ISSN:0263-6352    

出版商:OVID    

年代:1993

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1993

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Introduction:Abnormalities of calcium metabolism independent of changes in intracellular calcium have been described in patients with essential hypertension. These include increased urinary calcium excretion for a given salt intake, a raised parathyroid hormone level, an increase in urinary cyclic AMP, a tendency for a low serum ionized calcium level, a raised 1,25-dihydroxyvitamin D level and an increased intestinal calcium reabsorption. These changes have been seen as a consequence of a primary renal calcium leakHypothesis:We propose that these changes are secondary to a genetic defect in the ability of the kidney to excrete sodium. On the high salt intake in most Western countries (i.e. approximately 170mmol/day sodium) compensatory mechanisms occur to try to overcome this defect. These compensatory mechanisms are responsible for the rise in blood pressure, but also cause an increase in central blood volume which is the direct cause of the increase in urinary calcium excretion. This causes a slightly negative calcium balance, and the other abnormalities of calcium metabolism can then be seen as a compensatory response to try to restore calcium balance to normal.Discussion:This hypothesis explains the increase in kidney stones in essential hypertension and predicts that hypertensives, in the long term, will be more likely to develop bone demineralization (osteoporosis), as has been demonstrated in some animal models of hypertension. Increases in salt intake will not only cause a further rise in blood pressure, but will also increase urinary calcium excretion and aggravate the other abnormalities. A moderate reduction in salt intake from 170 to 70mmol/day will lower the blood pressure and will tend to correct the abnormalities of calcium metabolism. It should simultaneously reduce the incidence of renal stones and the long-term risk of bone demineralization

ISSN:0263-6352    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Objective:To study adrenergic receptors in the heart tissues of genetically hypertensive rats by evaluating the gene expression and the membrane protein density of ß1-adrenergic receptors using steady-state messenger RNA (mRNA) levels and a radioligand binding assay, respectively.Design:We compared prehypertensive (5-week-old) and early-hypertensive (13-week-old) spontaneously hypertensive rats (SHR) with age-matched Wistar-Kyoto (WKY) normotensive control ratsMethods:Polyadenylated RNA was extracted from individual hearts and analysed by the slot-blot technique using a ß1-adrenergic receptor complementary DNA probe.ß1-Adrenergic receptors in myocardial membranes were studied by radioligand binding assay using [125l]-cyanopindolol and the ß1- and ß2-selective antagonists CGP207.12A and IC1118.551, respectivelyResults:ß1-Adrenergic receptor mRNA levels were slightly higher, and membrane protein density was similar in prehypertensive SHR and age-matched WKY rats. However, both ß1-adrenergic receptor mRNA levels andß1-adrenergic receptor density were lower in the hypertensive SHR than in the control rats. ß1-Adrenergic receptor mRNA was significantly reduced in older rats of both strains, and this reduction was most evident in the SHRConclusions:The absence of downregulation of ß1-adrenergic receptors in young SHR, despite published data indicating a higher cardiac noradrenaline turnover than in WKY rats, may suggest that the cardiac hyperadrenergic activity observed in prehypertensive SHR is maintained, at least in part, by the participation of peripheral, postsynaptic component(s) involving ß1-adrenergic receptor dysregulation. In addition, the present data suggest that the previously reported evidence of an age-related decrease in cardiac ß1-adrenergic receptors in rats may be determined at the transcriptional level

ISSN:0263-6352    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Objective:The mechanisms underlying the accelerating effect of high salt intake on the development of vascular injury in the stroke-prone phenotype of spontaneously hypertensive rats (SHRSP) are still not clear. The aim of the present study was to determine whether young SHRSP can excrete a dietary excess of sodium and to characterize the associated hormonal responsesMethods:Sodium balance and hormonal parameters were studied during a 1-week high-salt diet (4% NaCl) in 6-week-old SHRSP (n=84), in age-matched spontaneously hypertensive rats (SHR; n=73) and in normotensive Wistar-Kyoto (WKY) rats (n=52)Results:Baseline systolic blood pressure (SBP) was similar in SHR and SHRSP and did not change significantly during the high-salt diet. SBP also remained unchanged in WKY rats during the high-salt diet. Despite similar daily sodium intakes in the three groups during the diet, the response of urinary sodium excretion to sodium loading was reduced significantly in SHRSP compared with SHR or WKY rats (F=4.09, P<0.001). Plasma renin activity was suppressed significantly by high salt intake in each group to a comparable extent. Plasma aldosterone concentrations were also reduced significantly by sodium loading in all strains. However, a lesser degree of aldosterone suppression was observed in the SHRSP than in both SHR and WKY rats (F=3.01, P<0.01)Conclusions:Young SHRSP show a blunted suppression of plasma aldosterone and a defective sodium excretion during high salt intake

ISSN:0263-6352    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Objective:To compare renal haemodynamics and proximal tubular sodium reabsorption (PTSR) in response to an acute intravenous saline infusion in rabbits bred for genetic differences in cardiac baroreflex sensitivity (BRS). Rabbits with low BRS increase their blood pressure significantly on a high-salt diet, in association with an initial delay in sodium excretion. It was hypothesized that this could occur through an impaired baroreflex regulation of renal sympathetic nerve activity. This, in turn, would alter renal blood flow and PTSRDesign:Experiments were performed in two groups of normotensive male rabbits (n=10 per group), one of which had high BRS (>5 beats/min per mmHg; group I) and one of which had low BRS (<4 beats/min per mmHg; group II). Effective renal plasma flow (ERPF) was measured by para-aminohippuric acid clearance, and PTSR by the lithium clearance technique. Sodium, lithium, para-aminohippuric acid and glomerular filtration rate were measured from urine samples collected every 30 min (for 90 min) via an indwelling bladder catheter, during a control infusion of glucose (30mg/ml) NaCI (1.8mg/ml), and for 2h after a threefold increase in NaCIResults:Croup I rabbits increased their ERPF by approximately 40%, in response to saline, and doubled their sodium and lithium clearances within the 2 h, but those in group II did not change their cation excretion or their ERPF significantly during this period. Blood pressure did not increase in either groupConclusions:A genetic impairment in BRS may be responsible for the inadequate depression of renal sympathetic nerve activity, which results in a failure to increase ERPF and suppress sodium reabsorption in the proximal tubule in response to salt loading

ISSN:0263-6352    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Objective:To determine whether essential hypertensive patients with high Na+,K+,CI-cotransport (COT) display alterations of some indices of kidney tubular reabsorption similar to those observed in Milan hypertensive (MHS) rats, which have high COT in both erythrocytes and kidney tubular cells, and hypertension caused by a primary increase of tubular reabsorptionDesign:Two sets of experiments were performed. First, renal function in two subgroups of hypertensive patients (one with 'high' and one with 'normal' COT was compared with that in normotensive controls. Secondly, the natriuretic and diuretic effects of a single oral dose of frusemide (25 mg) were analysed in six high- and in six normal-COT hypertensive patientsResults:Compared with normotensives and with normal-COT hypertensives, high-COT hypertensives had lower fractional uric acid excretion and plasma renin activity with similar glomerular filtration rate and urinary sodium and potassium excretion. COT was negatively correlated with fractional uric acid excretion in the essential hypertensive patients but not in the normotensives. The diuretic natriuretic response to frusemide was much higher in high- than in normal-COT hypertensivesConclusion:These results are consistent with the hypothesis that patients with high COT have abnormal renal handling of sodium similar to that observed in MHS rats

ISSN:0263-6352    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Objectives:To investigate the relationship between erythrocyte sodium-lithium countertransport and blood pressure in a randomly selected sample of untreated male workers and to evaluate the influence of a set of metabolic abnormalities commonly associated with hypertension on this relationshipDesign:A cross-sectional investigation of a randomly selected sample of untreated male workers (n=216, age range 21-59 years) at the Olivetti factory in Pozzuoli, NaplesMethods:Standardized measurements of anthropometric and metabolic parameters, blood pressure and Na+— L i+countertransport were performedResults:In a simple linear correlation analysis Na+—Li+countertransport was directly related to plasma triglycerides and uric acid concentrations, body mass index (BMI) and systolic and diastolic blood pressure. Significantly higher values of Na+-Li+countertransport were observed in the two upper quintiles of the serum triglycerides and uric acid distributions, and of the BMI distribution. Na+-Li+countertransport accounted for approximately 2% of the blood pressure variation in this study population, but its contribution to the effect of metabolic covariates was not statistically significant. Hypertensive individuals with one or more metabolic abnormality had a significantly higher mean level of Na+- Li+countertransport than those hypertensives who were free of such alterationsConclusions:The results of the present study suggest that a high level of Na+—Li+countertransport is more common in those hypertensive individuals who have concomitant metabolic abnormalities than in hypertensives who are free of such abnormalities

ISSN:0263-6352    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Introduction:Several authors have described increased Na+— H+exchanger activity in essential hypertension, and an increase in activity of this transport system has also been postulated in situations of hyperinsulinism, such as obesity and essential hypertensionMethods:We measured Na+— H+exchanger activity in a group of 37 subjects with essential hypertension (18 obese, 19 non-obese), in a group of nine normotensive obese subjects and in a control group of 16 healthy volunteers. Plasma insulin and glucose values during an oral glucose tolerance test were evaluated, together with other variables such as plasma aldosterone, plasma renin activity and plasma potassiumResults:Na+—H+exchanger system activity did not appear to be abnormally raised in the hypertensive subjects, but was significantly increased in the normotensive obese group. Upon dividing the hypertensive subjects into two subgroups on the basis of body mass index, it was noted that, whereas the non-obese hypertensives showed Na+—H+exchanger activity patterns similar to those in controls, the obese hypertensive subjects exhibited increased activity of the transport system. Na+—H+activity correlates with body mass index and shows a significant inverse correlation with plasma potassium. No correlations were found between Na+— H+exchanger activity and the sum of plasma insulin values during the oral glucose tolerance testConclusion:Na+— H+exchanger overactivity appears to be characteristic in overweight subjects, but would not appear to be a specific feature of essential hypertension. The increased Na+— H+exchanger activity observed in obese subjects may be postulated to be related to the hypermineralocorticoidism characteristic of this condition

ISSN:0263-6352    

出版商:OVID    

年代:1993

数据来源: OVID