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

Renal hemodynamics, plasma renin activity (PRA), plasma aldosterone (PA) and sodium excretion were studied in essential hypertension. PAH clearance (CPAH) and glomerular filtration rate (GFR) were normal or increased in early hypertension and depressed at later stages, especially in malignant cases. The PAH extraction ratio was depressed only in patients with low CPAH values. CPAH did not correlate inversely with blood pressure in benign hypertension. Later reexamination of untreated patients revealed a decrease in CPAH, but no further increase in blood pressure. Antihypertensive treatment prevented the decrease in CPAH. Patients with essential hypertension showed no abnormality in basal sodium excretion, plasma aldosterone, plasma renin activity and the sodium:aldosterone relationship. Basal sodium clearance did not correlate with GFR and the fractional sodium excretion was not pressure-dependent. When clearance determinations and measurements of PA and PRA were performed simultaneously under standardized conditions, PA and PRA were correlated inversely with CPAH and GFR. There was no relationship between PA or PRA and the blood pressure. Unless a defective release of renal prostaglandins and/or kinins could be shown to be responsible for the increase in systemic blood pressure, there is no evidence for a primary renal disturbance in essential hypertension.
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PMID:Relationships between sodium clearance, plasma renin activity, plasma aldosterone, renal hemodynamics and blood pressure in essential hypertension. 700 Apr 63

Labetalol, a blocker of alpha- and beta-adrenoreceptors, was tried on 45 patients with severe (29 cases) or mild to moderate (16 cases) hypertension. After an initial period of dosage adjustment and a 2 months treatment in effective doses, there was a significant fall in supine blood pressure from mean values of 207/132 to 170/106 mmHg. In 23 patients hypertension was controlled by labetalol alone in doses of 400 and 1800 mg per day. True failures were rare (16%). Digestive disorders and postural hypotension were the most frequently encountered side-effects; they obliged to discontinue treatment in 4 cases, but were compatible with it in 11 cases. In 22 patients the fall in BP was accompanied by a significant (p less than 0,001) decrease in plasma renin activity from 123 to 44 ng/l/min supine and from 144 to 83 ng/l/min standing. Studies of the renal function showed no changes during oral therapy. Following intravenous injection of 50 mg labetalol to 20 subjects, inulin and PAH clearances remained unaltered, and there was a significant, though transient (1 hour), decrease in chloride, sodium and phosphorus excretion. Effective in lowering blood pressure be used and well tolerated by the kidneys, labetalol can safely be used for the treatment of severe hypertension with organic renal involvement.
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PMID:[Effects of labetalol, a new alpha- and beta-adrenoreceptor blocking drug, on arterial pressure, renal function and renin activity (author's transl)]. 700 20

The experience derived from the administration of isoproterenol in six patients with pulmonary hypertension of unknown etiology (PAH-UE) is presented. The diagnosis was made after exclusion of other known diseases capable of producing hypertension in the pulmonary circuit. Catheterization was performed, and basal cardiopulmonary parameters, mean pulmonary artery pressure (PAP), pulmonary arteriolar resistance (PAR), cardiac index (CI), alveolar-arterial oxygen tension difference P(A-a)O2, and PaO2 were investigated. The effect of infusing 3 micrograms/min of isoproterenol into the pulmonary artery was studied in five cases. Isoproterenol was given sublingually to one patient who had previously received it intravenously; in another case it was given only sublingually. Significant P values (P less than .05) as a group were obtained, in relation to heart rate, CI, PAR, and mean PAP after isoproterenol. A favorable effect on the heart and lungs was seen in two cases, maintained for three years with sublingual isoproterenol with a favorable cardiorespiratory effect. Use of isoproterenol in PAH-UE is justified at present in those cases with a favorable cardiopulmonary response while no specific therapy is available.
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PMID:The role of isoproterenol in pulmonary artery hypertension of unknown etiology (primary): short- and long-term evaluation. 747 61

Endogenous nitric oxide (EDRF) plays an important role in the regulation of systemic and renal blood pressure by an alteration of vascular tone. To assess the effect of L-arginine (160 mumol/min i.v. for 3 hours), the precursor of EDRF, on blood pressure, protein-excretion and renal function (GFR = glomerular filtration rate, RPF = renal plasma flow) we performed a prospective, double blind, placebo controlled study. 18 patients with chronic glomerulonephritis (51.3 +/- 11.5 years), renal insufficiency (GFR < 65 ml/min) and hypertension were investigated for changes in GFR and RPF by continuous inulin- and PAH-clearances and for changes in permselectivity by determination of protein-excretion. L-arginine infusion results in a reduction of proteinuria (p < 0.05, t-test). There is no significant effect on renal hemodynamics and mean arterial pressure (MAP). Comparing the excretion of the endogenous proteins, only albuminuria is decreased significantly (p < 0.01), whereas IgG-excretion is reduced slightly (p < 0.05). This can be considered as an indicator of a special influence on the mesangial cells or the basement membrane of the glomerulum itself by EDRF. In conclusion L-arginine reduces protein-excretion without significant alterations in renal hemodynamics and so might prevent a decline in renal failure.
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PMID:Does L-arginine alter proteinuria and renal hemodynamics in patients with chronic glomerulonephritis and hypertension? 778 Dec 5

ACE-inhibitors are known to have special renal effects, i.e. they increase ERPF, decrease the filtration fraction and lower proteinuria. These effects can be due to a decrease in angiotensin II (AII) levels as well as an increase in bradykinin. New and more specific AII-receptor antagonists may help to distinguish between effects exerted by angiotensin II and those exerted by bradykinin. We investigated the effects of losartan in 9 patients with essential hypertension (sitting mean diastolic blood pressure 95-120 mmHg). Renal hemodynamics were measured by continuous inulin-and PAH-clearance (GFR and RPF) after stopping antihypertensive therapy for 1 week, followed by a 2-week placebo period and after a 4-week treatment phase with losartan (50 mg/die) followed by a therapy with an ACE-inhibitor (ramipril 5mg/die). Additionally, urine albumin excretion (UAE) was measured. Treatment of patients with essential hypertension with losartan resulted in a significant decrease of MAP after three weeks of treatment (121 +/- 8 mmHg under placebo and 114 +/- 10 mmHg under losartan; * = p < 0.05). MAP after four weeks of losartan treatment was 115 +/- 11 mmHg. Regarding changes in renal hemodynamics we could not demonstrate a significant change for neither losartan nor the ACE-inhibitor. Urine albumin excretion was reduced by both treatment regimens in correlation to the magnitude of blood pressure reduction. Our data indicate that losartan induced a significant reduction in MAP in patients with essential arterial hypertension with only moderate effects on renal hemodynamics.
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PMID:Renal hemodynamics in essential hypertensives treated with losartan. 778 Dec 6

Cyclosporin A (CsA) is widely used to suppress graft rejection following transplantation and in the treatment of a variety of autoimmune diseases. Therapy with CsA is often accompanied by adverse effects which include hepatotoxicity, hypertension, and nephrotoxicity. The role of endothelin (Et) in CsA-induced nephrotoxicity has been the subject of recent investigations. BQ-123 is a recently discovered Et receptor antagonist which is selective for the EtA receptor. In the present study, BQ-123 was used to further characterize the role of Et in CsA-induced nephrotoxicity. All experiments were performed in Inactin (100 mg/kg, i.p.) anesthetized male Munich-Wistar rats (250 to 350 g). Animals were prepared for the recording of blood pressure (MAP) and heart rate (HR) as well as the measurement of urine volume (UV), UNaV, UKV, GFR and effective renal plasma flow (ERPF). GFR and ERPF were estimated from the clearance of 14C-inulin and 3H-PAH, respectively. On the day of the experiment, animals were randomly assigned to one of three groups and treated according to the following protocols: Group 1, pretreatment with BQ-123 (1 mg/kg, i.v. bolus with 0.1 mg/kg/hr i.v. infusion) followed by treatment with vehicle (cremophor; 0.15 ml, i.v.); Group 2, pretreatment with normal saline (1.0 ml/kg; plus 25 microliters/min infusion) followed by treatment with CsA (20 mg/kg, i.v.); and Group 3, pretreatment with BQ-123 (same as group 1) followed by CsA (20 mg/kg, i.v.). BQ-123 administration alone produced transient changes in several of the measured parameters.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of BQ-123 on renal function and acute cyclosporine-induced renal dysfunction. 812 1

Glomerular hyperfiltration and hypertension may contribute to the progression of chronic renal insufficiency regardless of the underlying disease. Protein restriction and antihypertensive treatment are used to slow the decline in renal function. However, little is known about the interaction of protein loading and antihypertensive treatment on glomerular haemodynamics in humans. This paper compares the renal haemodynamic effects of beta-adrenoceptor blockers with those of the calcium channel antagonist nifedipine and the ACE inhibitor captopril on resting glomerular filtration and during glomerular hyperfiltration. In two separate studies the effects of nifedipine, captopril, metoprolol, and celiprolol on renal haemodynamics have been investigated. In two groups of healthy volunteers (n = 13) inulin and PAH clearances were measured, first under fasting conditions and afterwards during aminoacid infusion. In fasting subjects nifedipine and metoprolol induced glomerular hyperfiltration, while celiprolol and captopril did not significantly affect GFR. Without premedication, and also after nifedipine, metoprolol and celiprolol, the aminoacid infusion significantly increased the GFR. After premedication with captopril, however, aminoacid-induced hyperfiltration was prevented. In fasting subjects captopril, celiprolol and metoprolol elevated PAH clearance. With our without premedication aminoacid infusion increased renal plasma flow compared to baseline on the control day. We conclude that in healthy subjects, acute administration of antihypertensive drugs results in different renal haemodynamic responses. In contrast to captopril and celiprolol, nifedipine and metoprolol induce glomerular hyperfiltration like protein loading. Thus, they may counteract the renal haemodynamic effects of protein restriction. Celiprolol behaves similarly to captopril, since it increases renal perfusion without inducing glomerular hyperfiltration, a pattern which might reflect lower glomerular pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of antihypertensive drugs on glomerular hyperfiltration and renal haemodynamics. Comparison of captopril with nifedipine, metoprolol and celiprolol. 848 48

A prospective double-blind, randomized study was conducted to compare the effects of the beta 1 antagonist, beta 2 agonist celiprolol (200 mg daily) on renal hemodynamics and protein excretion with those of the beta 1 antagonist atenolol (50 mg daily), the ACE-inhibitor ramipril (2.5 mg daily), and placebo in 11 patients with proteinuria > 400 mg/24 h due to chronic glomerulonephritis. All 4 substances were given in a double-blind, randomized manner according to a latin-square design over a period of 4 weeks with a wash-out period of 2 weeks in between. Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured by inulin and PAH clearance. Proteinuria was assessed by urine sampling at the end of each treatment period. Mean arterial pressure (MAP) was reduced significantly (p < 0.01) by all 3 drugs compared to placebo (108 +/- 9 mmHg placebo, 98 +/- 12 mmHg atenolol, 101 +/- 11 mmHg celiprolol, and 98 +/- 8 mmHg ramipril). Celiprolol induced a significant increase in ERPF compared to placebo (322 +/- 109 ml/min under placebo versus 391 +/- 110 ml/min under celiprolol, p < 0.05). GFR was slightly but insignificantly increased under atenolol and celiprolol. Filtration fraction (FF) remained unchanged in case of atenolol and celiprolol treatment and was slightly but not significantly reduced by ramipril. Proteinuria was significantly (p < 0.05) reduced compared to placebo by all 3 drugs (1.8 +/- 1.3 g/24 h under placebo, 1.2 +/- 1.2 g/24 h under atenolol, 1.2 +/- 1.1 g/24 h under celiprolol, and 1.4 +/- 1.4 g/24 h under ramipril). These data demonstrate that new beta-blocking agents show favorable effects on proteinuria and renal blood flow in patients with chronic glomerulonephritis and arterial hypertension. This may be attributed to their vasodilating properties.
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PMID:Randomized controlled trial of ACE-inhibitors and beta-blockers with and without vasodilating activity in chronic glomerulonephritis. 893 34

1. The effects of benidipine, a long-acting calcium antagonist, on renal functions were determined in anaesthetized spontaneously hypertensive rats (SHR), as compared with those of amlodipine. 2. Benidipine at 3 and 10 mu g/kg (i.v.) significantly increased urine volume, sodium (Na) and potassium (K) excretions with no change in creatinine clearance (C-CRE). The increase in K excretion was relatively slight. Benidipine increased p-amino-hippuric acid clearance (C-PAH) without any change in C-CRE and, thus, decreased filtration fraction (FF). 3. On the other hand, amlodipine at 300 mu g/kg (i.v.) significantly increased Na and K excretions, but did not change FF. 4. Thus benidipine, but not amlodipine, can dilate glomerular efferent arteriole as well as afferent arteriole in SHR. It is, therefore, expected that benidipine would not induce intraglomerular hypertension, which could result in the progression of glomerular injury. 5. Benidipine at 3 mu g/kg (i.v.) increased lithium clearance, while it decreased CRE concentration and increased Na concentration in the stop-flow urine from the distal tubule. 6. These results suggest that benidipine produces diuresis by the inhibition of water and Na reabsorption at both the proximal and the distal tubules.
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PMID:Effects of benidipine, a long-acting calcium antagonist, on renal functions in anaesthetized spontaneously hypertensive rats. 907 17

In senescence renal function is thought to decline markedly even in the absence of renal disease. It has also been proposed that the changes in renal function with age are not uniform and that confounding factors such as hypertension or atherosclerosis may play a role. We performed a comprehensive study to compare several aspects of renal function in four groups: (i) young healthy normotensive subjects (N = 24; 13 males; mean age 26 +/- 3 years); (ii) elderly healthy normotensive subjects (elderly NT; N = 29; 13 males; 68 +/- 7 years); (iii) elderly treated and untreated hypertensive patients (elderly HT; N = 25; 13 males; 70 +/- 6 years); and (iv) elderly patients with compensated mild to moderate heart failure (elderly HF; N = 14; 6 males; 69 +/- 6 years). Compared to young subjects mean GFR (C(In)) and ERPF (C(PAH)) were significantly lower in the elderly, despite similar mean plasma creatinine levels (young, 121 +/- 11, 650 +/- 85 ml/min/1.73 m2; elderly NT, 103 +/- 11, 486 +/- 102; elderly HT, 103 +/- 13, 427 +/- 55; elderly HF, 92 +/- 14, 377 +/- 103). Nevertheless, GFR was within the normal range in the majority of elderly NT and HT, but not in elderly HF. ERPF was significantly lower in elderly HT as compared with elderly NT, and still lower in elderly HF. Mean renovascular resistance and filtration fraction were significantly higher in the elderly, particularly in elderly HT and HF as compared with the young. Mean fractional excretion of Na+ was similar in all groups studied, but the lithium clearance was significantly lower in the elderly, suggesting a greater proximal and less distal sodium reabsorption in senescence. In the elderly, mean PTH concentration and urinary excretion of pyridoline cross-links were significantly higher and mean 25-(OH)D3, calcitriol and phosphate concentrations significantly lower; the correlation between PTH and GFR was significant (r = -0.432, P < 0.001). The results document that the decrease in renal hemodynamics with senescence is less marked than suggested by some studies using less stringent methodology and inclusion criteria. Comorbid conditions confound renal function in the elderly. Age-associated changes in renal hemodynamics are accompanied by significant alterations of renal hormones and of renal sodium handling.
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PMID:Renal function in the elderly: impact of hypertension and cardiac function. 908 86


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