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

In the last years a great deal of reports on the presence of endogenous digitalis-like activity in mammals have appeared in the literature. The active factor could be an endogenous ligand of the digitalis receptor and thus a physiological humoral regulator of sodium pump activity. Such an agent would necessary have a whole series of physiological and physiopathological implications. It has been proposed that the factor is a natriuretic hormone, that it participates in blood pressure regulation and in the genesis of arterial hypertension, that it plays a role in pregnancy and that it regulates cardiac contractility. These hypotheses are discussed in the present review.
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PMID:[The evidence for the existence of an endogenous factor with digitalis activity in mammals: a physiological regulator of the sodium pump?]. 166 31

The activity and properties of Na,K-ATPase in erythrocytes and their membrane preparations (ghosts) from 34 subjects with borderline hypertension and 21 normotensive controls were studied. The Na,K-ATPase activity was found to be by 43% lower as compared to control group. No changes in the Na,K-ATPase activity were revealed in the ghosts of borderline subjects. This suggests that the plasma of borderline subjects contains an inhibitor of Na,K-ATPase. The plasma level of sodium pump inhibitor was measured in 21 borderline hypertensive subjects. It was found to be about 19% compared with the control group. These findings suggest presence of Na,K-ATPase inhibitor in the plasma of borderline subjects, which is likely to be involved in the development of hypertension.
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PMID:[The activity and properties of Na,K-ATPase in the erythrocytes and the Na-pump inhibitor in the plasma of subjects with borderline arterial hypertension]. 166 9

The effect of chronic alcohol administration on blood pressure was investigated in 7-week-old Wistar rats. Tail-cuff blood pressure was significantly higher in rats who received 15% ethanol in drinking water than in control rats. Intracellular free calcium concentration of lymphocytes was increased, while magnesium concentration of erythrocyte, aorta, and skeletal muscle and erythrocyte ouabain-sensitive 22Na efflux rate constant (Kos) were decreased in alcohol-induced hypertensive rats but not in control rats. Extracellular fluid volume was also increased in alcohol-administered rats. Oral magnesium supplementation (1% MgO in rat chow) attenuated the development of alcohol-induced hypertension accompanied by increased magnesium concentration of erythrocyte, aorta, skeletal muscle, and Kos and decreased intraerythrocyte sodium concentration. Norepinephrine half-life time of the heart and spleen was also increased in magnesium-supplemented rats. Blood pressure significantly correlated positively with intracellular calcium concentration and extracellular fluid volume, negatively with magnesium concentration of erythrocyte, aorta, skeletal muscle, and Kos. These results suggest that increased intracellular calcium, which was partly due to magnesium depletion and suppressed sodium pump activity, and expanded body fluid volume had a possible role in the development of alcohol-induced hypertension. It is also suggested that oral magnesium supplementation had a hypotensive effect on alcohol-induced hypertension possibly through decreased intracellular sodium concentration caused by an activation of sodium pump and decreased sympathetic nervous activity.
Hypertension 1992 Feb
PMID:Magnesium supplementation prevents the development of alcohol-induced hypertension. 173 52

An endogenous ouabain-like sodium pump inhibitor was demonstrated originally in serum or plasma of acutely extracellular fluid volume (ECFV) expanded animals and humans. Since then numerous studies have confirmed the presence of ouabain-like factor(s) (OLF) in blood, urine, cerebrospinal fluid, and various tissues including the heart and hypothalamus. Some of these OLFs represent well-known endogenous compounds, eg, free unsaturated fatty acids, which in vitro exhibit inhibition of transepithelial sodium transport, direct inhibition of the Na-K-ATPase enzyme, displacement of 3H-ouabain from its membrane receptor, and crossreaction with a digoxin antibody. Small molecular weight (MW) OLFs of yet unknown peptidic or nonpeptidic nature, which may be of hypothalamic origin, were also detected in various animal models of hypertension and in hypertensive patients. They may play a pathophysiological role especially in salt- and volume-dependent forms of hypertension. Our results show that OLFs increase basal and vasopressin-stimulated intracellular Ca2+ release in rat vascular smooth muscle cells in culture and in human platelets similar to the newly discovered endothelin. In addition, a natriuretic factor (natriuretic hormone) was detected by bioassay in plasma and urine, whose activity changes in parallel with sodium intake. We found that this natriuretic factor is associated with small peptides with a MW of less than 1,000. It is, however, unlikely that the two biological properties, ie, the ouabain-like and natriuretic activities, reside in a single compound. A number of circulating OLFs is certainly not identical with a humoral natriuretic factor. Nevertheless, there is increasing evidence for multiple interactions between OLF and the atrial natriuretic peptide (ANP).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endogenous natriuretic and ouabain-like factors. Their roles in body fluid volume and blood pressure regulation. 184 64

