Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the initial potassium loss and development of hypokalaemia during the administration of an oral diuretic, metabolic balance studies were performed in ten patients with essential hypertension who had shown hypokalaemia under prior oral diuretic treatment. Chlorthalidone (50 mg daily) was given for 14 days. Six patients received a normal-sodium diet and four a low-sodium (17 mmol/day) diet. All patients had a normal initial total body potassium (40K). The electrolyte balances, weight, bromide space, plasma renin activity, and aldosterone secretion rate were measured. In both groups a potassium deficit developed, with proportionally larger losses from the extracellular than from the intracellular compartment. In the normal-sodium group the highest mean potassium deficit was 176 mmol on day 9, after which some potassium was regained; in the low-sodium group the highest deficit was 276 mmol on day 13. The normal-sodium group showed an immediate but temporary rise of the renin and aldosterone levels; in the low-sodium group renin and aldosterone increased more slowly but remained elevated. It is concluded that dietary sodium restriction increases diuretic-induced potassium loss, presumably by an increased activity of the renin-angiotensin-aldosterone system, while sodium delivery to the distal renal tubules remains sufficiently high to allow increased potassium secretion.
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PMID:Initial potassium loss and hypokalaemia during chlorthalidone administration in patients with essential hypertension: the influence of dietary sodium restriction. 2 52

To investigate the role of the renin-angiotensin-aldosterone system as a cause of hypertension, 20 hypertensive patients with coarctation of the aorta were studied during normal and low sodium intake and after diuresis with flurosemide. Eight patients with essential hypertension and 13 control subjects were similarly studied. Plasma renin activity values in patients with coarctation were similar to those in patients with essential hypertension and in control patients during normal and low sodium diets. However, after the administration of furosemide, plasma renin activity values were significantly higher in the patients with coarctation than in the other two groups (P less than 0.005 and less than 0.01, respectively). The values for urinary aldosterone, plasma volume and extracell fluid volume (bromide space) were increased in patients with coarctation during both normal and low sodium intake. These renin and aldosterone responses and body fluid spaces in patients with coarctation suggest that their hypertension resembles a one-kidney Goldblatt model. The data help to better define the role of the renin-angiotensin-aldosterone system in the hypertension of coarctation and thus may help guide the clinician in therapeutic interventions.
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PMID:Role of the renin-angiotensin-aldosterone system in hypertensive children with coarctation of the aorta. 42 21

The effect of thiamine-bromide (5-7 mg/kg, intravenously) on the cerebral blood flow circulation rate; total arterial pressure, oxygen tension in the brain tissues (measured polarographically) and pressure in the venous vessels of the brain was investigated on anesthetized cats with controlled respiration. In patients with hypertensive disease (essential hypertension) the action of the agent (1 ml of a 6% solution, intramuscularly) on the rheoencephalographic readings and overall arterial pressure was studied. Thiamine-bromide is shown to lower the tonicity of intra- and extracranial vessels and to increase pulsed variations in the volume of blood filling of the cranial vessels. The hypotensive effect of the drug is pronounced but mildly. The oxygen tension in cerebral vessels depended mainly on changes in the cerebral circulation rate.
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PMID:[Effect of thiamine bromide on cerebral circulation and arterial pressure (an experimental and clinical study)]. 77 59

To assess the mechanism responsible for maintaining the elevated arterial pressure in 2-kidney DOCA treated Yucatan miniature swine, cardiovascular parameters and the responses to hexamethonium bromide (HMB) were evaluated in normal and DOCA treated animals. Using chronically instrumented conscious animals, measurements of mean arterial pressure (MAP), cardiac output (CO), and calculated total peripheral resistance (TPR) revealed that with DOCA hypertension MAP was increased 50-60 mmHg above controls. This increased pressure was due to an increase in TPR with CO remaining normal. HMB normalized the MAP of the DOCA animals via a selective lowering of TPR to a value similar to that of the controls. In DOCA hypertensive animals these functional changes, due to increased peripheral sympathetic nerve activity, were reflected by significantly elevated plasma norepinephrine. In this animal DOCA administration produces a neurogenic form of hypertension which appears to be analogous to essential hypertension in man.
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PMID:The role of the sympathetic nervous system in 2-kidney DOCA-hypertensive Yucatan miniature swine. 287 9