ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

The effect of dietary sodium loading on plasma human brain natriuretic peptide-like immunoreactivity (hBNP-li) was examined in 11 normotensive subjects aged 20–23 years. Plasma hBNP-li increased significantly with increasing dietary sodium intake, with levels of 1.33 ± 0.17pmol/l on day 5 of a normal-sodium diet (24-h urinary sodium excretion of 171 ± 16mmol) and 2.04 ± 0.10pmol/l (P < 0.05, versus normal-sodium diet) on day 5 of a high-sodium diet (24-h urinary sodium excretion 503 ± 36mmol). Corresponding plasma atrial natriuretic factor levels were 5.6 ± 1.7pmol/l and 11.0 ± 2.0pmol/l (P < 0.05, versus normal-sodium diet) on the normal- and high-sodium diets, respectively. These results suggest that, in addition to atrial natriuretic factor, BNP may be a new and important natriuretic peptide which regulates sodium homeostasis in man during increased sodium intake.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

The contribution of sarcoplasmic reticulum was studied with regard to the increase in arterial contraction induced by a high-potassium depolarization in spontaneously hypertensive rats (SHR). The 20 mmol/l potassium-induced contraction of femoral arteries was faster and greater in 6-week-old SHR than in age-matched normotensive Wistar-Kyoto (WKY) rats. Relaxation after washing the arteries with a Krebs solution was slower in SHR than in WKY rats. When the sarcoplasmic reticulum of SHR arteries had been depleted of calcium by caffeine in a calcium-free solution, the rate of high-potassium-induced contraction of the calcium-depleted SHR arteries was slowed, the same result as that with non-calcium-depleted WKY arteries. In ryanodine-treated arteries, the rate and magnitude of high-potassium-induced contraction were enhanced slightly in SHR and greatly in WKY rats, resulting in no final difference between SHR and WKY rats. Ryanodine slowed the relaxation rate in WKY rats but not in SHR. These results suggest that the diminution in ability of sarcoplasmic reticulum to sequester calcium may be responsible for the faster rate and greater magnitude of high-potassium-induced contraction with the slower relaxation in SHR arteries. We postulated that genetic malfunction of sarcoplasmic reticulum causes the increased contraction of arterial smooth muscle leading to the enhanced vasoconstriction and elevated blood pressure in SHR.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

the limited range of ± 15mmol/l induce changes in blood pressure which are directly related to intracellular sodium concentration and inversely related to the transmembrane sodium gradient. It followed from this that the blood pressure response to an incremental change in blood sodium concentration induced by an intraperitoneal salt load should be a function of the rate of accumulation of cell sodium. This was tested in rats treated with deoxycorticosterone acetate (DOCA)-saline for 3 days since at this time cell permeability to sodium is known to be increased. The rise of cell sodium when blood sodium concentration, measured 30 min after loading, ranged from 140-160 mmol/l, was significantly increased in treated animals (0.14 versus 0.21 mmol/kg dry weight for each 1 mmol/l rise in extracellular sodium concentration) and the rise in blood pressure was correspondingly greater (0.81 versus 1.43 mmHg for a 1 mmol/l rise in extracellular sodium concentration). The increased accumulation of cell sodium was not accompanied by a similar increase in water, so that the rise in intracellular sodium concentration was also exaggerated. Prior uninephrectomy slowed the excretion of the salt load sufficiently to exaggerate the rise of blood sodium concentration in response to a given load. The osmotic effects of intraperitoneal high sodium or high sucrose were both equally reduced, indicating that the increased permeability induced by DOCA is not specific for sodium but affects non-electrolytes as well; thus, it probably involves the phospholipid matrix.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

This study determined the influence of baroreflex sensitivity (BRS) on the rate of urinary sodium excretion and plasma renin activity (PRA) in response to a saline infusion in conscious male rabbits specifically bred for high (Croup I; n=7) and low (Group II; n= 10) BRS and in seven control animals. Only Group II showed significant increases in blood pressure on a chronic high-salt intake. After ensuring that each animal was in sodium balance, a (0.7-0.9%) saline infusion of 3-4 ml/kg perh for 90min (25% daily sodium intake for each rabbit) was given and urine collected at 15-min intervals via a bladder catheter. No differences were found in control urine volumes, urinary sodium or PRA. Group I excreted over 50% of the sodium load and Group II less than 20% within 90 min. PRA fell by more than 30% within 30 min in six Group I rabbits but decreased by less than 30% or increased in Group II. In the control animals, sodium excretion rates and PRA suppression were also much greater in those with high BRS. A highly significant correlation (r=0.808, P< 0.01) was found between the per cent of the sodium load excreted and BRS. It is suggested that the delayed sodium excretion and blood pressure elevation in salt-sensitive subjects may be due to a genetic impairment in baroreflex control of renal sympathetic nerve activity.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

