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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arterial hypertension is found in as many as 75% patients with autosomal dominant polycystic kidneys with normal renal function, its pathogenesis is however not quite clear so far. The authors examined 16 patients with polycystic kidneys with normal or only slightly reduced renal function (plasma creatinine lower than 140 umol/l), 8 of these patients were normotonic (N) and 8 hypertonic (H). In all examined subjects right-sided cardiac catheterization was performed with assessment of the minute cardiac volume by thermodilution. To all patients in the course of one hour 1500 ml saline per 70 kg body weight were administered and the haemodynamic examinations were repeated after termination of the infusion. In all subjects before and after expansion the plasma renin activity was assessed (PRA), as well as plasma aldosterone (PA), plasma catecholamines (PC) and the atrial natriuretic factor (ANF), the renal blood flow and glomerular filtration by means of clearance and extraction of PAH and inulin clearance. The authors did not find differences in plasma concentrations, cardiac output and splanchnic and renal ANF extraction in groups N and H, nor in PRA, PA and PC. Volume expansion led in both groups to a comparable rise of ANF and suppression of PRA and PA. Group H did not differ from group N in any of the investigated haemodynamic and renal parameters except for systemic vascular resistance. In hypertensive patients before expansion a close correlation was found between pressure in the pulmonary artery in a wedged position and diuresis (r = 0.935, p less than 0.01) and natriuresis (r = 0.895, p less than 0.01). The volume expansion was in both groups associated with a comparable rise of diuresis, the haemodynamic response of patients N and H was however quite different. While in patients of group N a decline of the systemic vascular resistance occurred as well as an increase of the minute volume without a change of the renal flow and glomerular filtration, in hypertonic patients the systemic vascular resistance and minute volume did not change but there was a significant rise of the renal flow and glomerular filtration. The relationship of diuresis and natriuresis of hypertensive patients with polycystic kidneys to volume parameters and the rise of the renal perfusion pressure during volume expansion indicates the importance of pressure natriuresis for ensuring the sodium and volume homeostasis in these patients.
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PMID:[Hypertension in patients with polycystic kidneys--the effect of volume expansion]. 182 66

Certain rat strains acutely increase blood pressure (BP) when given diets high in NaCl. Prior results showed that "salt-sensitive" rat strains, at least the ones studied, also increase BP in response to sugar loading. To examine this relationship further and learn more about the pathogenesis of sucrose-induced BP elevations, we examined the effects of unilateral nephrectomy (uninephrectomy) on sucrose-induced BP changes. The rationale is based upon the findings that renal mass removal sensitizes BP response to salt loading. Over 15 weeks, augmented sugar (sucrose) consumption by Long-Evans (LE) rats did not increase BP markedly compared to rats consuming a diet relatively low in sugar unless uninephrectomy was performed. The differences in BP caused by the high sugar diet in a uninephrectomized rat could not be explained adequately by alterations in catecholamine excretion, plasma renin activity, excesses in blood volume, or the other parameters examined. However, salt-induced hypertension has been attributed to the presence of circulating substances affecting ion transport. Among the dietary groups, there was a significant correlation between the ability of plasma to depress PAH and TEA renal slice uptake and the difference in BP. This is consistent with the presence of a circulating factor affecting cell transport that has its greatest activity in the high sugar-uninephrectomy group of LE rats. We conclude that reducing renal mass potentiates sugar-induced BP elevation similar to salt-induced BP elevation in a normally resistant rat strain, and the rise of BP may be caused by a circulating factor.
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PMID:Development of sugar-induced blood pressure elevation after uninephrectomy in a resistant rat strain. 201 May 76

We used pulsed Doppler echocardiography to examine the systolic ejection flow from the right ventricle in 66 patients with chronic obstructive pulmonary disease. Adequate recordings were obtained in 60 patients, in conjunction with right heart catheterization. Patients without pulmonary artery hypertension at rest (mean pulmonary artery pressure less than 20 mm Hg) underwent an exercise test which identified a group with PAH during exercise (MPAP greater than 30 mm Hg). The patients were divided into four groups: group 1, or control group: 17 healthy nonsmokers without normal respiratory function data; group 2: COPD without PAH (n = 12); group 3: PAH during exercise (n = 26); group 4: PAH at rest (n = 22). Analysis of Doppler data included time to peak velocity, right ventricular pre-ejection period, and ejection period. Pulsed Doppler echocardiography was a simple and reliable method of detecting PAH. Latent PAH, revealed by the exercise test, was accompanied by significant changes in Doppler findings, confirming the sensitivity of the method.
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PMID:Pulsed Doppler echocardiography in the diagnosis of pulmonary hypertension in COPD. 237 58

