ISSN:0263-6352    

出版商:OVID    

年代:1985

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1985

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1985

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

One possible explanation for the salt sensitivity of blood pressure (BP) in certain hypertensive individuals is that neural mechanisms which normally counteract the pressor effect of a high dietary sodium intake are defective. We have tested this possibility in normotensive Wistar-Kyoto rats (WKY) by surgically ablating the arterial baroreflex mechanism. This manoeuvre, by itself, conferred substantial salt-sensitivity on the WKY rats whose BP is normally relatively insensitive to dietary sodium intake. The treated rats responded to a high sodium diet with a significant rise in systolic BP which was reversed by substituting a low sodium diet. Thus, impaired baroreflex function which has been observed in essential hypertension and in hypertensive animals, may be responsible for the hypertensive effect of sodium.

ISSN:0263-6352    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The purpose of the study was to clarify the mechanism(s) of glucocorticoid-induced hypertension. Hypertension was induced in rats by single i.m. injection of methylprednisolone (MP) 20 mg/kg. In normal Wistar rats, systolic blood pressure (SBP) increased by 30 mmHg from days 2 to 10 after MP. Urinary sodium excretion increased transiently and sodium balance was negative. Plasma volume (PV; ml/100 g body weight) increased on day 5, but was unchanged on day 2 after MP, at a time when SBP had already increased. In rats with chronic renal failure (CRF) and low sodium intake, SBP increased more than in control rats (48 versus 22 mmHg on day 10). Hypertension was not accompanied by a significant drop in urinary excretion of prostaglandin E2(PGE2; measured by radio-immunoassay). In normal MP-injected rats, PGE2excretion decreased slightly and then increased; in CRF rats, basal PGE2excretion was too low to evaluate the effect of MP. In homozygous Brattleboro rats lacking antidiuretic hormone (ADH), MP increased SBP by 28 mmHg (day 10). Similar changes were obtained in heterozygous Brattleboro rats. The changes in PV were identical to those found in Wistar rats. We conclude that increase in PV, change in PGE2and vasopressin do not play a key role in MP hypertension. Direct effect of glucocorticoid on vascular receptors is likely to be involved in this model.

ISSN:0263-6352    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

To evaluate the role of renal Na+K+ATPase in the presence of Goldblatt hypertension, the enzyme activity and [3H]ouabain binding were examined in cortical and medullary homogenates from two-kidney, one clip (2K1C), one-kidney, one clip (1K1C), unilaterally nephreetomized and normal rabbits. Four weeks after the surgery, systolic blood pressures (SBPs) of 2K1C and 1K1C rabbits were increased significantly to 128 ± 3 and 129 ± 2 mmHg, respectively. In contrast, SBPs in the normal controls and unilateral nephrectomized (1K) animals were 83 ± 2 and 86 ± 3 mmHg, respectively.In the 2K1C rabbits, atrophy (91 %) occurred in the kidney on the ischaemic side and hypertrophy (110%) occurred in the contralateral kidney. Na+K+ATPase activity and number of [3H]ouabain binding sites were reduced in the homogenates of the ischaemic kidney of 2K1C rabbits. In the 1K1C rabbits, marked hypertrophy of the kidney (155%) occurred, and the activity of Na+K+ATPase and the number of [3H]ouabain binding sites increased slightly in the cortex and medulla, compared with the normal controls. 5'-Nucleotidase, a plasma membrane marker enzyme, remained unchanged in both groups of hypertensive rabbits. Dissociation constant (KD) values for [3H]ouabain binding did not differ significantly in the renal homogenates of 2K1C and 1K1C, compared with findings in the normal controls.The inhibitory activity of plasma was measured by studying [3H]ouabain binding to Na+K+ATPase of renal tubular basolateral membrane vesicles purified by Percoll gradient. The inhibition was more pronounced with plasma from 2K1C, 1K1C and 1K rabbits than from the control animals.Our findings suggest that in the Goldblatt hypertensive model, changes in Na+K+ATPase activity were due to alterations in glomerular filtration rate (GFR).

ISSN:0263-6352    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

In a study on 22 normotensive male subjects, a change in dietary sodium intake from 29.6 ± 6.0 to 332.5 ± 13.9 mmol/day (mean ± s.e.m.), over 7 days, was associated with a significant rise in supine and standing systolic blood pressure and a fall in sodium pump activity. Iritracellular sodium remained constant, while intracellular potassium fell. These changes appeared to be reversed by the addition of potassium (96 mmol/day) to the high sodium diet. The 12 subjects with a family history of essential hypertension, as determined by measurement of parental blood pressure, did not differ in their response from those whose parents were normotensive.

ISSN:0263-6352    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Intra-arterial blood pressure (IABP), baroreflex sensitivity and set point were measured in nine patients with essential hypertension during a control period and then after acute (4 h after a 12 mg oral dose) and chronic (after 3 months) treatment with the loop diuretic piretanide, mean dose 10 mg. Acutely, there was a fall in mean systolic IABP (P< 0.06) associated with a reduction in pulse interval (P< 0.01). Chronically, mean systolic IABP remained significantly reduced (P< 0.01) but pulse interval returned to control values. There were no significant changes in baroreflex sensitivity, either acutely or chronically. These results demonstrate acute deactivation of the vagal efferent limb of the baroreflex followed by a chronic resetting of the baroreflex-heart rate mechanism. We conclude that changes in baroreflex sensitivity are not responsible for the hypotensive effects of this drug and that resetting of the reflex arc is likely to be due to physiological adaptation rather than to any direct drug effect.

ISSN:0263-6352    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

A mixed solution of 0.1% sodium nitroprusside and 1% sodium thiosulphate (‘SNP-thiosulphate’) was given as i.v. infusion to 80 patients, 30 of whom were hypertensive emergencies and 50 were surgical cases requiring induction of hypotension. This treatment lowered the blood pressure (BP) by an average of 30% of the initial levels in the hypertensive patients and 30–40% of the initial levels in the surgical patients. The mean effective dose in the hypertensive patients was 2.4 μg/kg/min compared with about 3 μg/kg/min in 40 cases treated with sodium nitroprusside as mono-infusion. For deliberate hypotension in surgical patients the mean doses of SNP, used here in the mixed infusion with thiosulphate, were 1.0 and 2.3 μg/kg/min, compared with 1.3–7.5 μg/kg/min in 181 patients treated with SNP as monotherapy. In contrast to conventional therapy with SNP, the infusion of SNP-thiosulphate even at extremely high dose rates did not produce toxic concentrations of prussic acid in the blood. In no case was a rise observed in the cellular enzymes as an indirect indication of hypoxic cell damage. SNP-thiosulphate is thus at least as effective at lowering BP as SNP infused alone, and has a substantially lower toxicity risk.

ISSN:0263-6352    

出版商:OVID    

年代:1985

数据来源: OVID