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:

To clarify the effect of dietary sodium restriction on the mechanism regulating sodium and water in the development of hypertension, we determined the number of the α-adrenoceptors in renal basolateral membrane in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. The rats had been fed a low-sodium (0.5%) or normal-sodium (0.4%) diet from 3 weeks of age. The experiments were performed at 6, 8 and 20 weeks of age in both rat groups. Renal basolateral membranes were prepared using Percoll and radioligand binding studies were performed using3H-prazosin and3H-rauwolscine. Systolic blood pressure in SHR was already elevated at 6 weeks of age compared with that in WKY rats and rose to hypertensive levels at 8 weeks of age. The sodium balance in WKY rats on both diets decreased at 8 weeks of age, but that of SHR decreased at 20 weeks of age. The maximum number (Bmax) for the α2-adrenoceptor did not differ in any groups of the WKY rats or SHR. Bmaxfor the $AL2-adrenoceptors increased at 8 weeks of age in the low-sodium SHR compared with normal-sodium SHR, but did not increase in WKY rats. The data show that the increases in blood pressure in the SHR occur prior to significant increases in the α2-adrenoceptor density of renal basolateral membrane, and that the modulation of α2-adrenoceptor density in SHR differs from that in WKY rats under sodium restriction. The results suggest that renal α2-adrenoceptors in SHR could relate the regulatory mechanism to sodium reabsorption under sodium restriction rather than to the primary cause of the development of hypertension in SHR. There may be the possibility of an abnormality in renal α2-adrenoceptor mechanism in SHR.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

We showed earlier that the rostral ventral medulla can be functionally and anatomically divided into the rostral ventrolateral medulla (RVLM) and the rostral ventromedial medulla (RVMM). In this study, we examined the relationship between the lateral hypothalamus and these two medullary sites. Electrical stimulation of the lateral hypothalamus produced a pressor response mediated by increases in renal and mesenteric vascular resistance. Inactivating RVLM had no effect on this response whereas inactivating RVMM significantly blunted the pressor response and the increases in renal and mesenteric resistance. In other studies, inactivating dorsomedullary sites significantly reduced arterial pressure. Unlike RVLM, these depressor responses were not significantly altered by reducing tidal volume. Inactivating sites 0.5 mm medial and lateral to the RVMM, as well as a site 0.5 mm caudal to the RVLM, resulted in depressor responses that were unaffected by reducing tidal volume. However, inactivation of a site 1.0 mm caudal to the RVLM but still within the ventrolateral medullary pressor area, resulted in a depressor response that was enhanced by reduced tidal volume. Together, these data demonstrate a functional differentiation of medullary sites controlling vasomotor outflow.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

Treatment of young rats with vitamin D3plus nicotine has been proposed as a model of cardiovascular calcium overload. This treatment produced a 20–35-fold increase in the calcium content of the aorta, a compliance vessel, and this increase was accompanied by a 1.6-fold elevation of pulse pressure. In aortic rings, the maximal inhibition by the endothelium-dependent vasodilator, carbachol, of vasoconstriction induced by noradrenaline decreased from 90% in controls to 61% in treated animals. There were significant correlations between aortic calcium content and pulse pressure and aortic calcium content and carbachol-induced relaxation. In conclusion. the vitamin D3plus nicotine model may be useful for the study of the role of calcium overload in decreased arterial compliance coupled with endothelial injury.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

Mechanisms for the antagonistic action of atrial natriuretic peptide (ANP) toward endothelin were studied. We examined the effects of ANP on endothelin-induced vasoconstriction in isolated perfused kidney and the elevation of intracellular free calcium concentration using Fura-2 in cultured rat vascular smooth muscle cells (VSMC). Endothelin produced an increase in renal vascular resistance in isolated perfused kidney (2 x 10-10mol/l, +109%;P<0.01). ANP completely abolished renal vasoconstriction induced by endothelin. Endothelin produced a biphasic elevation in intracellular calcium concentration in the VSMC. Ethyleneglycol-bis-(β-amino-ethylether)-N,N,N‘,N’-tetraacetic acid (EGTA; 3mmol/l) or nicardipine (10-8mol/l) decreased the sustained elevation of intracellular calcium concentration by 10-8mol/l endothelin to the basal level (endothelin, +15% versus EGTA + endothelin −1%;P<0.05; endothelin, +18% versus nicardipine + endothelin, +5%;P<0.01). Pretreatment with 10-6mol/l ANP suppressed neither the peak phase of intracellular calcium concentration elevation (endothelin, 10-8mol/l, +35% versus endothelin + ANP, +31%; not significant) nor the sustained phase of intracellular calcium concentration elevation (endothelin, 10-8mol/l, +21% versus endothelih + ANP, + 16%; not significant). ANP markedly increased the production of cyclic 3‘,5’-guanosine monophosphate (cGMP) in the VSMC (ANP, 10-6mol/l, +1100%;P<0.01). However, endothelin did not influence cGMP production in the presence or absence of ANP. ANP may antagonize the vasoconstrictive action of endothelin through an effect on the steps subsequent to the mobilization of intracellular calcium in the pathway of vascular smooth muscle contraction.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

