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

The relationships between altered nutrition and body composition of sodium, potassium and water are reviewed. The physiological mechanisms involved in cellular homeostasis of sodium and potassium are also discussed with particular reference to energy costs. Alterations in mineral metabolism in protein energy malnutrition, oedema, potassium adaptation, fasting and hypertension are described.
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PMID:Interrelations between the physiology of sodium, potassium and water, and nutrition. 10 69

A new and simple laboratory test for measuring net Na+ and K+ fluxes in Na+-loaded/K+-depleted human erythrocytes was developed and applied to hypertension. Moderate essential hypertension was characterized by a constant increase in net K+ influx; more severe cases showed a drop in net Na+ efflux. Na+ and K+ erythrocyte fluxes were found to be normal in hypertension of renal origin.
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PMID:[Evidence of abnormalities in net sodium and potassium fluxes in erythrocytes of patients with essential hypertension]. 10 28

Nitroglycerin is a vasodilating agent by virtue of its actions on vascular smooth muscle fibers. It may be administered intravenously (using either 5 p. cent dextrose, or propylene-glycol solvant), sublingually, orally or by topical administration. It is rapidly metabolized, principally by liver. Its is not toxic. The vasodilatation that is produced is both arterial and venous and is dose-related in dog (1 microgram to 100 micrograms/kg/min). However, resistance and tachphylaxis may occur. Its principal use is for angor treatment, but it has been used for the treatment of arteriopathy of the lower limbs, biliar hypertony and arterial hypertension. It has been recently administered for the treatment of acute phase of myocardial infarction and during pre, per- and post-operative periods in cardiac surgery, neurosurgery and hip surgery, as myocardial protector or anti-hypertensive agent or hypotensive agent. The absence of toxicity and the rapid reversibility of its cardio-vascular effects which are similar to the effects of sodium nitroprusside are important reasons for its use in anesthesia and cardiac intensive care.
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PMID:[Pharmacology of nitroglycerin (author's transl)]. 11 40

The increase in total body sodium and hyperactivity of the renin-angiotensin system plays a major part in hypertension in patients underdoing chronic dialysis. After sodium depletion most patients become normotensive. Their hypertension seems to be due to sodium overload but it is favoured by insufficient inhibition of renin secretion. Some renin hypertensive, hypersecretion of renin is the main factor in these cases but its effect is aggravated by the sodium overload. Other factors may play a role as suggested by the studies of hypertensive patients after bilateral nephrectomy. However, their roles and mechanisms are unknown at present.
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PMID:[Physiopathology of arterial hypertension in chronic hemodialysis patients]. 11 4

The response of arterial pressure to an infusion of saralasin was compared to the effect of surgical correction of renal vascular lesions (3 to 6 months after surgery) in eleven patients whose hypertension was associated with uni or bilateral stenosis of renal artery. Saralasin was infused after four days of dietary sodium restriction (10-40 mEq/day). An excellent correlation (r = 0.83, p less than 0.005) between the effects of saralasin and surgery was obtained. There was no correlation between the response to saralasin or to surgery and the ratio of renal vein renin activities. It is suggested that saralasin may be a good tool for predicting the effect of surgery in renovascular hypertension, when infused in moderately sodium depleted patients.
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PMID:[Saralasin and prediction of the surgical result in renovascular arterial hypertension]. 11 7

The angiotensin antagonist, saralasin, (10 and 30 mg/kg), increased serum renin activity (SRA) in normal, conscious rats from 2.7 +/- 0.4 to 16.2 +/- 3.7 and 22.5 +/- 2.4 ng/ml/hr (p less than 0.001), respectively, without markedly altering blood pressure or heart rate. Indomethacin, in a dose which inhibited the urinary excretion of prostaglandin E2 (PGE2) by 75%, and arachidonate-induced hypotension by 83%, failed to alter basal SRA but inhibited saralasin-induced renin release by 99% and 87% at the 10 and 30 mg/kg doses, respectively. Indomethacin failed to alter basal hemodynamics or the hemodynamic response to saralasin. Propranolol (1.5 mg/kg) inhibited saralasin-induced renin release by 93% and enhanced the suppressant effect of indomethacin from 79% to 100%. Meclofenamate, another prostaglandin synthesis inhibitor, also blocked saralasin-induced renin release by 99% and 72% at the 10 and 30 mg/kg doses, respectively (p less than 0.001). In sodium-depleted rats, saralasin (0.3 mg/kg) increased SRA from 12 +/- 2 to 119 +/- 6 ng/ml/hr (p less than 0.001) and decreased blood pressure by 6% (p less than 0.01). In these animals, indomethacin failed to alter basal SRA, but inhibited saralasin-induced renin release by 82%, urinary excretion of PGE2 by 79%, and arachidonate-induced hypotension by 81%. These findings suggest 1) that saralasin-induced renin release is mediated by renal prostaglandins, and 2) an interrelationship exists between the receptor controlling AII-mediated inhibition of renin release, which is blocked by saralasin, and the juxtaglomerular beta-adrenergic receptor.
Hypertension
PMID:Saralasin-induced renin release: its blockade by prostaglandin synthesis inhibitors in the conscious rat. 12 Mar 20