Many physiological variables known or thought to affect erythrocyte Na+,K+-cotransport are altered in pregnancy. The interrelationships of Na+,K+-cotransport and pregnancy were therefore examined. Values were elevated by more than 30% in both second and third trimesters with a return towards non-pregnant levels in the postpartum period. Although pregnancy was also associated with elevated plasma cholesterol, renin activity and aldosterone, there was no significant relationship within the pregnant group between Na+,K+-cotransport and any of these factors. No change could be demonstrated in Na+,K+-cotransport values after 7 days of either high (greater than 250 mmol/day) or low (less than 50 mmol/day) sodium intake and values for those who developed pregnancy-associated hypertension (PAH, pre-eclampsia) were not significantly different from those in continuously normotensive women in either the second or the third trimesters of pregnancy.
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PMID:Alterations in erythrocyte Na+,K+-cotransport in normal and hypertensive human pregnancy. 245 Sep 10

With the aim to improve renal graft function and to prevent hypertension, we used the calcium-antagonist diltiazem in a prospective randomized study in 30 consecutive cadaveric renal transplanted patients from september 1987 to may 1988. The diltiazem (D+) group comprised 14 patients receiving a loading dose of 0.3 mg/kg followed by a 2 micrograms/kg/d continuous IV infusion of D started as soon as possible after clamp on renal artery removal. D was then given orally (120-180 mg/d) throughout the study. 16 patients without D composed the D- group. Cyclosporine A (csa) was started either just before transplantation (15 mg/kg/d orally) in 18 patients (9 D+ and 9 D-) or after 2-3 weeks of poly or monoclonal antibodies (5 D+ and 7 D- at 10 mg/kg/d. In addition to the usual monitoring, inulin (for GFR) and PAH (for ERBF), clearances were performed 7 days and 3 months after transplantation. If hypertension (blood pressure greater than 160/90 mm Hg) occurred, all but calcium-antagonists antihypertensive agents were used in both groups. Between D+ and D-, the number of patients requiring haemodialysis during the first week was not different (7/14 vs 5/16) like the number of dialysis session per patient (1.4 vs 1.1) day 7 GFR (19 +/- 22 vs 23 +/- 20) and day 7 ERBF (146 +/- 147 vs 226 +/- 224) ml/mn/1.73 m2; at 3 months 13/14 (93 p. 100) vs 12/15 (80 p. 100) of the grafts are functioning (NS), GFR (34 +/- 17 vs 33 +/- 10) and ERBF (242 +/- 90 vs 236 +/- 117) are not different.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of diltiazem on arterial pressure and renal function in renal transplanted and cyclosporin A treated subjects. Results after 3 months of a prospective study]. 251 Jun 52

Up to now, no studies have been performed in normal humans to investigate the role of renal hemodynamic abnormalities in relation to acute-cyclosporin A (CsA) renal dysfunction and to verify whether the specific renal vasodilator, dopamine, can counteract these abnormalities. Eight normal subjects were examined both (A) after oral CsA (12 mg/kg body wt) and (B) after oral CsA + dopamine infusion (2 mg/kg body wt/min), under water diuresis. Both in protocols A and in B, four basal renal clearances were performed before CsA and every twenty minutes for four hours after CsA administration. In protocol A, after CsA, inulin (GFR) and PAH clearance (RPF) fell by up to 27% and to 41%, respectively, so that filtration fraction (FF) increased (P less than 0.01). A slight (not significant) hypertension occurred while renal resistances were markedly raised (P less than 0.001). Fractional urine and Na+ excretion as well as CH2O decreased, while UOsm increased (P less than 0.01). In protocol B, dopamine was infused from 120 to 180 minutes after CsA (that is, when the maximal adverse effects of CsA on renal hemodynamics had been observed in A). Dopamine infusion could reverse completely the effects of CsA on RPF, GFR, fractional urine output and CH2O; only UOsm remained higher than normal in conclusion with an increased fractional excretion of sodium (P less than 0.01). No changes were observed in plasma renin activity, aldosterone and in urinary epinephrine and norepinephrine excretion both in protocols.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute cyclosporine renal dysfunction reversed by dopamine infusion in healthy subjects. 260 Dec 57

In patients with well-functioning renal allografts, the presence of diseased native kidneys appears to be a common cause of elevated blood pressure. We evaluated the role of native kidneys in post-transplant hypertension using a rat model in which the confounding variables of rejection and immunosuppression could be eliminated. To produce disease in native kidneys. PVG rats were subjected to 5/6 nephrectomy. Four weeks following renal ablation, these hypertensive animals were transplanted with kidneys from syngeneic PVG donors. Four weeks later, the effects of captopril and native nephrectomy on blood pressure and renal hemodynamics were examined. Animals with remnant native kidneys which received non-rejecting renal isografts had sustained hypertension, elevated plasma renin levels and reduced transplant function. In these animals, administration of captopril reduced systemic blood pressure. Despite the reduction in blood pressure, PAH clearance by the transplanted kidney increased markedly while GFR rose modestly. Removal of the remnant native kidney also acutely lowered blood pressure. However, compared to captopril, native nephrectomy produced a more marked increase in GFR without significantly affecting renal blood flow. In this model of post-transplant hypertension in the rat, elevated blood pressure and reduced isograft function are mediated by the diseased native kidney, in part through the effects of angiotensin II. These data suggest that ACE inhibitors and native nephrectomy may have beneficial hemodynamic effects in patients with post-transplant hypertension caused by native kidneys.
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PMID:Post-transplant hypertension in the rat: effects of captopril and native nephrectomy. 268 27

