ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Differences in cellular Na+ and K+ regulation may relate to the pathogenesis of essential hypertension and the predisposition of blacks to this disease. To explore these tenets, we examined several aspects of cellular Na+ homeostasis in serially passed, cultured skin fibroblasts from 30 subjects (15 hypertensive blacks and whites and normotensive subjects matched for sex, age, and race.) Fibroblasts from blacks demonstrated higher cellular Na+ turnover rates than did those from whites. This difference was expressed by accelerated Na+-K+ pump activity (ouabain-sensitive Na+ washout rate, 3.46 ± 0.216 for blacks vs 1.84 ± 0.283 mEq/IVmin for whites; p=0.0006) and a higher rate of cellular accumulation of Na+ in the presence of ouabain (0.964 ± 0.0743 vs 0.562 ± 0.0440 mEq/IVmln f°r blacks and whites, respectively; p=0.0045). Associated with these findings, fibroblasts from blacks had higher cellular Na+ concentration than did those from whites (9.78 ± 0.512 vs 7.50 ± 0.400 raEq/L; p=0.0170, as measured by atomic absorption, and 7.84 ± 0.470 vs 5.03 ± 0.980 mEq/L; p=0.0141, as derived from the equilibrium distribution ratio of22Na+). It is concluded that blacks differ from whites with respect to cellular Na+ turnover rate, which is evidenced by an increased Na+ influx and accelerated Na+-K+ pump activity in their fibroblasts. Our findings support the tenet that innate racial differences in cellular Na+ regulation may underlie the predisposition of blacks to hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

In a previous study, we reported that black children demonstrated greater cardiovascular reactivity than did white children to the psychological stress of a television video game. Reliance on urban volunteers and the wide age range of the children may have limited conclusions concerning the generalizability of those results. In the present study, 481 of 484 children enrolled in the third grade of the public schools of an entire rural county in Tennessee were examined with the same video game procedure used previously. Results indicated greater heart rate and blood pressure reactivity among black children than among white children. Thus, the previous results were replicated. The greater prevalence of hypertension among black adults may relate to the greater reactivity among black children; reactivity may be either a marker or a mechanism in the development of hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Nineteen patients with normal renin idiopathic hypertension were arbitrarily classified as salt-sensitive or salt-resistant depending on whether their mean arterial pressure did or did not increase by 8% or more when sodium intake was increased. The responses of the two subsets and of five normal subjects to sodium intakes of 9, 109, and 249 mEq/day given for 7 days were as follows: The salt-sensitive subjects retained more sodium than normal and plasma or urinary norepinephrine did not decrease when they were given a high sodium intake; urinary dopamine was normal but did not increase normally when sodium intake was increased. The salt-resistant subjects excreted sodium normally and plasma and urinary norepinephrine was decreased by 30 and 37%, respectively, when they were given a high sodium intake; urinary dopamine was supernormal and did not increase further when sodium intake was increased. Cumulative sodium retention during the high sodium intake was directly related to the percentage of change in plasma norepinephrine in the hypertensive subjects, suggesting that renal adrenergic activity was a factor in the impaired sodium excretion in the salt-sensitive patients. Cumulative sodium retention and the percentage of change hi plasma norepinephrine were inversely related to urinary dopamine in the hypertensive subjects, suggesting that increased formation of dopamine in renal and neural tissue in the salt-resistant subjects may have been responsible for the differences between the subsets hi renal and adrenergic responses to a high sodium intake. Supernormal sodium retention and a failure to suppress adrenergic activity may explain, hi part, the phenomenon of salt sensitivity of blood pressure in salt-sensitive patients and may also be factors in the pathogenesis of hypertension in this subset.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Structural changes in resistance vessels have been considered an important factor in triggering and maintaining chronic hypertension in humans and in experimental animals. To determine whether the increased forearm vascular resistance observed following vasodilator maneuvers in hypertensive patients is predominantly due to structural or to functional changes, we examined the influence of different vasodilator stimuli on forearm blood flow and blood pressure in 22 male patients with established essential hypertension and in 22 age-matched normotensive men (age range, 28–52 years). Blood pressure was measured directly, and blood flow was measured by venous occlusion plethysmography. The maneuvers applied were 1) arterial occlusion combined with handgrip exercise and local heating, 2) intra-arterial infusion of the calcium entry blocker nifedipine, 3) intra-arterial infusion of the nonspecific vasodilator sodium nitroprusside, 4) arterial occlusion initiated after intraarterial infusion of nifedipine. Vascular resistance during vasodilation induced by arterial occlusion or infusion of nifedipine or sodium nitroprusside remained significantly higher in the hypertensive than in the normotensive subjects. However, the maximal vasodilation achieved by the combination of arterial occlusion and nifedipine resulted in a similar resistance in both groups (1.6 ± 0.2 in the hypertensive vs 1.4 ± 0.2 nun Hg/ml/min/100 ml tissue in the normotensive subjects). These data suggest that there is an important functional component of the elevated resistance in patients with essential hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

