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

Vascular smooth muscle is activated through 2 major systems. One, which can be inhibited by calcium-entry blocking agents, involves the influx of calcium through potential-sensitive channels. The other, which can be inhibited by sodium nitroprusside, involves the entry of calcium through agonist-controlled channels and probably its mobilization from within the cell as well. Human veins, muscular arteries and resistance vessels show differing patterns of response to agents that selectively inhibit the 2 activation systems. The responses indicate that physiologic contractions of cutaneous veins and muscular arteries depend on the agonist-controlled system; contractions of veins induced by high concentrations of potassium depend on the potential-sensitive system as, probably, does local spasm in arteries. The tone of resistance vessels depends on a balance between the potential-sensitive and agonist-controlled systems. The forearm resistance vessels of men with primary hypertension respond to verapamil with larger-than-normal dilatation compared with that induced by nitroprusside. This is interpreted as showing an increased contribution to resistance vessel tone from the potential-sensitive system. This functional abnormality does not depend on the inhibition of sodium pump activity that is known to occur in hypertension, because it cannot be reproduced by local infusion of ouabain. It probably results from a primary disorder of calcium handling by the cell membrane.
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PMID:Functional differences in blood vessels determined from studies with calcium-channel blockers. Functional changes in forearm resistance vessels of men with primary hypertension. 396 57

Intracellular cation concentrations (Nai, Ki), and the influx of Rb86 and of Na22 were measured in the erythrocytes of 22 normal women with no family history of hypertension, 16 women with untreated essential hypertension, and 14 normotensive women treated with hormonal contraceptives. Values for total Rb influx, and for its components denoting sodium pump activity (ouabain-sensitive) and Na, K co-transport (ouabain-resistant, frusemide-sensitive), were significantly greater in the hypertensive and contraceptive-treated groups than in the normal group. Na, K cotransport measured by Na influx (frusemide-sensitive) was found to be significantly increased in the contraceptive-treated but not the hypertensive group. Passive sodium diffusion (frusemide-resistant Na influx) and Ki did not differ significantly between groups. Nai was lower in the hypertensive group than in the other two groups. These findings support the hypothesis that hypertension or hormonal contraception are associated with increased leakage of K ions from erythrocytes, without a corresponding increase in passive Na influx: the change in cell membrane permeability is compensated for by increases in Na, K co-transport and sodium pump activity, adjusted to allow for altered differential permeability to K and Na ions.
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PMID:Altered erythrocyte cation transport related to hypertension or oral contraception. 399 41

Previous investigations have demonstrated an increased amount of a sodium pump inhibitor (N.H.) in plasma from humans with essential hypertension and from animals with various forms of experimental hypertension. The present study has employed Sephadex column and C18 reverse phase separation of urines from patients with essential hypertension and normal controls to distinguish "high", "intermediate" and "low" molecular weight forms of N.H., measured through properties of Na-K-ATPase inhibition and digoxin-like immunoreactivity. The major difference between hypertensive and normotensive urines was a highly significant increase in the "intermediate" molecular weight form of N.H., as measured by Na-K-ATPase inhibition. In contrast, digoxin-like immunoreactivity was significantly decreased in urine from hypertensive patients. The results are compatible with an hypothesis that the defect in some forms of essential hypertension may be partial inhibition of enzymatic conversion of intermediate to final form of N.H., with the increased sodium pump inhibition primarily related to the precursor.
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PMID:Observations on the "cascade" of Na-K-ATPase inhibitory and digoxin-like immunoreactive material in human urine: possible relevance to essential hypertension. 401 67

We determined the sodium pump activity, measured as ouabain-sensitive 86Rb+ uptake, in the tail arteries of rats treated with deoxycorticosterone and sodium chloride for 6, 9, 14, 28, and 50 days. Systolic blood pressures, plasma sodium, potassium, and creatinine concentrations were measured, and the body weights were recorded. Vascular sodium pump activity was suppressed (by 27%) at the 6th day of deoxycorticosterone and sodium chloride treatment, a prehypertensive state. By the 9th day, blood pressure of deoxycorticosterone-treated and sodium chloride rats had increased, but sodium pump activity was not different from that of control animals. However, increases in sodium pump activity were noted after 14 and 28 days of deoxycorticosterone and sodium chloride treatment (18 and 21%, respectively). By 28 days, a fully developed hypertension was noted. At 50 days, rats displayed lower vascular sodium pump activity (by 23%) than the controls. These rats, although hypertensive, had significantly lower systolic blood pressures than the rats treated for 28 days. They had high plasma creatinine levels, low potassium and sodium concentrations, and low body weights compared to the controls, suggesting the presence of a malignant state. Our data indicate that there are time-related changes in the vascular sodium pump activity with this type of hypertension.
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PMID:Phasic vascular sodium pump changes in deoxycorticosterone-hypertensive rats. 608 15

Sodium efflux rates were measured in leucocytes from eighteen normotensive subjects who had one or more first-degree relatives with essential hypertension and from twenty-four matched controls with no such family history. The total efflux rate constant was significantly lower in those with a family history of hypertension, owing to reduced ouabain-sensitive sodium pump activity. The presence of a membrane electrolyte handling abnormality characteristic of essential hypertension in normotensive individuals genetically predisposed to hypertension points to an underlying genetic factor. At the same time, the fact that blood-pressure was normal in these subjects indicates that the abnormality does not participate directly in blood-pressure elevation. Rather, the abnormality, like other red-cell changes in electrolyte handling, seems to be a marker for a genetically determined alteration in membrane structure, and thus only indirectly related to hypertension.
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PMID:Leucocyte membrane sodium transport in normotensive populations: dissociation of abnormalities of sodium efflux from raised blood-pressure. 612 51

The presence in plasma extracts of a sodium pump inhibitor with digitalis-like properties was investigated by two complementary tests: decrease in the affinity of ouabain binding to human red blood cells and inhibition of Na+,K+-ATPase. The results of the two methods were correlated (r = 0.76, n = 44, p less than 0.01), suggesting that the same factor may be responsible for both effects. All subjects with elevated values were hypertensive or normotensive and had a family history of hypertension. Forty percent of the subjects in these two groups had high inhibition values. The elevation was significant (p less than 0.01) when compared with values in normotensive subjects with no hypertensive heredity. Increased inhibition was observed in patients taking beta-blocking agents; conversely, diuretics normalized the values. No correlation was found between pump inhibition and age, sex, blood pressure, levels of plasma K+ or Na+, or plasma renin activity. These data show the existence of a sodium pump inhibitor in the plasma of some subjects and point to a possible association with hypertension. They also underline the importance of genetic background and the heterogeneity of essential hypertension.
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PMID:Plasma sodium pump inhibitor in essential hypertension and normotensive subjects with hypertensive heredity. 620 59

This study was designed to characterize potassium-induced relaxation in vascular smooth muscle during the development of deoxycorticosterone acetate (DOCA) hypertension. Pigs were implanted subcutaneously with 100 mg/kg DOCA. Mean arterial pressure in the DOCA-treated pigs reached levels approximately 37% greater than controls. In some pigs, the left hindlimb vascular bed was "protected" from the rise in arterial pressure by ligation of the iliac artery. Arterial strips from DOCA hypertensive and normotensive pigs relaxed in response to potassium after contraction induced by norepinephrine in potassium-free solution. Arterial strips from DOCA hypertensive pigs showed greater relaxation than did those from normotensive pigs. The magnitude of relaxation in femoral arteries from "protected" hindlimbs was similar to that in arteries from the contralateral unoccluded limb. Potassium-induced relaxation in tail arteries from DOCA hypertensive pigs was more sensitive to ouabain inhibition than that from normotensive pigs. Relaxation induced by potassium varied with: 1) length of incubation in potassium-free solution; 2) concentration of added potassium; and 3) concentration of norepinephrine added during the potassium-free interval. The amplitude of potassium-induced relaxation is believed to be a functional index of the activity of the electrogenic sodium-potassium transport system. These experiments support the hypothesis that vascular smooth muscle from DOCA hypertensive animals has increased electrogenic sodium pump activity. The development of this vascular change parallels the increase in blood pressure induced by mineralocorticoid excess.
Hypertension
PMID:Potassium relaxation of vascular smooth muscle from DOCA hypertensive pigs. 628 78

Recent studies suggest that sodium-dependent low-renin hypertension in animals results at least in part from sodium-potassium pump inhibition in blood vessels and heart by a humoral agent released from or influenced by the anteroventral third ventricular area of the brain. For example, a high salt intake in a rat with reduced renal mass results in the appearance of a heat-stable sodium pump inhibitor in the plasma, decreased cardiac Na+, K+-ATPase activity, decreased arterial sodium-potassium pump activity, and hypertension. These changes are reversed by reducing the salt intake or by producing a lesion in the anteroventral third ventricular area of the brain. The course of the development of pump inhibition is similar to the course of the development of hypertension. Sodium-potassium pump inhibition by a humoral agent may also occur in humans with low-renin hypertension. A high potassium intake may stimulate pump activity.
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PMID:Sodium-potassium pump in low-renin hypertension. 630 76

A digitalis-like compound was detected in human plasma by tritiated ouabain competition binding to the sodium pump. The study comprised analyses of plasma extracts from 17 normal controls, 17 normotensive subjects with one or both parents hypertensive, and 16 patients with untreated essential hypertension. In two thirds of the untreated hypertensive and several of the normotensive subjects with a family history of hypertension the potency of the digitalis-like compound, as measured by its interference with ouabain binding, was significantly greater than in the controls. In the untreated hypertensive patients the potency of the compound was significantly correlated with the urinary sodium output. Measurement of this salt-related, digitalis-like compound may be useful in clinical studies of hypertension.
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PMID:Measurement of digitalis-like compound in plasma: application in studies of essential hypertension. 630 18

Acute subcutaneous (s.c.) administration of aldosterone increases ex vivo 22Na efflux from rat tail artery smooth muscle, which appears to be due to a specific action on mineralocorticoid receptors. Indeed, this effect is blocked by the antimineralocorticoid compounds RU 28318 [17 beta-hydroxy-3-oxo,7 alpha-propyl(17 alpha)-pregn 4-ene, 21 potassium carboxylate] and spironolactone. The specific glucocorticoid receptor agonist RU 26988 [11 beta,17 beta-dihydroxy-17-(1-propynyl) androesta-1,4,6 trien-3-one] does not modify 22Na efflux. We show here that aldosterone has, at physiological concentrations, a mineralocorticoid specific stimulating effect on passive and sodium pump dependent transmembrane movements of sodium from the rat tail artery smooth muscle. Aldosterone exerts two types of action on sodium transport: 1) a delayed stimulation of ouabain-dependent 22Na efflux and ouabain-independent 22Na efflux, which are completely blocked by actinomycin D; and 2) a very rapid increase of passive 22Na efflux, which is insensitive to actinomycin D and therefore does not seem to depend on transcription of genomic information.
Hypertension
PMID:Direct action of aldosterone on transmembrane 22Na efflux from arterial smooth muscle. Rapid and delayed effects. 632 52


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