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

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

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

Vasodilator responses to acute intra-arterial infusions of K+ are attenuated in dogs with chronic one-kidney perinephritic hypertension in rats with chronic two-kidney Goldblatt hypertension, and in men with essential hypertension. There is evidence that K+ evokes vasodilation by stimulating vascular smooth muscle membrane Na+-K+-activated adenosine triphosphatase, thereby increasing activity of the cellular Na+-K+ electrogenic pump. We therefore proposed that there may be an underlying decrease in the operation of this pump in vascular smooth muscle of hypertensives. The operation of the cellular Na+-K+ pump may be estimated by measurement of rubidium uptake. Thus, so further investigate our hypothesis, we measured 86Rb uptake in small mesenteric arteries and splanchnic veins from 12 dogs with chronic uncomplicated one-kidney perinephritic hypertension and from 12 normotensive control dogs. Vessels were excised under thiamylal anesthesia and incubated in cold medium (plasma or Krebs-Henseleit solution) for sodium loading and then the velocity of 86Rb uptake was estimated in the absence of or in the presence of ouabain, a specific inhibitor of the Na+-K+ pump. In neither arteries nor veins was there evidence for differences between hypertensives and normotensives in the ouabain-insensitive uptake of 86Rb. In contrast, the ouabain-sensitive 86Rb uptake was depressed by 42% in arteries (P less than 0.05) and by 49% in veins (P less than 0.01) from hypertensive dogs, if incubated in the dog's own plasma. These results indicate that the activity of a ouabain-sensitive Na+-K+ pump may be depressed in vascular tissue from dogs with chronic one-kidney perinephritic hypertension. Because the Na+-K+ pump in vascular smooth muscle is probably electrogenic, such an abnormality, by partially depolarizing the muscle cell membrane, would help to account for the elevated vascular resistance found in these dogs.
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PMID:Depressed function of a ouabain-sensitive sodium-potassium pump in blood vessels from renal hypertensive dogs. 13 55

Hypertensive Goldblatt-rats have higher than normal Na-appetite and an enhanced Na-output. They have normal plasma Na- and K-concentration and kidney weight but a significantly reduced plasma volume. The amount of renal membrane protein and the renal Na-K-ATPase-activity of hypertensive rats was found to be significantly below that of controls. In order to evaluate the role of Na-appetite, Na-excretion rate and renal Na-K-ATPase-activity in the electrolyte balance, Goldblatt-rats with a stable hypertension and control animals were put for 8 days on a Na-free diet. Na-excretion rate of control rats reached a minimum (13 muEq/100 g x 24 hr) within 5 days and was maintained on this level up to the end of the experiment. Na-free diet did not alter either the kidney weight or the amount of membrane protein of the animals. However, in salt-free fed control rats total renal Na-K-ATPase-activity was found elevated by about 10% as compared to animals maintained on normal diet. Goldblatt-rats continuously excreted significantly higher amounts of Na (35 muEq/100 g x 24 hr), had sharply reduced plasma volume and plasma Na- concentration. The renal Na-K-ATPase-activity should no adaptation in gold blatt-rats. In all animals studied the rate of Na-excretion showed a close indirect correlation with the renal Na-K-ATPase-activity. It is concluded, that Goldblatt-rats depend on dietary Na to a higher extent than controls because of their reduced capacity to retain Na. The increased Na-appetite of hypertensive rats is a factor secondary to Na-loss.
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PMID:Interdependence of Na-excretion, plasma electrolytes, plasma volume and renal Na-K-ATPase-activity in hypertensive rats. 13 99

A patient with excessive industrial exposure to silicon and an elevated silicon content in his renal tissue was found to have a distinctive nephropathy, characterized pathologically by changes in the glomeruli and proximal tubules, and manifested clinically by albuminuria and hypertension. Proximal tubular function was intact. From a biochemical standpoint, this finding correlates with the demonstration in vitro that, in contrast to cadmium, a known cause of Fanconi syndrome, silicon does not inhibit renal cortical sodium-potassium-adenosine triphosphatase (Na-K-ATPase).
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PMID:Silicon nephropathy. 113 57

1. The peripheral glucose disposal rate (assessed with the euglycaemic-hyperinsulinaemic clamp technique), the serum sex hormone-binding globulin concentration and total and ouabain-sensitive 22Na-efflux rate constants in leucocytes were determined in 41 women with impaired glucose tolerance and in 40 women with normal glucose tolerance. The groups were matched for body mass index and diastolic blood pressure (range 55-112 mmHg). 2. Stepwise regression analysis showed that diastolic blood pressure in the group with impaired glucose tolerance was inversely correlated with the glucose disposal rate (model r2 = 21%) and was correlated with the plasma glucose concentration at 120 min after an oral glucose load (model r2 = 31%). In the group with normal glucose tolerance, however, neither of these two variables was correlated with blood pressure, although the ouabain-sensitive 22Na efflux rate constant was (model r2 = 11%). 3. Among insulin-resistant subjects, those with hypertension had significantly lower serum sex hormone-binding globulin concentrations than the normotensive subjects. 4. We conclude that insulin resistance is correlated with high blood pressure in women with glucose intolerance and increased androgenic activity. In women with normal insulin sensitivity, a low level of the Na+/K(+)-ATPase-mediated sodium efflux is associated with high blood pressure.
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PMID:Insulin resistance and Na+/K(+)-ATPase in hypertensive women: a difference in mechanism depending on the level of glucose tolerance. 131 Sep 9