Several investigators have demonstrated the antihypertensive properties of potassium in various models of hypertension. The present studies were conducted to determine whether central mechanisms contribute to these salutary effects of potassium. In Inactin-anaesthetized rats, intracerebroventricular administration of KCl solutions (0.375, 0.75 and 1.25 mumol/5 microliters) produced concentration-dependent reductions in arterial pressure and heart rate. These effects were significantly attenuated by prior central administration of ouabain, a selective inhibitor of the sodium pump. In a separate series of experiments, prior central administration of alpha 1- and alpha 2-antagonist phentolamine, or the dopamine receptor (DA1 and DA2) antagonist RS-sulpiride, was also effective in inhibiting the hypotensive and bradycardiac effects of intracerebroventricular administration of potassium. Thus, these data suggest that activation of Na+,K(+)-ATPase and central noradrenergic and dopaminergic mechanisms are involved in the central actions of potassium and these central mechanisms may contribute to the salutary effects of a potassium-rich diet in hypertensive subjects. The present studies demonstrate a potentially important relationship between Na+,K(+)-ATPase activity in the central nervous system and neural regulation of arterial blood pressure.
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PMID:Role of Na+,K(+)-ATPase in the centrally mediated hypotensive effects of potassium in anaesthetized rats. 184 33

This review first summarizes evidence from animals and humans for and against a role for dietary sodium in the genesis and treatment of hypertension. The evidence for its role is strongest in those subjects with impaired ability to excrete sodium because of organic renal disease or mineralocorticoid excess. Here, restriction of dietary sodium promptly lowers pressure. Its role in the genesis of essential hypertension is more controversial. Nevertheless, it appears that some patients with mild to moderate essential hypertension respond to moderate sodium restriction with a modest fall in pressure. This restriction also seems to reduce the amount of antihypertensive medication needed to keep pressure under control. Next, the mechanism of the pressure response to dietary sodium chloride is considered, with emphasis on potassium depletion and increased plasma levels of prohypertensive sodium pump inhibitor and antihypertensive atrial natriuretic peptide. The evidence for a primary role for dietary potassium in the genesis of hypertension then is summarized; certain subsets of subjects with a high incidence of hypertension also have a lower potassium intake. Some investigators have found that dietary potassium supplementation lowers pressure in established hypertension. This may result from natriuresis and from vasodilation subsequent to stimulation of Na+,K(+)-ATPase in vascular smooth muscle and adrenergic nerve terminals. After the role of dietary calcium is discussed, practical aspects of dietary sodium restriction and dietary potassium supplementation in the therapy for established hypertension are considered. The review concludes with comments on their possible roles in the prevention of hypertension.
Hypertension 1991 Nov
PMID:Roles of sodium, potassium, calcium, and natriuretic factors in hypertension. 193 82

The alteration of sodium ion transport in red blood cells was observed in SHR and patients with essential hypertension. The purpose of the present study was to determine the effects of dietary calcium intake on blood pressure and sodium ion transport of red blood cells in SHR. The SHR were fed a diet with three different levels of calcium contents as follows: 0.1% (low), 0.6% (normal) and 4.0% (high) of calcium between 6 and 20 weeks of age. At 20 weeks of age, the levels of erythrocyte sodium efflux, sodium or potassium contents in the red blood cells were measured. On the high Ca diet, SHR showed an attenuation of the increase in blood pressure. On the low Ca diet, SHR showed an enhancement of hypertension. In proportion of increasing of dietary calcium contents, SHR had a lower level of sodium content in the RBC and a higher activity of the sodium pump. However, the passive sodium permeability and sodium-potassium cotransport in SHR were similar among the three different Ca diets. It is concluded that the amounts of dietary Ca might be related to the regulation of blood pressure by changing the sodium pump of the cell membrane in SHR.
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PMID:Effects of dietary calcium on erythrocyte sodium ion transport systems in spontaneously hypertensive rats. 195 55

Endogenous factors with biological and immunological activity similar to cardiac glycoside drugs (endogenous digitalis-like factors; EDLF) have been found in several tissues and body fluids of animals and humans. Detectable EDLF concentrations were found in blood and urine extracts of adults (normal healthy controls, hypertensive patients and salt-loaded healthy subjects), while higher levels were generally observed in plasma samples of pregnant women, newborns, and patients with renal insufficiency. The chemical characteristics of this endogenous factor are, at present, unknown, although it has been suggested that EDLF could be a substance with low molecular weight. Experimental studies and theoretical considerations suggest that EDLF, in addition to the ability to react with antibodies, might also bind to the specific cellular receptor of the cardiac glycosides and thus inhibit the membrane Na+/K(+)-ATPase (sodium pump). Therefore, it has been suggested that EDLF is an endogenous modulator of the membrane sodium-potassium pump, and that it could play a role in the regulation of fluids and electrolytes, in the myocardial muscular tone and also in the pathogenesis of hypertension.
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PMID:Endogenous digitalis-like factors: their possible pathophysiological implications with particular regard to the perinatal period. 196 38

Inhibition of active sodium transport by ouabain was found to cause concentration- and time-dependent impairment of acetylcholine-induced relaxation in human resistance arteries with a significant effect at 100 pM. The reduced acetylcholine response was attributable to inhibition of the NG-monomethyl L-arginine-sensitive but not the indomethacin-sensitive component of relaxation. Relaxation by sodium nitroprusside was not affected by ouabain, suggesting that inhibition of sodium transport, directly or indirectly, must affect synthesis or release of endothelium-derived relaxing factor rather than its effector pathway. These results do not support the existence of an additional endothelium-derived relaxing factor other than endothelium-derived relaxing factor, which is dependent on sodium pump activity. The finding that inhibition of sodium transport has a profound effect on vascular relaxation may have implications in the pathogenesis of certain forms of hypertension.
Hypertension 1991 May
PMID:Effect of ouabain on endothelium-dependent relaxation of human resistance arteries. 202 6

The defect of the sodium pump of the blood cell membrane in patients with essential blood hypertension, can induce changes in the metabolic use of ATP, especially at glucolytic pathway level. We studied the blood levels of ATP (32.51 +/- 10.80 mg/100 ml), 2,3-DPG (0.82 +/- 0.47 mumol/ml), piruvate (0.36 +/- 0.16 mg/100 ml) and lactate (18.88 +/- 4.53 mg/dl), of a group of 50 patients with essential blood hypertension and of 50 healthy persons in the control group (17.09 +/- 6.37 mg/100 ml, 0.45 +/- 0.23 mumol/ml, 0.33 +/- 0.15 mg/100 ml and 17.32 +/- 3.85 mg/dl respectively). There were statistically significant differences between ATP (p less than 0.0005) levels and 2,3-DPG and lactate (p less than 0.05). These results force us to study the presence of those changes on peripheral tissues to see whether they play an important role in hypertension complications, especially in respect of the vascular wall.
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PMID:[Changes in the glycolytic pathway in patients with essential arterial hypertension]. 210 17


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