ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

The ability of endothelin to stimulate phosphatidylinositol hydrolysis in rings of rat aorta was studied. Endothelin 10-8-10-5mol/l caused increases of 200–1000% in inositol phosphate levels. However, physiological responses to endothelin have been reported in the concentration range 10-10-10-8mol/l. Thus phosphatidylinositol hydrolysis as measured in the present study does not correlate directly with functional responses. Phosphatidylinositol hydrolysis in response to endothelin was attenuated but not abolished by removal of endothelium. Attenuation of inositol phosphate production was also observed with time, consistent with the hypothesis that continuous exposure to the agonist can cause desensitization of the endothelin receptor.

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Dietary calcium (Ca2+) supplementation lowers blood pressure in many forms of genetically mediated and experimentally induced hypertension. The present study tested the hypothesis that neuronal mechanisms underlie the blood pressure-lowering effect of dietary Ca2+in NaCl-sensitive spontaneously hypertensive rats (SHR-S). SHR-S were fed one of the following diets: control (0.75% NaCl/0.68% Ca2+); high NaCl (8.00% NaCl/0.68% Ca2+); high Ca2+(0.75% NaCl/2.00% Ca2+), and high NaCl/high Ca2+(8.00% NaCl/2.00% Ca2+). SHR-S on the 8% NaCl diet for 2 weeks displayed significantly elevated blood pressure (161 ± 4 mmHg) compared with those on the control diet (139 ± 3 mmHg). Ca2+supplementation prevented a rise in blood pressure in rats on the high-NaCl diet but did not alter blood pressure in rats consuming 0.75% NaCl. Plasma norepinephrine stores and turnover in the hypothalamus (anterior and posterior regions), brainstem (pons and medulla) and thoracic spinal cord were assessed using the dopamine-β-hydroxylase inhibitor 1-cyclohexyl-2-mercapto-imidazole. The 8% NaCl diets reduced anterior hypothalamic region norepinephrine stores and turnover. Concomitant Ca2+supplementation restored norepinephrine turnover to normal, but did not alter norepinephrine stores in the anterior hypothalamic region. In other regions, no significant differences in norepinephrine content or turnover were observed among groups. In SHR that are resistant to high-NaCl diets (SHR-R), the diets did not alter blood pressure, and neither dietary NaCl nor Ca2+supplementation affected norepinephrine turnover in any brain region studied. These data indicate that in SHR-S on a diet high in NaCl, Ca2+supplementation may prevent the NaCl-induced exacerbation of hypertension by increasing norepinephrine turnover in the hypothalamus.

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

The mechanisms resulting in the greater predisposition of male subjects towards hypertension were investigated in different strains of rats with genetic hypertension [spontaneously hypertensive rats of the stroke-prone strain (SHRSP) and spontaneously hypertensive rats (SHR)] and their respective normotensive controls. Blood pressure was reduced in young (9 weeks of age) hypertensive rats by (1) surgical castration, (2) treatment with the testosterone receptor antagonist cyproterone acetate (CPA), which does not elevate testosterone, or (3) with the testosterone receptor antagonist flutamide, which leads to a feedback elevation of gonadotrophic hormones and plasma testosterone. These treatments had no effect on high blood pressure in old hypertensive rats aged 25 weeks. Both androgen receptor antagonists attenuated high blood pressure development when given for the first 10 days after birth. These data clearly relate the sexual dimorphism of hypertension to testosterone produced during male brain maturation in the early phase of hypertension development. Testosterone appears not to contribute directly to the maintenance of high blood pressure in established hypertension.

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

We studied the expression of kidney renin gene in hypertensive animals by measuring the kidney renin messenger (m) RNA. The kidney renin mRNA was quantified by densitometric Northern biot analysis using a32P-labelled rat renin genomic DNA fragment as a hybridization probe. Spontaneously hypertensive rats (SHR) and control Wistar–Kyoto rats (WKY) were treated with a low-sodium diet plus furosemide, captopril or propranolol for a week. Plasma renin activity (PRA) in SHR and WKY was increased similarly by sodium depletion and by treatment with captopril. PRA in both strains was not decreased significantly by treatment with propranolol. Both sodium depletion and captopril treatment caused significant increases in the kidney renin mRNA in SHR and WKY. However, the increases in the kidney renin mRNA of SHR were greater than those in the corresponding WKY (SHR, 10.0− and 22.1-fold increases; WKY, 6.2− and 7.8-fold increases, respectively). Propranolol had no effect on the kidney renin gene expression in either WKY or SHR. These results indicate that SHR show an enhanced expression of the renin gene in the kidney compared with WKY in response to stimuli that increase renin release.