1. Several observations support the hypothesis that in rats of the Milan hypertensive strain elevated levels of a circulating ouabain-like factor might normalize the elevated Na+ reabsorption, but, on the other hand, might contribute to the development of hypertension. 2. As the receptor occupancy of this endogenous factor seems to be reversible, the aim of our study was to test, in vitro, the hypothesis of its presence in isolated kidneys from Milan hypertensive rats by studying the response to exogenous ouabain before and after prolonged washing. 3. The kidneys were isolated from adult Milan hypertensive rats and from age-matched normotensive controls and ouabain was given at two different experimental time intervals: shortly (15 min) after washout or after a further 60 min of washout (75 min in total). Comparative experiments with the diuretic hydrochlorothiazide were performed using the same protocol. 4. Ouabain given after 15 min of perfusion caused an increase in renal vascular resistance, diuresis and natriuresis; these haemodynamic and tubular responses were similar in kidneys from both Milan hypertensive and Milan normotensive rats. If given after the washout period, ouabain caused a comparable increase in renal vascular resistance, but a significantly greater natriuresis in kidneys from Milan hypertensive rats as compared with kidneys from Milan normotensive rats. On the other hand, hydrochlorothiazide caused similar natriuresis in kidneys from both strains after washout. 5. These results support the hypothesis that a factor, capable of interacting with the ouabain receptor on the Na+/K(+)-ATPase of tubular cells, is present in the kidney of adult Milan hypertensive rats and that it can be removed by prolonged washout.
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PMID:Differences in ouabain-induced natriuresis between isolated kidneys of Milan hypertensive and normotensive rats. 131 56

Na(+)-Ca2+ exchange is proposed to be an important regulator of myoplasmic intracellular Ca2+ concentration ([Ca2+]i) and contraction in vascular smooth muscle. We investigated the role of Na(+)-Ca2+ exchange in regulating [Ca2+]i in swine carotid arterial tissues that were loaded with aequorin to allow simultaneous measurement of [Ca2+]i and force. Reversal of Na(+)-Ca2+ exchange, by reduction of extracellular Na+ concentration ([Na+]o) to 1.2 mM, induced a large increase in aequorin-estimated [Ca2+]i and a low [Ca2+]i sensitivity. The contraction induced by 1.2 mM [Na+]o was partially caused by depolarization and opening of L-type Ca2+ channels because 10 microM diltiazem partially attenuated the 1.2 mM [Na+]o-induced increases in [Ca2+]i. High dose ouabain (10 microM), a putative endogenous Na+,K(+)-ATPase inhibitor, increased both [Ca2+]i and force. However, the increases in [Ca2+]i and force were mostly blocked by 10 microM phentolamine, suggesting the predominant effect of ouabain was to increase norepinephrine release from nerve terminals. In the presence of 10 microM phentolamine, 10 microM ouabain slightly accentuated 1 microM histamine-induced increases in [Ca2+]i and force. The ouabain dose necessary to induce contraction in the absence of phentolamine was significantly less than the ouabain dose necessary to accentuate histamine-induced contractions in the presence of phentolamine. These results suggest that Na(+)-Ca2+ exchange exists in swine arterial smooth muscle. These data also suggest that ouabain (which should increase [Na+]i and inhibit Na(+)-Ca2+ exchange) primarily enhances contractile function in the swine carotid artery by releasing catecholamines from nerve terminals; direct action of Na+,K(+)-ATPase inhibitors on smooth muscle appears to occur only with very high doses.
Hypertension 1992 Apr
PMID:Na(+)-Ca2+ exchange, myoplasmic Ca2+ concentration, and contraction of arterial smooth muscle. 131 92

This review paper deals with recent data concerning the physiopathology of chronic heart failure. Broadly speaking, the cause of chronic heart failure is arterial hypertension and/or coronary disease. Myocardial hypertrophy is only one example of biological adjustment to the environment, and chronic heart failure, an adaptation disease, indicates its limits. Diastolic dysfunction includes 3 elements. Relaxation is slowed down by a decrease in density of Ca(2+)-ATPase in the sarcoplasmic reticulum and by a fall in Na+/Ca2+ exchange activity. The decline of tissue compliance is mainly explained by probably hormonal changes in collagen. Changes in isomyosins account for abnormalities of atrial contraction. At the beginning of mechanical overload, the fall in systolic function enables the heart to produce a normal tension. The determinant element is slowing down of intracellular calcium movements. Enlarged hearts generate arrhythmias. The origin is probably the presence of unstable calcium homeostasis.
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PMID:[Chronic heart failure: biological bases of myocardial function]. 131 2

Na+/K(+)-ATPase of the cell membrane is considered to be closely related to the pathology of various diseases including hypertension and heart failure. The activity of this enzyme in the erythrocyte membrane has been determined in earlier reports by the assay of inorganic phosphate generated from the substrate ATP or radioimmunoassay after binding 3H ouabain to the erythrocyte membrane, using a large volume of blood samples. However, as neither method was appropriate for wide routine use, we developed a method to assay this enzyme in a small volume (10 ml) of fresh human blood samples with re-evaluation of conditions for the inorganic phosphate assay. In this method, the coefficient value (CV) of membrane protein amount and the NA+/K(+)-ATPase activity were 2.2% and 2.5% respectively, indicating sufficient precision of the assay. Moreover, in 97 subjects without abnormalities in blood biochemical tests (77 males and 20 females) aged 35-59 years, the enzyme activity showed no differences according to age or sex, ranging from 0.217 to 0.071 mumols Pi/mg/hr with a mean of 0.130.
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PMID:[Determination of human erythrocyte membrane Na+/K(+)-ATPase activity in small volume of blood sample]. 131 73


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