The responsiveness of central nervous system α2-adrenergic receptors in the neural control of renal function was compared in conscious spontaneously hypertensive rats (SHR) and normotensive Wlstar-Kyoto rats (WKY) on normal or high sodium intake (3–4 weeks of 1% NaCl for drinking). The responsiveness of central aradrenergk receptors was determined by comparing among groups the dose-response curves for the effects of cumulative intracerebroventricular injections of guanabenz (5, 25, and 125 μg) on changes in mean arterial pressure, renal sympathetic nerve activity, and urinary sodium excretion. Guanabenz altered mean arterial pressure similarly in SHR on normal or high sodium intake and in WKY on normal or high sodium intake. High sodium intake shifted the guanabenz-renal sympathetic nerve activity and guanabenz-urinary sodium excretion dose-response curves to the left in SHR and to the right in WKY. The dose-response curves between SHR and WKY on normal sodium intake were similar. Surgical renal denervation or pretreatment with an α2-adrenergic receptor antagonist (rauwolscine, 30 fig i.c.v.) attenuated the ability of guanabenz to inhibit renal sympathetic nerve activity or increase urinary sodium excretion in SHR and WKY on either normal or high sodium intake. We conclude that the responsiveness of central nervous system α2-adrenergic receptors regarding the neural control of renal function is increased by high sodium intake in conscious SHR, but not in conscious normotensive WKY.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

The effects of a stressful environmental stimulus (air stress) on mean arterial pressure, renal sympathetic nerve activity, and renal function were examined in conscious Dahl salt-sensitive (DS) and Dahl salt-resistant rats (DR) on low (0.4%) and high (8%) NaCl diets. Air stress increased renal sympathetic nerve activity and decreased urine flow rate and urinary sodium excretion in conscious Dahl rats on a high sodium diet, but it had no effect in rats on a low sodium diet. Mean arterial pressure did not change during air stress in any group. Renal denervation prevented the antidiuretic and antinatriuretic responses to stress in DS and DR on a high NaCl diet. An increased renal tubular reabsorption of sodium and water appeared to mediate the antinatriuretic and antidiuretic responses to air stress, since glomerular filtration rate and renal plasma flow were unchanged. Thus, environmental stress increases renal sympathetic nerve activity and decreases urinary sodium excretion more in' Dahl rats on a high NaCl diet than on a low NaCl diet. On a high NaCl diet, these responses are greater hi DS than in DR.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

The aim of this work was to investigate, in an experimental model of diabetes mellitus, the levels of renin activity in vascular and adrenal tissues and their relationship to several circulating renin-angiotensin system components. Rats with chronic (12 weeks) streptozocin-induced diabetes showed a significant decrease in plasma renin activity (PRA), plasma renin concentration, and plasma aldosterone. However, plasma trypsin activatable inactive renin concentration was increased (11.65 ± 1.40 vs 6.73 ± 0.57 ng angiotensin I/ml/hr;p< 0.001), as were aortic reninlike activity (p< 0.001) and adrenal renin, both in the zona glomerulosa (p< 0.01) and the fascicular-reticularmedullary portion (p< 0.001) with respect to an age-matched control group. After bilateral nephrectomy, plasma renin-angiotensin system components (PRA and plasma active and inactive renin concentrations) as well as aortic and fascicular-reticular-medullary renin activity significantly decreased in both control and diabetic rats. However, glomemlar renin activity increased in control nephrectomized rats to the levels observed in diabetic animals but did not change in diabetic nephrectomized rats. The parallel changes of aortic and fascicular-reticular-medullary renin activity and plasma inactive renin concentration in diabetes and nephrectomy suggest an interdependent relationship, whereas the increase of glomerular renin activity in diabetic and nephrectomized animals, both with low levels of PRA, suggests the existence of a local autonomic renin-angiotensin system regulated by plasma feedback. Tissue renin-angiotensin system alterations in diabetes could mean that a pathogenic factor is involved in long-term diabetic complications or that only a compensatory physiological process is at work.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

To assess the effects of imposition of moderate diabetes on in vivo cardiac performance in gradually proceeding hypertension, spontaneously hypertensive (SHR) and Wistar-Kyoto rats (WKY) were treated with streptozotocin (40 mg/kg) or vehicle at 8 weeks of age. Four and 20 weeks later, with the rats under ether anesthesia, peak cardiac output and stroke volume were measured during volume loading and peak left ventricular developed pressure and maximum rate of rise of pressure (dP/dtMaxwere determined during aortic occlusion. Additionally, passive pressure-volume relations were obtained during saline infusion hi potassium-arrested hearts, and the chamber stiffness constant was derived from one exponential function. There was a mortality of 16.1% in the diabetic SHR only. While basal and stressed cardiac performance was unchanged despite the already decreased mean arterial pressure and left ventricular weight at 4 weeks, the diabetic SHR revealed significant decreases in peak cardiac pumping indexes, peak left ventricular developed pressure, and dP/dtMax, with unchanged resting cardiac function, at 20 weeks. Changes seen in the diabetic WKY were reduced left ventricular weight at 4 weeks and reduced peak left ventricular dP/dtMaxat 20 weeks. The chamber stiffness was unaltered with strain or diabetes. These data show that imposition of even moderate diabetes substantially influences the stress-loaded in vivo cardiac performance in the SHR, whereas it produces only minor changes in the WKY.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID