip Sprague-Dawley rat. The DS were pair-fed (n = 7/group) a “normal” NaCI, a high NaCI (4%), or a “normal” sodium-high chloride diet for 11 weeks. From Week 7 until the end of the experiment, the high NaCl-fed animals had higher (p 0.05) blood pressures than animals fed either the normal NaCI or normal sodiumhigh chloride diet, which were not different from each other. Thus, in the DS, hypertension depends on high dietary intakes of both sodium and chloride. In one-kidney, one clip hypertensive rats, selective chloride loading failed to lower plasma renin activity (9 ± 1 vs 7 ± 1 ng angiotensin I/ml/hr) or to prevent hypertension (160 ± 10 vs 166 ± 9 mm Hg). Thus, selective dietary chloride loading (without sodium) does not alter blood pressure in either salt-sensitive or renin-dependent hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1986

数据来源: OVID