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

The authors examined 74 women in III trimester (29-40 week), among them 44 women with hypertension induced by pregnancy (group examined) and 30 healthy women (control group). The blood serum of these women was studied for: creatinine, urea, uric acid, electrolytes K+ and Na+. Besides, the blood was studied for acid-base equilibrium (apparatus Corning type 128). The 24-hour urine of the two groups was studied for the concentrations of ions: 1) ammonium (NH4+), 2) hydrogen (H+) and 3) potassium and sodium (K+ and Na+). The authors also made the endogenic creatinine clearance (Ckr). The results were calculated statistically. The women with hypertension induced by pregnancy had in their blood serum an increase in the concentration of creatinine, urea and uric acid. As to the parameters of acid-base equilibrium, the authors found an increase in pCO2. Besides, the women with this kind of hypertension had: a decrease in the excretion of ions NH4+ and H+ in the urine, a decrease of Ckr with electrolytes K+ and Na+ being within the normal range.
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PMID:[Kidney function in women with pregnancy-induced hypertension]. 263 83

An apparent increase of calmodulin (CaM) activity was previously observed in the heart and kidney but not in the liver of spontaneously-hypertensive rats (SHR) and mice compared with their corresponding normotensive controls. As this change was due to an elevated recovery of CaM in the organs of the hypertensive animals, the present study was designed to evaluate its activity in hypertension. A CaM activator, detected in heart and kidney supernatants from hypertensive animals, was found to be responsible for this enhanced recovery. Similar results were obtained with passaged, cultured aortic smooth muscle cells from SHR, indicating that the anomaly was not a mere consequence of elevated blood pressure but rather a genetic expression of cells of hypertensive origin. The activator was heat stable, nondialyzable, and recovered in the fraction precipitated with 30-50% ammonium sulfate. Preliminary extraction studies suggest that the activator is contained in a glycolipid fraction. The stimulation of phosphodiesterase by this activator was calcium and CaM dependent. The activator appears to affect the affinity of the phosphodiesterase for CaM rather than the maximal stimulation. The activator was also present at a low concentration in the heart and kidney of normotensive animals. These findings indicate that at least some of the calcium abnormalities implicated in the pathogenesis of hypertension could be the result of interactions between CaM, calcium, and this activator.
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PMID:Abnormality of calmodulin activity in hypertension. Evidence of the presence of an activator. 283 48

To determine the nature, extent, and severity of renal involvement in Laurence-Moon-Biedl syndrome (obesity, mental retardation, polydactyly, hypogonadism, and pigmented retinal dystrophy), we evaluated 20 of 30 patients with the disorder identified from ophthalmologic records in Newfoundland. The mean age was 31 years, and seven were male. All 20 patients had structural or functional abnormalities of the kidneys or both. Three had end-stage renal disease, with two requiring maintenance hemodialysis. The remaining 17 patients had normal serum creatinine values and estimated creatinine clearances. Half the subjects had hypertension. Fourteen of 17 patients could not concentrate urine above 750 mOsm per kilogram of body weight even after vasopressin, whereas all 10 normal controls could. Urinary pH decreased below 5.3 after ammonium chloride administration in all 15 normal controls, but in only 13 of 18 patients. Calyceal clubbing or blunting was evident in 18 of 19 patients studied by intravenous pyelography; 13 patients had calyceal cysts or diverticula. Seventeen of 19 patients had lobulated renal outlines of the fetal type. Four patients had diffuse renal cortical loss, but only two of these had renal insufficiency. We conclude that Laurence-Moon-Biedl syndrome includes the presence of renal abnormalities.
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PMID:The spectrum of renal disease in Laurence-Moon-Biedl syndrome. 341 78

Hypotensive activity of labetalol therapy alone or in combination with the diuretic agent oxodolin or with low-sodium diet (about 110 mmol/day) and potassium cooking salt substitute "Sanasol" (60% sodium chloride, ammonium chloride, calcium gluconate, magnesium asparaginate, etc.) was studied in 67 patients with second- or third-stage essential hypertension and 14 patients with nephrogenic hypertension. Central hemodynamic changes were assessed by means of radiocardiography and tetrapolar rheography. Combined treatment had better hypotensive effect in moderate and severe hypertension (diastolic arterial BP above 110 mm Hg). The diuretic-labetalol combination made possible a 25-45% reduction in the adrenoblocker dose. The effect of combined hypotensive treatment was similar in patients with different central hemodynamic types. Low-sodium diet with potassium substitute was well tolerated by the patients.
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PMID:[Potentiation of the hypotensive effect of labetalol in hypertensive patients treated to maintain sodium balance in the body]. 357 27

Homeostatic renal functions in nephrotic syndrome (NS) and arterial hypertension were studied the data on 240 patients with functionally compensated chronic glomerulonephritis (CGN). Benign arterial hypertension did not make a considerable effect on renal functions. In NS there was a selective decrease in the functions, particularly affected in the tubulointerstitial component (TIC) of CGN (concentration and ammonium secretory functions). These functions were affected to the maximum in proteinuria over 9.0 g/day. The NS adverse effect on renal transport processes was not dependent on the TIC presence. In CGN accompanied by moderate proteinuria, even a moderate decrease in renal concentration function or a considerable decrease in ammonium secretory function suggested the TIC presence. Against a background of the NS the presence of CGN TIC could be supposed only in the detection of maximum urine osmolarity not exceeding 600 mmol/l.
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PMID:[Several homeostatic renal functions in hypertensive and nephrotic syndromes of chronic functionally compensated glomerulonephritis]. 368 46

The mechanisms of metabolic acidosis and hyperkalemia were investigated in a patient with chronic mineralocorticoid-resistant renal hyperkalemia (5.3-6.9 mmol/l), metabolic acidosis (arterial blood pH 7.27, total CO2 17 mmol/l), arterial hypertension, undetectable plasma renin activity (less than 0.10 ng/ml/h), high plasma aldosterone level (32-100 ng/dl), and normal glomerular filtration rate (131 ml/min/1.73 m2). During the hyperkalemic period, urine was highly acidic (pH 4.6-5.0), urinary NH4 excretion (10-13 microEq/min) and urinary net acid excretion (19-24 microEq/min) were not supernormal as expected from a chronic acid load. During NaHCO3 infusion, the maximal tubular HCO3 reabsorption was markedly diminished (19.8 mmol/l glomerular filtrate), and the fractional excretion of HCO3 (FE HCO3) when plasma HCO3 was normalized was 20%. Urine minus blood PCO2 increased normally during NaHCO3 infusion (31 mm Hg), and the urinary pH remained maximally low (less than 5.3) when the buffer urinary excretion sharply increased after NH4Cl load. When serum K was returned toward normal limits, metabolic acidosis disappeared, urinary NH4 excretion rose normally after short NH4Cl loading while the urinary pH remained maximally low (4.9-5.2), the maximal tubular HCO3 reabsorption returned to normal values (24.8 mmol/l glomerular filtrate), and FE HCO3 at normal plasma HCO3 was 1%. Nasal insufflation of 1-desamino-8-D-Arginine Vasopressin (dDAVP) resulted in an acute normalization of the renal handling of K and in an increase in net urinary acid excretion. We conclude that: the effect of dDAVP on renal handling of K may be explained by the reversal of the distal chloride shunt and/or an increase in luminal membrane conductance to K; the distal acidification seems to be normal which in the event of distal chloride shunt impairing distal hydrogen secretion might be explained by the presence of systemic acidosis which is a potent stimulus of hydrogen secretion, and metabolic acidosis in the steady state was accounted for by the diminution of bicarbonate reabsorption and ammonia production in the proximal tubule secondary to chronic hyperkalemia.
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PMID:Pseudohypoaldosteronism type II: proximal renal tubular acidosis and dDAVP-sensitive renal hyperkalemia. 377 34

A study to measure the pressor substance, called active pressor principle (APP), which is generated in incubated human plasma was performed using anesthetized and ganglion blocked rats. It was found that APP has properties characteristic of protein. APP was not extractable with mixtures of chloroform: methanol. APP was present at 50 to 70% saturation with ammonium sulfate. By treating the plasma with Pronase, the pressor activity of the plasma was almost completely abolished. The molecular weight of APP as determined by gel filtration was about 68,000. By adding diisopropyl fluorophosphate before incubation of the plasma, the generation of vasopressor substance was prevented. Treatment of the rat with captopril was ineffective in inhibiting the pressor effect of incubated plasma. It was found that the plasma of normal pregnant women generated significantly higher amounts of APP than the plasma of nonpregnant women. The plasma obtained from patients with pregnancy-induced hypertension generated significantly lower amounts of APP than the plasma of normal pregnant women. These findings suggest that a vasoactive protein (APP) is generated during simple incubation of plasma, and a serine protease is involved in the formation of this substance. Concerning the relevance of these results to blood pressure regulation in pregnancy-induced hypertension, probably APP is involved in blood pressure regulation via a compensatory mechanism.
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PMID:[Some properties of a vasopressor substance generated in human plasma by incubation and its clinical significance in pregnancy-induced hypertension]. 397 49