These experiments were designed to study the effects of inhibition of endogenous bradykinin and/or prostaglandins on systemic and regional hemodynamics in conscious normotensive rats, using the radioactive microsphere technique. Administration of either a bradykinin antagonist (50|o.g/min for 5min) or indomethacin (10mg/kg) alone, decreased the cardiac output by an average of 17.58 and 25.94%, respectively (P < 0.05), without significant change in total peripheral resistance. Regional blood flow decreased and local vascular resistance increased in most organs. Coronary and renal blood flow decreased by an average of 16.45 and 17.26% with bradykinin antagonist and 23.85 and 19.80% with indomethacin, respectively (P<0.05). Indomethacin but not bradykinin antagonist also decreased cerebral blood flow by an average of 47.57% (P<0.01). Infusion of the bradykinin antagonist following prior prostaglandin inhibition with indomethacin did not induce further changes in either systemic or regional hemodynamics, except in the liver where a significant additional increment in vascular resistance was observed. Our data suggest that most organs have similar patterns of regional vascular sensitivity to bradykinin and prostaglandins (including the heart, kidney, testis, stomach, skin and adrenal). The major differences were in the cerebral vasculature, which was much more sensitive to prostaglandins, and in the liver, spleen and small intestine, which were more sensitive to bradykinin. We conclude that both hormonal systems participate to a varying extent in the maintenance of resting vascular tone in most organs; however, in some cases, their effects may be additive and in others they may work in opposite directions.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

The pressor actions of arginine vasopressin (AVP) were examined in pithed Sprague-Dawley and Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). Prior to pithing, systolic blood pressure (SBP) and diastolic blood pressure (DBP) were recorded via an intra-arterial catheter from sodium pentobarbital anaesthetized rats. SBP and DBP recorded from SHR were significantly greater than those from Sprague-Dawley and WKY rats. However, after pithing, there were no significant differences between DBP among the various strains. Pertussis toxin pretreatment significantly reduced the prepithing SBP and DBP of the SHR but not Sprague-Dawley or WKY rats. Administration of nifedipine significantly reduced DBP of pithed rats. The dose-diastolic pressure response curves obtained from infusion of AVP in Sprague-Dawley and WKY rats were not significantly different from one another, but the maximal vasopressor responses to AVP in pithed SHR were enhanced. Administration of nifedipine to Sprague-Dawley and WKY rats did not affect the dose-response curve to AVP, but nifedipine administration in SHR led to a significant inhibition of the pressor responses to AVP. Furthermore, pertussis toxin pretreament of rats significantly reduced a component of the AVP pressor effect in SHR but not Sprague-Dawley or WKY rats. We speculate that, in SHR, vasopressin receptors are coupled to a pertussis toxin-sensitive G protein that, in turn, may couple to a dihydropyridine-sensitive calcium channel and also to a pertussis-insensitive G protein that is probably coupled to the phospholipase C/intracellular calcium release process. A component of the elevated blood pressure in SHR is also regulated by a pertussis toxin-sensitive process. However, this toxin does not have a significant effect on the blood pressure of Sprague-Dawley or WKY rats, suggesting that there is a pertussis toxin-sensitive receptor and/or channel which is differentially expressed in the SHR.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

The hypotensive action of b adrenoreceptor blockers is not fully understood, there being a lack of studies focusing on possible relationships between b blockers and the secretion of atrial natriuretic peptide (ANP). In 10 patients with essential hypertension, we investigated the influence of betaxolol, a selective β1adrenergic blocking agent, on renal function and on plasma levels of ANP during exercise, volume depletion and volume expansion. Chronic therapy with betaxolol (mean 14.5mg/day) did not alter glomerular filtration rate and renal blood flow although blood pressure was reduced. Renal vascular resistance decreased from 12 795 ± 1064dyn/s percm5 to 10614 ± 833dyn/s percm5 (P< 0.005). Under betaxolol, basal ANP levels increased from 39 ± 10pg/ml to 80 ± 19pg/ml (P< 0.01). ANP increased during exercise and volume expansion but was decreased during volume depletion. ANP values observed under betaxolol treatment showed significantly higher values while preserving their dynamic features. We believe that the stimulating effect of betaxolol on ANP may at least partly account for its hypotensive action.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID