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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied changes in intracellular electrolytes and the rate constant of 22Na efflux from isolated leucocytes in Chinese patients with essential hypertension and their normotensive offsprings. The hypertensives had an increase of sodium content and a reduction of the total or ouabain-sensitive 22Na efflux from leucocytes. The normotensives born of hypertensive parents showed lower sodium content, higher potassium content and reduced rate constant of ouabain-insensitive 22Na efflux from leucocytes. The results suggest that the inhibition of cell sodium pump activity may be a marker of essential hypertension. Abnormal cell sodium transport observed in normotensives with family history of hypertension may have some etiological linking with the inheritance of hypertension.
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PMID:Abnormal leucocyte sodium transport in Chinese patients with essential hypertension and their normotensive offsprings. 653 3

The effect of local infusion of ouabain into the forearm vascular bed has been examined in 15 normotensive male volunteers in an attempt to define the nature of the functional abnormalities of the resistance vessels in primary hypertension. Ouabain and other drugs were infused into the brachial artery and forearm blood flow was measured by venous occlusion plethysmography. Infusion of ouabain at 2 micrograms/min for 1 h caused a 26% reduction in forearm blood flow with a small rise in systemic arterial pressure; the increase in vascular resistance was unaffected by prior treatment with phentolamine. After infusion of ouabain the dilator response to potassium was reduced by 33% but the responses to verapamil and sodium nitroprusside were unchanged. The results show that acute depression of sodium pump activity by ouabain reproduces the increased resting resistance and impaired response to potassium that are seen in hypertension. It does not reproduce the relative enhancement of responsiveness to verapamil that is also observed in the resistance vessels of patients with hypertension and this abnormality must have some other cause.
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PMID:Effect of local infusion of ouabain on human forearm vascular resistance and on response to potassium, verapamil and sodium nitroprusside. 668 Oct 36

Excessive dietary intake of sodium appears to play a significant role in human essential hypertension. The underlying mechanism may involve the excessive secretion of a humoral natriuretic factor in response to the salt load. Deproteinized plasma from patients with essential hypertension contains elevated levels of an ouabain-like inhibitor of dog kidney sodium plus potassium-dependent adenosine triphosphatase. This substance, by inhibiting renal sodium transport, should have a natriuretic effect. Plasma from hypertensive patients also produces an ouabain-like sensitization of vascular smooth muscle (rabbit aorta) to exogenous norepinephrine. These data suggest that a circulating inhibitor of the sodium pump may play a key role in generating increased peripheral vascular resistance. Cellular mechanisms that link sodium pump inhibition to increased vascular resistance involve increased norepinephrine release and reduced re-uptake and directly increased smooth muscle contractility and reactivity, as a result of increased cell sodium.
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PMID:Role of a natriuretic factor in essential hypertension: an hypothesis. 668 39

The dilator response to local infusion of K+ has been assessed in the forearm resistance vessels of 17 men with primary hypertension and 11 controls, by using a standard plethysmographic method. The response to infusion of K+ at 0.1 mmol/min was smaller in the patients with hypertension than in the normal controls (P less than 0.03). The results are consistent with the view that the activity of the sodium pump is depressed in the resistance vessels of patients with hypertension, but they yield no evidence as to whether or not this abnormality contributes to the elevation of the peripheral resistance.
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PMID:The dilator response to K+ is reduced in the forearm resistance vessels of men with primary hypertension. 669 57

An endogenous sodium pump inhibitor, or digitalis-like factor (DLF), has been postulated to mediate essential hypertension. It may also play a role in preeclampsia. However, studies of this factor in hypertensive pregnancy have not provided consistent findings. Part of this may be due to the absence of subclassification of pregnant women with pregnancy-induced hypertension (PIH) when assessing these parameters. In this study we explored serum DLF and digoxin-like immunoreactive factor (DLIF) in insulin-dependent diabetic (IDDM) women with normotensive pregnancies or PIH, comparing them to each other and to nondiabetic pregnant women. Our results demonstrated that nondiabetic women with preeclampsia (PE, PIH with proteinuria) had significantly increased serum DLF and DLIF compared to normotensive pregnant women (NL BP). Women with transient hypertension of pregnancy (THP, PIH without proteinuria) had intermediate values (DLF. NL BP: 3.3 +/- 0.6, THP: 4.8 +/- 1.1, PE: 7.6 +/- 1.3% inhibition [Na,K]-ATPase, P < .05 ANOVA; DLIF. NL BP: 0.22 +/- 0.02, THP: 0.28 +/- 0.03, PE: 0.35 +/- 0.02 ng digoxin equivalents/mL, P < .05 ANOVA). Pregnant normotensive IDDM women had significantly higher serum DLF and DLIF activity than their nondiabetic counterparts (DLF. non-IDDM NL BP: 3.3 +/- 0.6 v IDDM NL BP: 8.8 +/- 1.2% inhibition [Na,K]-ATPase, P = .0008; DLIF. non-IDDM NL BP: 0.22 +/- 0.02 v IDDM NL BP: 0.31 +/- 0.02 ng digoxin equivalents/mL, P = .005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Digitalis-like factor and digoxin-like immunoreactive factor in diabetic women with preeclampsia, transient hypertension of pregnancy, and normotensive pregnancy. 873 86

There is increasing evidence that the sodium pump plays a role in essential hypertension. Recent publications have focused on intrinsic alterations in pump activity, external modification of pump activity by circulating inhibitors, and endothelial mediation of endogenous inhibitor effects on the vascular response. Hence, this review focuses on these areas. Although there is intriguing evidence that alterations in sodium pump activity might contribute to the pathogenesis of hypertension, in at least some sodium-sensitive models and some patients with essential hypertension, the evidence remains circumstantial and areas of substantial controversy exist.
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PMID:The sodium pump in hypertension. 785 Apr 5

We have used 23Na nuclear magnetic resonance spectroscopy to examine the relationship between intracellular sodium and cardiac muscle alterations in genetic hypertension. In the spontaneously hypertensive rat (SHR) compared with the normotensive Wistar-Kyoto rat (WKY) (aged 15 to 19 weeks), mean systolic blood pressures (measured using the tail-cuff method) were significantly (P < .05) different (WKY: 118 +/- 8 mm Hg, n = 5; SHR: 185 +/- 9 mm Hg, n = 5). Heart weights were also increased significantly (P < .05) in SHR (grams dry heart to kilograms body weight ratio was 0.73 +/- 0.04, n = 5, for SHR and 0.55 +/- 0.02, n = 5, for WKY). Intracellular sodium levels, measured using shift-reagent-aided and triple quantum filtered (TQF) nuclear magnetic resonance techniques, were significantly increased (P < .05) in the isolated Langendorff perfused hypertensive rat hearts (17.3 +/- 3.6 mmol/L, n = 5) compared with normotensive rat hearts (8.4 +/- 2.3 mmol/L, n = 5). These data demonstrate increased sodium in cardiac muscle in essential hypertension. We also investigated the effect of pacing on cardiac TQF 23Na nuclear magnetic resonance and found an increase in TQF Na+ content in both WKY and SHR hearts on stepped up pacing. These results support the existence of sodium pump lag in the rat heart perfused at physiologic Ca2+ concentration and suggest that the hypertensive rat heart has adapted to compensate for increased basal intracellular Na+ and maintain a normal response to increased heart rate. Our data appear to suggest an ionic contribution to the cardiac hypertrophy of genetic hypertension in the rat.
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PMID:Nuclear magnetic resonance measurement of intracellular sodium in the perfused normotensive and spontaneously hypertensive rat heart. 806 May 76

Out of all until now discovered natriuretic factors it is still the atrial natriuretic factor (ANF) which is the most significant with its diuretic, natriuretic and vasodilatory effects. Its effect is antagonistic to sodium retention factors. The increase of its levels in arterial hypertension is more of secondary character, but according to some authors the functional deficit of ANF secretion can be applied also primarily in the development and maintenance of high blood pressure. ANF levels represent a good marker of the clinical severeness and are of prognostic value. Increased levels were detected also in cases of renal failure and partially in hepatic cirrhosis. Natriuretic hormone, in comparison to ANF, is a natriuretic and vasoconstrictive substance, the effect of which is based on the mechanism of sodium pump inhibition. Chemically the main candidate is represented by endogenous ouabain, or a digitalis-like activity. It increases physiologically due to the expansion of extracellular fluid during gravidity and in newborn. Its pathological increase is brought about by some forms of essential hypertension and in the diseases associated with fluid retention and edema development. Cirrhosis of the liver can reflect both the degree of sodium retention and haemodilution, as well as the severeness of hepatic lesion. (Tab. 2, Ref. 30.).
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PMID:[The clinical significance of natriuretic hormones]. 862 37

Human essential hypertension is a polygenic disease whose phenotypic expression is modulated by the environment. Though the kidney could play a major role in the initiation and maintainment of hypertension, many questions remain open. Rat models of primary hypertension provided the substantial information with experiments on kidney cross-transplantation, showing that at least a portion of hypertension could be transplanted with the kidney in all strains where such an experiment has been carried out. Data consistent with those of rats have also been obtained in humans. Many abnormalities in kidney function and cell membrane ion transport have been described in hypertensive rats and humans, but the logical sequence of events from a genetic-molecular abnormality to a cellular abnormality which causes hypertension via a modification of kidney function is difficult to prove. We established this sequence in Milan hypertensive rats using a variety of experimental techniques such as the study of isolated kidney and renal cell function, cell membrane ion transport, cross-immunisation with membrane proteins, molecular biology, genetic crosses and manipulation. Such study led to the identification of a polymorphism in the cytoskeletal protein adducin. Recently, alpha-adducin variants have been associated to both primary hypertension and salt sensitive hypertension. Finally, recent findings strongly support the hypothesis that adducin variants may affect kidney function by modulating the overall capacity of the tubular epithelial cells to transport ions through both a modification in the assembly of actin cytoskeleton, and a modulation of sodium pump activity.
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PMID:Genetic determinants and renal mechanisms in essential hypertension. 900 89

Looking for causes or consequences of primary hypertension much attention is drawn to the ion transport systems of the cellular membrane. The existence of endogeneous digitalis-like factors, that lower the activity of Na+/K(+)-ATPase and result in a complex change of electrolyte balance of cells are discussed as a reaction of the organism to salt and volume retention. The measurement of passive permeability of erythrocyte membranes for potassium is an easy and useful method for the detection of disturbances of Na+/K(+)-transport, especially for extensive screening investigations. We examined the potassium permeability of erythrocytes in healthy individuals (GR1, n = 48), patients with compensated renal insufficiency (GR2, n = 36) and diabetics (GR3, n = 25) as well as a group of diabetics with renal failure (GR4, n = 47). The relative change of potassium concentration in the whole blood, based on the efflux of potassium during a 4-hour-incubation at 37 degrees C, is defined as a measure for K(+)-permeability. K(+)-concentrations are determined every 60 minutes with ion sensitive electrodes. K(+)-permeability was significantly increased in patients with compensated renal insufficiency compared to the control group and to diabetics. Diabetics differed markedly in their erythrocyte reaction regarding K(+)-permeability. Whereas patients with renal insufficiency show an efflux of potassium during investigation there is a decrease of potassium in plasma in diabetics. The K(+)-permeability results of patients with both diseases are intermediate between the GR2- and GR3 results and are significantly different from the control group. When g-strophanthin is added to inhibit the sodium pump, the differences between the groups are abolished. The decreased K+permeability in diabetics compared to the control group could be explained by the increased supply of energy-rich substrates for the Na+/K(+)-ATPase.
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PMID:K(+)-permeability in diabetics and nondiabetics with and without renal insufficiency. 928 37


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