This study examines renal function in different rat models of renovascular hypertension. Hypertension was induced by constriction of the aorta proximal to the renal artery (PAC), by PAC and nephrectomy (PAC + Nx) or by renal artery stenosis (RAS). PAC + Nx is equivalent to the Goldblatt 1 kidney-I clip hypertension model. The PAC rats were studied 3 weeks after surgery. Hypertension was by then well established. GFR, measured as the clearance of inulin, was significantly lower in PAC rats than in control (C) rats. GFR was the same in PAC + Nx rats as in C rats, but significantly lower in PAC + Nx than in Nx rats. Kidney weight was significantly higher in PAC + Nx rats than in C rats. Filtration fraction (FF), measured as the ratio between GFR and the clearance of PAH, was significantly higher in PAC and PAC + Nx rats than in C and Nx rats. In RAS rats hypertension was not established until 6 weeks after surgery, and RAS is equivalent to Goldblatt 2 kidney-I clip hypertension. Renal artery constriction was moderate as judged from the weight ratio between the stenosed and contralateral kidneys. The GFR in the stenosed kidney was not significantly lower in the contralateral kidney. FF was significantly higher in RAS rats than in C rats in both the stenosed and the contralateral kidneys, but the increase was less pronounced than in PAC and PAC + Nx rats.
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PMID:Renal function in different forms of renovascular hypertension in rats. 275 May 42

Use of converting-enzyme inhibitors in patients with hypertension and bilateral renal artery stenosis or renal artery stenosis in a single kidney may be complicated by acute renal failure (ARF). The aim of this work was to find a simple test to predict this accident. PAH clearance (CPAH), Inuline clearance (CIn) and Glomerular Filtration Fraction (GFF) were measured before and three hours after a single oral dose of Captopril (50 mg) in 7 hypertensive patients (sodium intake = 6 g/24 h). All these patients presented significant stenosis (greater than 60%) of the artery of a transplanted kidney (5), of a single kidney (1) or a bilateral renal artery stenosis (1). During the following three days, 50 mg captopril was given twice a day. ARF with creatinine serum level higher than 300 mumoles/l was seen in 4 patients (Group II); in 3 patients (Group I) creatinine serum level didn't change. Values measured before the single dose of captopril and variations after three hours are reported in the table: (Table: see text). Before captopril, in Group II CPAH and CIn are lower and GFF is higher, but these is not significant difference between the two groups. After Captopril CIn and GFF are significantly decreased in Group II (29.1 and 36.6% vs 7.8 and 10%). These results allow two conclusions: 1) Basal values of Glomerular Filtration Rate plasma flow and filtration fraction are not predictive parameters for acute renal failure after captopril therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Predictability of post-captopril acute renal failure in hypertension with renal artery stenosis of a single kidney or bilateral stenosis]. 309 6

To elucidate the role of the kidneys in the development of hypertension in Dahl salt-sensitive (S), as compared to resistant (R) rats of the JR strain, we analyzed functional and morphological changes before and after the administration of an 8% NaCl diet and the onset of hypertension. The diet was begun at six weeks of age and was continued until 12 weeks of age. At six weeks, blood pressure was not different between S and R rats. Hypertension occurred in S rats receiving the 8% NaCl diet at week 8, and in S rats receiving 0.9% NaCl at week 10. Albuminuria and proteinuria were found in S rats prior to the 8% NaCl diet and progressed regardless of diet. Electron microscopy of glomeruli revealed segmental loss of epithelial foot processes in S rats at six weeks prior to the 8% NaCl diet. Mesangial widening, arteriolar myo-intimal cell hyperplasia and interstitial fibrosis occurred in all S rats. Inulin and PAH clearances in S rats decreased with time, the changes being accelerated by the 8% NaCl diet. Micropuncture of S and R rats prior to the 8% NaCl diet revealed no glomerular hypertension in S rats. The number of glomeruli in S and R rats were not different. We conclude that prehypertensive S rats of the JR strain already have albuminuric glomerular disease not associated with reduced number of glomeruli or glomerular hypertension. The renal pathology is accelerated once hypertension develops. A lower NaCl intake delays, but does not prevent renal disease in S rats.
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PMID:Renal disease and the development of hypertension in salt-sensitive Dahl rats. 340 12


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