ISSN:0263-6352    

出版商:OVID    

年代:1990

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1990

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Erythrocyte Na+and K+transport mediated by the Na+–K+pump, the Na+,K+cotransport system and cation leaks, together with blood pressure, were determined in young and adult rats subjected to either chronic salt deprivation or chronic salt loading combined with subtotal nephrectomy. The kinetics of ion transport were studied in Na+media as a function of extracellular K+, replaced by extracellular Rb+, and intracellular Na+varied around the physiological range. A high salt intake increased blood pressure in young but not in adult subtotally nephrectomized rats. Erythrocyte Na+or K+contents of salt-deprived and salt-loaded rats did not differ. There were no major changes in Na+,K+cotransport or cation leaks in salt-loaded rats. Chronic salt loading caused some alterations in the kinetics of the Na+–K+pump, which were greater in young than in adult rats. The most pronounced change was a decreased affinity of the Na+–K+pump for intracellular Na+, which was partially balanced by an increased maximal velocity. At physiological (in vivo) ion concentrations these kinetic alterations caused a slight reduction in total ouabain-sensitive Rb+uptake [partly due to a decrease in intracellular K+:extracellular Rb+(1:1) exchange] but no changes in Na+ net extrusion in salt-loaded rats. The erythrocyte Na+and K+transport systems showed no changes in intrinsic properties that would favour the development or maintenance of salt hypertension in young over adult rats if similar alterations occurred in tissues relevant for blood pressure control

ISSN:0263-6352    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

In a comparative study the influence of changes in dietary sodium intake on blood pressure, renal function, extracellular fluid volume, the renin-angiotensin-aldosterone system and plasma concentrations of arginine vasopressin, atrial natriuretic factor and cyclic guanosine monophosphate (GMP) was investigated in 12 patients with essential hypertension and in 10 normotensive controls. The subjects were studied after 4 days on a low (50 mmol/day), medium (180mmol/day) or high (380 mmol/day) sodium intake. Renal sodium handling was assessed by simultaneous measurements of51Cr-ethylenediaminetetraacetic acid (EDTA), lithium and sodium clearances. Identical values for the extracellular fluid volume, glomerular filtration rate and proximal and distal tubular resorption rates of sodium and water were found in the hypertensive patients and the controls at all three levels of sodium intake. In both groups, raising the sodium intake from low to high significantly increased51Cr-EDTA and lithium clearance (an indirect measure of end-proximal fluid delivery), with intermediate values for the medium-sodium diet. The estimated values of fractional proximal and distal sodium resorption decreased when sodium intake was raised; the absolute proximal sodium resorption rate did not change, whereas the absolute distal sodium resorption rate as well as the extracellular fluid volume and sodium clearance increased. Blood pressure and the heart rate were unaffected by sodium intake. In both hypertensive and controls, plasma concentrations of active renin, angiotensin II and aldosterone decreased with increasing sodium intake, arginine vasopressin did not change, and atrial natriuretic factor and cyclic CMP increased. The data indicate that changes in dietary sodium intake caused identical adaptive changes in the glomerular filtration rate and in proximal and distal tubular sodium handling in essential hypertensive patients and normal controls. The alterations were accompanied by marked changes in extracellular fluid volume and in the hormonal factors involved in volume homeostasis

ISSN:0263-6352    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The short-term and long-term effects (for up to 98 days) of the angiotensin converting enzyme inhibitor enalapril were investigated in male and female BALB/c mice. In control animals, separate antisera to renin and its prosequence produced an identical pattern of staining in granular cells of the juxtaglomerular apparatus (JGA) a short distance from the glomerulus. After 1 day of the enalapril treatment there was a decrease in the number of JCA granular cells immunostained with antisera to both renin and its prosequence. Electron microscopy revealed degranulation of mature granules from JGA granular cells. Fusion of granules with the cell membrane was not observed, but numerous membrane-like structures (myelin figures) were identified in the cytoplasm and extracellular space, indicating possible secretion. In addition, the volume proportion of granulated cells in relation to the glomerular volume was decreased, as was renal renin contentWith continuing enalapril treatment, separate antisera to renin and its prosequence stained the same granulated JGA cells with equal intensity. The cells so stained increased in number, extending down the wall of the afferent arteriole to cortical radial arteries (interiobular arteries) upstream from the glomerulus. Ultrastructural studies revealed a progressive development of cytoplasmic granulation in JGA granular cells and in smooth muscle cells extending into cortical radial arteries. Furthermore, the volume proportion of granulated cells in relation to the glomerular volume was significantly increased, as was renal renin contentThus, short-term enalapril treatment in mice provoked rapid secretion of renin via degranulation of mature granules from JGA granular cells. In contrast, long-term enalapril treatment produced a continuing stimulus for renin synthesis, secretion and storage, resulting in an increased thickness of the afferent arteriolar wall The mechanism for this change appears to be hypertrophy and hypergranulation of granular JGA cells and neogranulation of smooth muscle cells upstream from the glomerulus. Identification of the intrarenal mediators that induce these phenotypic changes presents an interesting challenge

ISSN:0263-6352    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

We have previously shown that during percutaneous transluminal renal angioplasty (PTRA) there is a transient increase in plasma renin activity (PRA) that is partly mediated by adrenergic β-receptors. Despite a concomitant increase in plasma aldosterone, no increase in blood pressure occurred. The aim of this study was to record sympathetic outflow in man during PTRA as reflected by muscle nerve sympathetic activity and arterial plasma noradrenaline. Nine patients with hypertension and unilateral renal artery stenosis underwent PTRA by the Grüntzig technique and simultaneous microelectrode recording of muscle nerve sympathetic activity in the peroneal nerve. Blood pressure and heart rate were recorded and blood specimens were drawn for determination of noradrenaline and PRA. During total occlusion of the renal artery, muscle nerve sympathetic activity and the heart rate were unchanged. In the first 6 min after occlusion PRA increased transiently, but there was no significant change in muscle nerve sympathetic activity, arterial noradrenaline, heart rate or blood pressure. From 10 min after PTRA, muscle nerve sympathetic activity was significantly increased and after 40 min there was a significant increase in noradrenaline. The heart rate remained unchanged throughout the procedure, but the blood pressure decreased progressively and the diastolic blood pressure was significantly reduced at 40 min, indicating successful dilation. Despite activation of the renin–,angiotensin–,aldosterone system and the sympathetic nervous system, two strong pressor systems, the only circulatory reaction was a decrease in diastolic blood pressure. These findings indicate simultaneous activation of a potent depressor mechanism during PTRA

ISSN:0263-6352    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Forty 11-week-old Dahl salt-sensitive rats were divided into four groups matched for blood pressure and weight. Croup I was given a sodium-deficient diet, group II a sodium-enriched diet, group III a sodium-enriched diet plus a calcium supplement and group IV a sodium-enriched diet plus nitrendipine, a calcium antagonist. For the first 18 weeks, when the sodium-enriched diet contained 2.6% sodium, there were no differences in blood pressure between the groups; the sodium content was then increased to 8%, and the diets continued for 12 more weeks. At 41 weeks old, the rats in group II had significantly ( p <0.05) higher systolic blood pressures than the other groups. Erythrocytes from the rats on the low-sodium diet had significantly (P<0.025) lower intracellular sodium (3.9 ± 0.4mmol/l) while cells from the rats given nitrendipine had significantly (p <0.005) higher intracellular sodium (13.3 ± 0.8mmol/l) than those from the rats on a high-salt diet (7.4 ± 1.4mmol/l). Nitrendipine caused significant (p <0.05) decreases in both ouabain-sensitive and furosemide-sensitive sodium efflux. Platelet aggregation in response to 2 |imol/l adenosine diphosphate was not significantly affected by the nitrendipine. The evidence that nitrendipine markedly affects sodium transport supports the hypothesis that an interaction of calcium and sodium may be involved in blood pressure control.

ISSN:0263-6352    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

In order to investigate the hypotensive mechanisms of action of peptide renin inhibitors, blood pressure responses to five renin inhibitors were compared with those to the angiotensin converting enzyme inhibitor, enalaprilat, in conscious African green and rhesus monkeys. (3S-4S)-4-amino-5-cyclohexyl-3-hydroxy pentanoic acid (ACHPA)-containing renin inhibitory peptide (ACRIP) and enalaprilat both decreased blood pressure in euvolemic and volume-depleted African green monkeys. However, while a maximum dose of enalaprilat reduced blood pressure to 80 ± 4 and 56 ± 4 mmHg in the euvolemic and volume-depleted monkeys, respectively, ACRIP lowered pressure to life-threatening levels (< 40 mmHg) under both conditions. The relative potencies of ACRIP and four other renin inhibitors for inhibiting in vitro plasma renin activity (PRA; IC50) were compared with their potencies in reducing blood pressure by 15mmHg (ED15mmHg) and lowering blood pressure more than enalaprilat in volume-depleted rhesus monkeys. All renin inhibitors lowered blood pressure significantly beyond the maximal response to enalaprilat. Despite a significant correlation (r=0.99, p <0.05) between the in vitro PRA inhibitory potency and the in vivo ED15mmHg, doses which lowered blood pressure beyond the maximal responses to enalaprilat were not significantly correlated (r=0.53, p >0.05) with the in vitro PRA IC50values. Furthermore, the profound depressor responses to renin inhibitors in rhesus monkeys were accompanied by increases in the heart rate and decreases in pulse pressure. These data demonstrate that peptide renin inhibitors can elicit blood pressure reductions by a plasma renin-dependent as well as a plasma renin-independent mechanism. Therefore, studies designed to investigate the antihypertensive efficacy of renin inhibitors may overestimate the renin-dependent hypotensive activity of these peptides

ISSN:0263-6352    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Since the membrane Ca2+handling properties of the arterial smooth muscle sarcoplasmic reticulum may be altered in genetic hypertension, we studied caffeine- and noradrenaline-induced contractions in tail arteries from spontaneously hypertensive rats (SHR) at the prehypertensive stage (4 weeks old) and from age-matched Wistar-Kyoto rats (WKY). After the sarcoplasmic reticulum had been loaded with Ca2+by pretreatment with physiological Ca2+solution, caffeine- and noradrenaline-induced contractions of the tail arteries, measured in a Ca2+-free solution [containing 0.1 mmol/l ethyleneglycol-bis-(ß-aminoethylether)-N,N,N',N'-tetraacetic acid], were smaller in SHR than in WKY. After caffeine-releasable Ca2+in the sarcoplasmic reticulum had been depleted by pretreatment with the Ca2 +-free solution, the caffeine-induced arterial contractions in a Iow-Ca2+(0.5 mmol/l) solution were smaller in SHR than in WKY. The Ca2+concentration-tension relationship in skinned arterial fibres was similar in WKY and SHR. These data suggest that the ability of the sarcoplasmic reticulum to take up and store caffeine- and noradrenaline-releasable Ca2+is decreased in SHR. The development of hypertension in SHR may be explained by an impaired function of the sarcoplasmic reticulum in arterial smooth muscle.

ISSN:0263-6352    

出版商:OVID    

年代:1990

数据来源: OVID