The mechanisms of metabolic acidosis and hyperkalemia were investigated in a patient with chronic mineralocorticoid-resistant renal hyperkalemia (5.3 to 6.8 mM), metabolic acidosis (arterial blood pH 7.27, total CO2 17 mM), arterial hypertension, undetectable plasma renin activity (less than 0.10 ng/ml/hr), high plasma aldosterone (32 to 100 ng/dl), normal GFR (131 +/- 2.5 ml/min/1.73 m2). During hyperkalemic period, urine was highly acidic (pH 4.6 to 5.0), urinary NH4 excretion (13 mumoles/min) and urinary net acid excretion (24 mumoles/min) were not supernormal as expected from a chronic acid load. During NaHCO3 infusion, maximal tubular HCO3 reabsorption (Tm HCO3) was markedly diminished (19 mmoles/liter GF), fractional excretion of HCO3 (FE HCO3) when plasma HCO3 was normalized, was 20%. Urine-minus-blood PCO2 increased normally (31 mmHg) during NaHCO3 infusion, and urinary pH remained maximally low (less than 5.3) when buffer urinary excretion sharply increased after NH4Cl load. When serum K was returned toward normal limits, metabolic acidosis disappeared, urinary NH4 excretion rose normally after short NH4Cl loading while urinary pH remained maximally low (4.9 to 5.2), Tm HCO3 returned to normal value (24.8 mmoles/liter GF), and FE HCO3 became nil. The renal handling of K was improved with acute NaHCO3 loading and normalized after DDAVP nasal insufflation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Type II pseudohypoaldosteronism: proximal tubular acidosis and distal tubular hyperkalemia corrected by DDAVP]. 408 72

Hypertonic solutions of 0.3 M sodium chloride (NaCl) infused into the third ventricle (ICV) for 20 min in urethane-anesthetized rats consistently elevated mean aortic pressure by approximately 10 mm Hg. Heart rate and sympathetic nerve activity diminished slightly during the first few minutes but then accelerated to attain higher than preinfusion levels. By contrast, ICV infusions of either artificial cerebrospinal fluid alone or 0.6 M sucrose were ineffective, those of 0.6 M urea were slightly depressor, while those of 0.3 M ammonium chloride elevated blood pressure without affecting sympathetic nerve activity. In rats pretreated with a vasopressin antagonist, the early pressor effects of hypertonic NaCl were inhibited, while sympathetic nerve firing, instead of being initially inhibited, increased from the onset. Consequently, the blood pressure elevation occurring during the first 5 min of ICV infusion was considered partly due to vasoconstriction caused by increased secretion of endogenous vasopressin, and subsequent maintenance of the blood pressure elevation after the first 10 min was attributed to sympathetic overactivity. Because pressor and sympathetic nerve responses were substantially enhanced following bilateral vagotomy or sinoaortic denervation, it was considered likely that responsiveness to hypertonic NaCl in intact rats in inhibited by both cardiopulmonary and sinoaortic baroreceptor afferents. Augmentation of pressor responsiveness following interruption of baroreceptor afferent pathways suggests that increases in sympathetic activity and blood pressure produced by hypertonic NaCl could contribute to salt-induced hypertension, particularly when baroreceptor buffering becomes deficient.
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PMID:Sympathetic hyperactivity elevates blood pressure during acute cerebroventricular infusions of hypertonic salt in rats. 620 90

Several previous studies have demonstrated an increased prevalence of gout in New Zealand Maoris. The aetiology of the hyperuricaemia and its effect on morbidity, apart from gout, are unknown. A survey of 115 Maori men of working age revealed a history of gout in 10 (8%) and asymptomatic hyperuricaemia in 26 (23%). The relationship of hyperuricaemia with obesity was confirmed. Alcohol did not make an obvious contribution to the prevalence of hyperuricaemia. Hypertension was more common and creatinine clearance lower amongst those with gout, but not significantly so. The frequency of hypertension and mean creatinine clearance were similar to that seen in asymptomatic hyperuricaemia and normouricaemia. Urate clearance was lower in the gouty and hyperuricaemic subjects. The normouricaemic Maoris had a reduced fractional urate clearance compared with normal men elsewhere. They also excreted a relatively small proportion of hydrogen as ammonium. Both these features are characteristic of gout, and suggest that the Maoris' susceptibility to hyperuricaemia has a renal mechanism. Obesity is common amongst the Maoris and accentuates their natural tendency to hyperuricaemia.
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PMID:Hyperuricaemia, gout and kidney function in New Zealand Maori men. 648 33


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