The authors studied the effect of sodium salicylate administered into different parts of the circulatory system on various cardiovascular, respiratory and glottic parameters in Pentobarbital-anaesthetized rabbits. The results show that apnoea, bradycardia and hypotension, followed by hypertension, can also be caused by the extrathoracic action of salicylate. Cardiovascular responses induced by injecting salicylate into the carotid circulation are qualitatively the same, even after vagotomy, as in injection into the femoral vein. Salicylate injected into the common carotid artery, the internal carotid artery or the femoral vein causes inspiratory apnoea in rabbits, with powerful electrical activity of the diaphragm and an intrapleural pressure shift to marked inspiratory values. Laryngoconstriction occurs simultaneously, despite inspiratory apnoea. The injection of salicylate into the common carotid artery after bilateral vagotomy induces expiratory (not inspiratory) apnoea, indicating that the vagi play an important role in the origination of inspiratory apnoea in rabbits.
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PMID:Cardiovascular, respiratory and glottic effects of sodium salicylate administered into different parts of the circulation in rabbits. 12 83

The activities of the Na+--K+-ATPase, succinic dehydrogenase (SDH/, lactic dehydrogenase (LDH/ and glucose-6-phosphat dehydrogenase (G-6-PDH/ were studied in the cortex outer and inner medulla of the kidneys of rats with spontaneous hypertension (SHR) and were compared with those of control normotensive Wistar rats. The SHR aged 6--8 weeks had durint the prehypertensive and the early hypertensive stage the same enzymatic activities as control rats. Rats with a steady SH aged 16-22 weeks had low specific activity of the, Na+--K+-ATPase, SDH and LDH in the outer medulla. The latter can be associated with decreased intensity of the energy metabolism and a reduction of the active sodium transport in the ascending limb of the loop of Henle in the SHR rats and cold cause the phenomenon of exaggerated natriuresis characteristic of hypertension.
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PMID:[Na+--K+-adenosine triphosphatase and some oxidoreductases in the kidney of rats with spontaneous hypertension]. 12 6

In the course of the development of desoxycorticosterone-acetate-salt hypertension the animals were noted to display high appetite of sodium chloride, a considerable increase of the weight of the heart, kidneys and adrenal glands, of the diameter of the glomeruli and the surface of the cortical and medullar zones of the kidneys, a decrease of the sodium and potassium gradient in the renal tissue. Adaptation to hypoxy is noted so cause a decrease in the interventricular factor, in the width of the glomerular zone of the adrenal glands, in the sodium concentration in the erythrocytes, an increase in the mass of the medullar layer of the kidneys, and an increase in the sodium and potassium gradients. When adaptation to hypoxy is combined with the effect of desoxycorticosterone-acetate-salt, hypertension develops to a lower degree than in non-adapted animals.
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PMID:[Certain changes in the water-electrolyte metabolism in desoxycorticosterone acetate salt hypertension in rats adapted to high altitude hypoxia]. 12 78

The rats with chronic renal hypertension caused by constricting one renal artery, exhibit a decrease in the activity of Na-K-ATPase in the outer medulla of the "untouched" kidney, as compared to this activity in the kidneys of intact normotensive rats and in the "untouched" kidney of the rats where renal artery constriction did not result in hypertension. There were no differences between the control normotensive Wistar rats and the spontaneously hypertensive rats (SHR) in the prehypertensive and early hypertensive stages (at the age of 6-8 weeks) as far as the activities of Na-K-ATPase and oxidoreductases (SDH and LDH) in the renal cortex, the outer and inner medulla are concerned. The spontaneously hypertensive rats with chronic hypertension had at the age of 16-20 and 27-29 weeks lower activity of Na-K-ATPase, SDH, and LDH in the outer renal medulla than the control normotensive Wistar rats. The experimental results indicate that in chronic arterial hypertension there is a decrease in the activity of Na-K-ATPase, in the outer renal medulla, which suggests a reduction in the resorpo sodium and water.
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PMID:Na-K-adenosine triphosphatase in the kidney of rats with renal hypertension and spontaneously hypertensive rats. 13 Jun 15


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