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Renin messenger (m) RNA distribution was studied in congenital mesoblastic nephroma, a usually benign renal tumour of early infancy which may be associated with excess renin production and hypertension. Usingin situhybridization with synthetic radiolabelled oligonucleotide probes combined with immunohistochemical studies, renin expression was found in areas of tumours containing recognizable cortical structures including glomeruli and tubules. Renin mRNA was also detected in vessels and larger vascular spaces within the tumour not associated with cortical structures. Cells in the tumour vessel walls and sinusoids which expressed renin also stained positively for vascular smooth muscle-specific α actin.

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

In order to test the hypothesis that the contraction induced in human resistance arterioles by porcine tetradecapeptide renin substrate (TDP) is mediated by enzymes specific to the renin–angiotensin cascade, human resistance vessels from skin and subcutaneous fat were mounted in a myograph and exposed to TDP in the presence and absence of the human renin inhibitor H261, the serine protease inhibitor aprotinin, a polyclonal anti-human renin antibody and captopril. TDP induced a dose-dependent contraction that could be abolished by saralasin. The sensitivity to TDP was significantly attenuated by H261, aprotinin and combinations of captopril with aprotinin and captopril plus aprotinin and H261, as indicated by a significant reduction in pD2(-log10ED50[mmol/l]) for TDP. However, captopril alone was ineffective. It was concluded that at physiological pH, porcine TDP induces contraction in human resistance vessels by the action of enzymes not specific to the renin–angiotensin cascade. Whilst a clear inhibitory effect of H261 was demonstrated, a significant comparable inhibition by captopril and a polyclonal renin antibody was not observed. This may reflect the difficulty with which these inhibitors gain access to their intracellularry located substrates.

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

This study was conducted to determine if muscle sympathetic nerve activity (MSA) and/or the neuronal release of noradrenaline per impulse are modulated by adrenaline in the physiological plasma concentration range. We gave step-wise infusions of adrenaline (0.05–0.6 nmol/kg per min) to 10 healthy young men and measured: intra-arterial blood pressure; heart rate; central venous pressure (CVP); efferent MSA (microneurography in the peroneal nerve); arterial (brachial artery) and femoral venous plasma concentrations of noradrenaline, and the spillover of noradrenaline to arterial and venous plasma (radiotracer infusion). The infusion of adrenaline caused a fall in diastolic blood pressure and tachycardia, and was associated with increases in MSA and noradrenaline spillover. These observations suggest that part of the adrenaline-induced increase in transmitter release is due to enhanced nerve impulse activity, but such a conclusion rests on the absence of diffusion limitations from the site of noradrenaline infusion into the blood stream. After termination of adrenaline infusion the tachycardia and elevated plasma noradrenaline levels persisted, but these changes were probably due mainly to a profound increase in nerve activity. Concurrently, there was a reduction in CVP which may have triggered the increase in efferent sympathetic nerve activity. Infusions of adrenaline did not influence the clearance of noradrenaline from arterial plasma, but the fractional extraction over the leg was moderately reduced, indicating that more arterial noradrenaline is recovered in venous plasma during adrenaline infusion. The present data suggest that the reasons for the adrenalipe-induced increase in noradrenaline release are complex, but they are consistent with the hypothesis that stress levels of adrenaline enhance sympathetic nerve activity, and that circulating adrenaline may modulate both haemodynamic and neural responses to stress.

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

We studied the role of sodium (Na) in renin release from isolated afferent arterioles incubated in Krebs–Ringer bicarbonate solutions with the Na concentrations adjusted to 145, 135, 125, 110 and 95mmol/l. The arterioles were incubated for three consecutive periods, with the sequence of incubations randomized. Renin release increased by 119 and 275% in the media with Na concentrations of 135 and 125 mmol/l, respectively, as compared with rhe renin released from arterioles incubated in the medium with Na 145 mmol/l. When the Na concentrations of the incubation media were further lowered to 110 mmol/l and 95 mmol/l, renin release continued by 118 and 216%, respectively, in comparison with that in the medium having an Na concentration of 125 mmol/l. Regression analysis showed that renin release increased by 98% for each 10 mmol/l decrement of Na concentration. When the osmolarity of the incubation medium was held constant, varying the Na concentrations did not alter the renin secretion. This suggests that renin was released from the arterioles in response to the osmotic pressure exerted by Na rather than as an ionic effect. Renin release was suppressed by the osmotic effects of sucrose and urea, although the suppressive effect of urea was weaker.

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID