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

Endocrine and renal functions were studied in 149 patients with essential hypertension by measuring plasma electrolytes, renin activity, creatinine and aldoserone, as well as the urinary excretion of creatinine and sodium chloride, before and during treatment for hypertension. Half of the patients responded to trichlormethiazide (thiazide-responsive group) but the other half did not (thiazide-unresponsive group). Systolic and diastolic blood pressures increased progressively uith age in the thiazide-unresponsive group, but were lower and did not progress with age in the thiazide-responsive group. There was no consistent difference in plasma renin activity between the thiazide-responsive and the thiazide-unresponsive groups. The fluctuation of plasma renin activity in response to an excess of sodium chloride or to thiazide treatment was reduced progressively with age. Creatinine clearance decreased and the blood urea nitrogen level increased with age. The age-related decrease of plasma renin activity is discussed on the light of the age-related impairment in the ability of the kidney to excrete sodium and water.
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PMID:Age-related changes in endocrine and renal function in patients with essential hypertension. 46 52

This study was undertaken to explore the effects of chronic low-level cadmium ingestion in Dahl hypertension-resistant (R) and hypertension-sensitive (S) lines of rats. Groups of weanling female R and S rats were given 0 or 1 mg cadmium/1. in drinking water and fed either a low salt (0.4% NaCl) or a high salt (4% NaCl) diet for 28 weeks. Cadmium produced hypertension associated with gross cardiac hypertrophy and mild to moderate renal vascular changes in S, but not in R, rats on a low salt diet. Cadmium enhanced the rate and degree of development of salt-induced hypertension without exacerbating the hypercholesterolemia or renal vascular lesions normally observed in S rats on a high salt diet. Cadmium lowered circulating cholesterol levels in both lines on a low salt diet. Cadmium had no influence on growth, blood urea nitrogen concentration, plasma renin activity, tumor formation, or survivorship in R and S rats on either salt diet. This study indicates that the genetic composition is a critical determinant of the adverse effects of chronic low-level cadmium ingestion in rats. In addition to the experimental implications, these findings may have relevance to the problem of human "essential" hypertension.
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PMID:Effects of cadmium ingestion in rats with opposite genetic predisposition to hypertension. 48 40

A 56-year-old Samoan man with a documented history of hypertension, who presented with atrial fibrillation and hypotension, quickly developed renal failure with a serum urea nitrogen of 1.370 g/L and a serum creatinine of 92 mg/L. After hydration of the patient, the creatinine value became normal in two days, the urea nitrogen in four days. The urinary creatinine output during the first 24 h of hospitalization was 3.7 g. This case illustrates the rapidity with which unusually large amounts of creatinine (more commonly seen in chronic renal failure) can accumulate and be excreted in pre-renal failure. It also reaffirms the usefulness of the urea nitrogen/creatnine ratio in evaluating the causes of azotemia.
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PMID:Pre-renal azotemia mimicking chronic renal failure in a hypotensive patient. 49 10

Phencyclidine concentrations were measured in the plasmas of 22 patients with nonfatal phencyclidine intoxication using gas-liquid chromatography with a nitrogen detector. Concentrations found ranged from less than 10 to 812 micrograms/l, and except for the systolic blood pressure (r = 0.60, P less than 0.05), showed no significant correlation with the physical findings. The most common physical findings were combativeness-agitation (64%), depressed level of consciousness (50%), hypertension (43%), moiosis (43%), and tachycardia (43%). Phencyclidine concentrations measured in the erythrocytes of seven of the patients were generally higher than concentrations in the corresponding plasmas (erythrocyte:plasma concentration ratios ranged from 3.1 to 37.9), suggesting that the binding of phencyclidine to plasma proteins is low. Erythrocytic concentrations also showed no significant correlation with either the physical findings or the plasma concentrations of phencyclidine. For 15 unselected urines the concentrations of phencyclidine showed no significant correlation with urinary pH.
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PMID:Phencyclidine abuse. Clinical findings and concentrations in biological fluids after nonfatal intoxication. 50 93

Normotensive, Sprague-Dawley (S-D) and spontaneously hypertensive (SH) rats were subjected to aortic ligature. The systolic blood pressure of S-D rats was increased by +/- 80 mm Hg, whereas the blood pressure of SH rats with pre-existent hypertension increased only slightly, +/- 9 mm Hg. The S-D rats developed myocardial and renal infarcts as well as polyarteritis nodosa; the SH rats developed testicular and microadrenocortical infarcts only. Aortic-ligated S-D rats had elevated creatine phosphokinase, serum glutamic-oxaloacetic transaminase, serum glutamic-pyruvic transaminase, and lactic hydrogenase levels and manifested hyperglycemia, hypercholesterolemia, and elevated blood urea nitrogen (BUN) levels. Corticosterone levels increased in aortic-ligated S-D rats but decreased in SH rats. Collateralization about the site of aortic ligature appeared to be the same in both strains. It is suggested that the acutely induced hypertension in S-D rats rather than SH rats and differences in adrenal steroidogenesis between the two strains would best account for the dichotomous cardiovascular response to aortic constriction.
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PMID:Diverse cardiovascular responses to aortic constriction in normotensive Sprague-Dawley versus spontaneously hypertensive rats. 50 90

Intact anesthetized dogs were exposed for 75 min to either 5.75, 9.0, or 12.0% oxygen in nitrogen. Although pulmonary artery pressures were significantly elevated in all hypoxic exposures, systemic hypertension occurred only at the onset of severe hypoxia(5.75% O2). Coronary blood flow increased from an average of 130 during normoxia to a peak of 400 ml/100 g per min during inhalation of 5.75% O2, and coronary sinus oxygen tensions of 8 Torr and oxygen contents of 1.1 ml/100 ml were sustained for 75 min without biochemical, functional, or electrophysiological evidence of myocardial ischemia. Cardiac index (CI) increased significantly only during severe hypoxia (5.75% O2) with the greatest elevation after 30 min. Subsequently, CI decreased concomitantly with a 27% elevation in arterial hemoglobin concentration and oxygen-carrying capacity. It is concluded that the hypoxic threshold for significant elevations of cardiac output is between 6.0 and 9.0% O2.
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PMID:Effects of acute prolonged hypoxia on cardiovascular dynamics in dogs. 59 70

The effect of total adrenalectomy on the mechanisms of arterial pressure control was studied in uninephrectomized rats with and without renal artery stenosis (Goldblatt one-kidney model). Four groups of rats were prepared and maintained on high-salt intake (1% NaCl): uninephrectomized-KI; KI + adrenalectomy-KIAx; uninephrectomized with renal artery stenosis-GI; and GI with adrenalectomy-GIAx. Over 3 wk blood pressure rose significantly in both GI and GIAx but the degree of increase in GI was greater. Hyponatremia, hyperkalemia, and increased plasma urea nitrogen were observed in both KIAx and GIAx. Plasma renin concentration (PRC) and plasma renine activity (PRA) were markedly increased and plasma renin substrate (PRS) was decreased in both adrenalectomized groups. Infusion of saralasin resulted in significant and similar reductions in mean arterial pressure (MAP) in KIAx and GIAx, but had no effect on MAP in KI and GI. These results allow approximations of the contribution to total MAP of identifiable components, which are: the total adrenal component, the renin-angiotensin system component, which partially compensates for loss of the adrenal secretions, and the independent effect of the renal artery clip. Thus, a multifactorial analysis of GI hypertension is provided.
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PMID:Adrenal gland in experimental renal hypertension. 62 42

Transient hypertension occurred in 3 patients shortly after blunt injury to the abdomen. Renal trauma was suspected in all 3 patients and radiological evidence for renal injury was present in 2. Plasma renin activity definitely was elevated in 1 patient and probably was elevated in another. There was a decrease in blood pressure in all 3 patients during infusion of the angiotensin II analogue--saralasin--showing that the hypertension in these patients was angiotensin-mediated. Renal function as reflected by the blood urea nitrogen, creatinine and electrolytes was not impaired significantly. Thus, acute hypertension after blunt abdominal trauma may be angiotensinogenic and is not necessarily sustained.
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PMID:Renin angiotensin involvement in transient hypertension after renal injury. 65 Jul 71

The antihypertensive effect of spironolactone was studied in 20 patients with essential hypertension and normal stimulated peripheral renin activity (PRA). Single-blind 8-wk treatment periods of placebo, 100, 200, and 400 mg spironolactone were used in consecutive order. Average supine and erect blood pressures were lower than placebo values at the end of each treatment. A prominent orthostatic effect was observed. Changes in blood pressure were not related to changes in body weight, PRA, or blood urea nitrogen. A larger proportion (50%) of patients had a more normal erect diastolic pressure at the end of 400 mg/day than at the end of 100 mg/day (20%), but the response to 400 mg/day could not be predicted from the responses to lower doses. Larger doses of spironolactone were predictably associated with rises in serum potassium, PRA, and aldosterone excretion. Adverse effects were absent during therapy with 100 mg/day but were frequent during 200--400 mg/day. Although there are no apparent advantages in increasing spironolactone from 100 to 200 mg/day in this group of patients with normal renin hypertension, increasing the dose to 400 mg/day resulted in better blood pressure control with more frequent adverse effects.
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PMID:Antihypertensive responses to spironolactone in normal renin hypertension. 69 76

Issuing from the present state of the influence of the basic nutritive substances (protein, fat, carbohydrates) and various nutritive factors discussed again and again (cholesterol, erucaic acid, sodium, calcium/magnesium quotient, pressor amines) on the development of the arteriosclerosis, the indididual factors of influence are critically evaluated. The investigations are getting under way, so that ascertained results are standing beside insufficiently claified or open problems, From the abundance of the observations conclusions are drawn which are of significance for practice. Unfavourable influences of nutrition on the factors of risk (hyperlipoproteinaemia, disturbance of the carbohydrate tolerance, hyperuricaemia, hyperalimentation) and on the manifest diseases (hypertension, diabetes mellitus, uric arthritis, obesity) of the metabolic syndrome which finally contribute to the development of arteriosclerosis are emphasized. In front of this background a clinically and ambulatorily tested basic metabolic diet is described. About 20% of the energy content (kcal or kJ) of this diet are protein, 35% fat and 45% are carbohydrates. The saturated fatty acids lie below 30%, the manifold saturated fatty acids, however, above 20% of the total fat proportion. The cholesterol content is below 400 mg, the purin-nitrogen below 200 mg, and the sodium content is about 2g per day. This diet can be produced for the treatment of persons with normal weight and overweight in different energetic degradations.
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PMID:[Nutrition and arteriosclerosis]. 70


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