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

Sodium-lithium countertransport is believed to depend on a specific protein and since such proteins usually decline with erythrocyte age it would be expected to be reduced in older cells. In fact, sodium-lithium countertransport increased with ageing, whereas the rate constant of the sodium pump decreased. The increase in sodium-lithium countertransport with erythrocyte ageing was due to a phloretin insensitive component that was not present in young erythrocytes. Raised sodium-lithium countertransport in patients with essential hypertension was due mainly to an increased phloretin sensitive component but the phloretin insensitive component was also higher in middle aged erythrocytes. Amiloride had no effect upon sodium-lithium countertransport or unidirectional sodium influx in cells of any age. This suggests that sodium-lithium countertransport is not a mode of action of the sodium-proton exchanger in the erythrocyte.
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PMID:Sodium-lithium countertransport activity and its sensitivity to inhibitors with erythrocyte ageing in man. 322 83

In this review, we first summarized the evidence from animals and man for and against a role for dietary sodium in the genesis and treatment of hypertension. The evidence for a role for dietary sodium in the genesis of hypertension is strongest in those subjects with impaired ability to excrete sodium due to organic renal disease or mineralocorticoid excess. Here restriction of dietary sodium promptly lowers arterial pressure. Its role in the genesis of essential hypertension is still controversial. Nevertheless, it appears that some patients with mild to moderate essential hypertension respond to moderate sodium restriction with a modest fall in blood pressure. This restriction also seems to reduce the amount of antihypertensive medication needed to keep blood pressure under control. We next considered the mechanism of the pressure response to dietary sodium chloride, concentrating upon the increase in extracellular fluid volume, potassium depletion, and increased plasma levels of prohypertensive sodium pump inhibitor and antihypertensive atrial natriuretic factor. We next summarized the evidence for a primary role for dietary potassium in the genesis of hypertension and pointed out that certain subsets of subjects with a high incidence of hypertension also have a lower dietary potassium intake. Some investigators find that dietary potassium supplementation lowers blood 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. We then considered practical aspects of dietary sodium restriction and dietary potassium supplementation in the therapy for established hypertension. The review concludes with comments on their possible roles in the prevention of hypertension.
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PMID:Dietary sodium and potassium in the genesis, therapy, and prevention of hypertension. 329 78

Lymphocyte sodium content and sodium efflux were studied in 9 healthy normotensive males without history of essential hypertension before, during and after 5 weeks of severe sodium depletion. Sodium depletion caused a significant increase in sodium content and a slight but non-significant decrease in potassium content. Total and ouabain-sensitive sodium efflux rate constants decreased significantly during sodium depletion, while absolute sodium efflux, derived from cellular sodium concentration and the corresponding sodium efflux rate constants, remained unchanged. A significant reduction in arterial mean and diastolic blood pressure, measured by ambulatory as well as by home readings, was observed during salt restriction. Prolonged severe sodium depletion of normotensive subjects leads to changes in lymphocytic sodium homeostasis, probably due to a primary inhibition of the sodium pump and a secondary intralymphocytic sodium accumulation. The mechanism underlying these changes remains unclarified.
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PMID:Cell membrane handling of sodium in lymphocytes during salt restriction in normotensives. 343 3

Although there is much circumstantial and some direct clinical evidence suggesting that a high consumption of salt predisposes patients to the development of essential hypertension, the mechanism by which such consumption causes high blood pressure is not clear. It has been suggested that due to an inherited abnormality in renal sodium excretion, high salt intake triggers an increase in the levels of sodium transport inhibitor. Although this may help to restore sodium balance, it may also increase the concentration of intracellular sodium in arteriolar smooth muscle and, thereby, stimulate smooth muscle reactivity. It has been shown that intra-arterial infusion of calcium channel blockers into the forearm produces an enhancement of forearm blood flow that is proportional to the degree of hypertension. Other studies have demonstrated a linear relationship between the degree of hypertension and the magnitude of blood pressure reduction following treatment with a calcium channel blocker. These clinical findings, combined with evidence from studies in animals, suggest that a functionally abnormal response of smooth muscle cells to calcium channel blockers occurs as blood pressure increases. Whether this functional abnormality is related to an increased level of intracellular calcium and/or inhibition of the sodium pump is not known. The short-term blood pressure lowering effect of nifedipine appears to be enhanced when sodium intake is increased.
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PMID:Sodium intake, high blood pressure, and calcium channel blockers. 355

To examine the interrelationship of blood pressure, ethnic origin, genetic predisposition to hypertension, and cellular sodium handling, 49 hypertensive and 70 normotensive subjects were studied. Those with a positive family history of essential hypertension were found to have higher intracellular sodium levels and lower ratios of intracellular potassium to sodium than those without, regardless of their blood pressure. Only hypertensive subjects with a positive family history had depressed sodium efflux rate constants. Hypertensive subjects with no family history of essential hypertension had normal intracellular sodium levels and sodium pump activity. Black subjects had significantly higher levels of intracellular sodium than whites, regardless of blood pressure. Black hypertensive subjects had higher plasma sodium and lower plasma potassium concentrations than normotensive subjects did. These results suggest that cellular sodium handling is more closely associated with a genetic predisposition to essential hypertension than to hypertension itself and cast doubt on the significance of abnormalities of cellular sodium handling in the development of essential hypertension.
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PMID:Genetic and ethnic influences on the distribution of sodium and potassium in normotensive and hypertensive subjects. 357 58

Sodium efflux rate constants and intracellular sodium were measured in leucocytes from healthy volunteers in the presence and absence of the calcium antagonist verapamil hydrochloride. Verapamil stimulated sodium pump activity and this effect was dependent on the presence of external calcium. Verapamil has been reported to reverse the abnormality of sodium transport seen in leucocytes from patients with essential hypertension and the present study demonstrates that sodium pump activity in leucocytes from control subjects is also stimulated by exposure to verapamil in vitro. This direct cellular effect appears to be due to the calcium antagonist properties of the drug.
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PMID:Effect of the calcium antagonist verapamil on human leucocyte sodium transport in vitro. 396 68

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

Circumstantial and direct evidence suggests that human plasma contains an inhibitor or inhibitors of sodium transport and that the level of this inhibitor or inhibitors is raised in many patients with essential hypertension. Although considerable work has been carried out, its exact nature and structure are not as yet known. In order to clarify the issue from a biochemical/methodological point of view, an attempt has been made to illustrate the complexity of the sodium pump and the conceptual and technical problems associated with the identification and measurement of this transport inhibitor in plasma.
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PMID:Problems in the identification and measurement of a sodium transport inhibitor in human plasma. 399 33

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


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