The effects induced by α-human 28-amino acid residue atrial natriuretic peptide (α-hANP) on arterial pressure, heart rate and vascular resistance, measured as hindlimb perfusion pressure (HPP), were examined in anesthetized rabbits. In particular, the involvement of the autonomic nervous system in mediating the cardiocirculatory effects of α-hANP was investigated. Intravenous α-hANP (8 $mUg/kg, bolus injection) in anesthetized rabbits caused a sustained decrease in atrial pressure, a transient decrease in HPP and no significant changes in heart rate. After sinoaortic denervation, α-hANP produced a greater decrease in arterial pressure and in hindlimb vascular resistance and also a consistent decrease in heart rate. Bilateral vagotomy did not significantly alter the cardiocirculatory responses to α-hANP in either normal or in sinoaortic denervated rabbits. Intravenous infusion of α-hANP (2 $mMg/kg bolus + 0.2 $mMg/kg per min) did not substantially change the baroreflex cardiocirculatory responses to loading and unloading carotid and aortic baroreceptors with bilateral carotid occlusion and phenylephrine or nitroglycerin bolus injection. In addition, α-hANP infusion did not modify the cardiovascular reflex responses to chemical stimulation of neural receptors (sensory endings of group III and IV somatic afferents) in the hindlimb muscles which are primarily mediated by sympathetic nerves in the anesthetized rabbit. Pharmacological blockade of the autonomic nervous system with atropine and guanethidine did not reduce the hypotensive and bradycardic effects caused by α-hANP in sinoaortic denervated animals. The results indicate that in anesthetized rabbits: (1) α-hANP can induce inhibitory cardiocirculatory responses (hypotension, bradycardia, musculocutaneous vasodilation) which are consistently offset by the sinoaortic baroreceptor system; (2) α-hANP does not alter the reflex control of arterial pressure and heart rate by arterial baroreceptors and muscle chemosensitive receptors; (3) activation of cardiopulmonary vagally-mediated depressor reflexes does not contribute to the inhibitory cardiovascular action of α-hANP; and (4) inhibitory effects on sympathetic activity do not constitute a significant component of the cardiocirculatory action of α-hANP.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

Antihypertensive treatment, by lowering blood pressure and correcting functional and/or structural abnormalities of the arterial wall, may prevent the arterial damage due to the accelerated ageing process. The objective of the present study was to determine, using a cross-sectional approach, whether arterial distensibility of patients whose blood pressure had been normalized for several months by antihypertensive treatment, was significantly higher than that of untreated hypertensive patients. The properties of the vessel wall of the common carotid artery (CCA) were studied non-invasively, using an original pulsed ultrasound echo-tracking system based on Doppler shift, during a study comparing 46 normotensive subjects and 81 age-matched hypertensive patients. The latter group included 25 patients well controlled by antihypertensive treatment for at least 3 months and 56 untreated hypertensives. The three groups did not differ with respect to age, total and high-density lipoprotein cholesterol, blood glucose and smoking. In each group, there were significant relationships between age and CCA dimensional and functional data, including end-diastolic diameter, absolute and relative stroke changes in diameter and Peterson modulus, indicating a widening of the CCA with advancing age and a decrease in its buffering function. When compared with untreated hypertensives, well controlled hypertensives had significantly lower blood pressure and Peterson elastic modulus according to age. However, although blood pressure of well controlled hypertensives was not significantly different from that of normotensive subjects, their arterial distensibility remained altered compared with that of normotensive subjects (significant increase in Peterson elastic modulus). These results suggest that long-term antihypertensive treatment may not fully reverse arterial lesions due to the hypertensive disease.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

The renal, hormonal and haemodynamic effects of chronic (4 days) dosing with an inhibitor of endopeptidase EC 3.4.24.11 (UK 79300) were assessed in two groups, each of eight normal volunteers, receiving 25 mg every 12 h (group 1) or 100 mg every 12 h (group 2) of UK 79300 in double-blind, balanced-randomized, placebo-controlled, crossover studies. Group 2 (but not group 1) exhibited a significant transient natriuresis (P<0.01) and a consequent sustained negative cumulative sodium balance (70 21 mmol) which was established within 48 h and remained for the duration of dosing with UK 79300. Urine and plasma cyclic guanosine monophosphate (cGMP) levels rose significantly above placebo values (P<0.01 andP<0.001, respectively) in both groups and the effect was sustained throughout the dosing period. Plasma atrial natriuretic factor (ANF) was slightly enhanced by UK 79300 in group 1 (P< 0.05) but not significantly increased in group 2. Despite a significant increase in heart rate in both groups (P< 0.001) and of natriuresis in group 2, there was minimal evidence of renin-aldosterone activation in either group. trends towards lower systolic pressures, observed in both groups, did not attain statistical significance. These findings suggest chronic treatment with UK 79300 induces an increase in tissue ANF levels, with sustained enhancement of plasma and urine concentrations of ANF second messenger (cGMP) and increased heart rate.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID