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

Leucocyte sodium efflux and sodium content were studied in 41 insulin treated diabetic patients and compared to 41 age, body mass index and blood pressure matched nondiabetic control subjects. Fasting leucocyte 22Na ouabain-sensitive efflux rate constants were lower in diabetic patients (median [range] 2.30 [1.04-3.73] versus 2.45 [1.57-3.95] h-1, p less than 0.4) suggesting a reduced sodium pump activity. The 22Na ouabain-insensitive efflux rate constant which reflects passive sodium efflux was raised in insulin treated diabetes (0.92 [0.42-1.73] versus 0.79 [0.28-1.49] h-1, p less than 0.01). Leucocyte sodium content was raised in the diabetic patients (47.7 [26.9-93.4] versus 26.5 [15.9-67.7] mmol/kg, p less than 0.0001). Abnormal cellular sodium handling could lead to hypertension or other complications in diabetes.
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PMID:Leucocyte sodium efflux and electrolyte content in insulin treated diabetes. 323 36

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

The effects of changing sodium balance on blood pressure (BP) and erythrocyte sodium transport were investigated in normotensive first-degree relatives of hypertensive patients and control subjects randomised to receive low and high salt diets for two weeks, separated by a two week washout period. Changing from high to low salt intake produced a significant fall in standing diastolic pressure (DBP) in control subjects but not in the offspring of hypertensive patients. In both groups erythrocyte sodium efflux was not changed significantly by either manoeuvre, but the relatives had a significantly higher ouabain insensitive sodium efflux rate constant on both the low and the high salt diet compared to the controls (P less than 0.05). These results are not in keeping with the hypothesis which suggests the release of a humoral sodium pump inhibitor in response to sodium loading but lend support to the view that there is a disturbance of membrane permeability to sodium in subjects genetically prone to hypertension.
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PMID:Effects of manipulation of sodium balance on erythrocyte sodium transport. 333 21

Selective sodium loading attenuated the development of hypertension in the deoxycorticosterone acetate (DOCA) treated rat. The DOCA treated rat fed a diet equimolar in sodium to a 7% sodium chloride diet and in chloride to a standard diet, differed in various parameters from the DOCA treated rat fed a 7% sodium chloride diet: it had higher sodium concentration in both erythrocytes and muscles, a higher erythrocyte ouabain sensitive 22Na efflux rate constant (Kos), and a lower norepinephrine turnover rate in the heart and the spleen. These results suggest that the suppressed sympathetic nervous system activity and the activated cell membrane sodium pump contribute in part to the mechanism for the suppression of the development of hypertension in the DOCA-selective sodium loaded rat.
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PMID:The role of chloride on deoxycorticosterone acetate-salt hypertension. 343 Jun 90

The incidence of hypertension in the geriatric population is very high and is a significant determinant of cardiovascular risk in this group. The tendency for blood pressure to increase with age in westernized societies such as the United States may depend on environmental factors such as diet, stress, and inactivity. Our population tends to become more obese; to consume relatively greater amounts of sodium and lesser amounts of potassium, calcium, and magnesium; and to decrease exercising with increasing age. Senescent changes in the cardiovascular system leading to decreased vascular compliance and decreased baroreceptor sensitivity contribute not only to rising blood pressure but also to an impairment of postural reflexes and orthostatic hypotension. The hallmark of hypertension in the elderly is increased vascular resistance. Greater vascular reactivity in the elderly hypertensive patients may reflect decreased membrane sodium pump activity and decreased beta-adrenergic receptor activity as well as age-related structural changes. Treatment of diastolic hypertension in the elderly is associated with decreased cardiovascular morbidity and mortality. Although treatment of systolic hypertension may not decrease immediate cardiovascular mortality, it appears to decrease the incidence of stroke. The initial therapeutic approach to the elderly hypertensive patient should generally consist of a reduction in salt and caloric intake and an increase in aerobic exercise, i.e., walking. Drug therapy should be initiated with lower doses of medication with a special concern about orthostatic hypotension.
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PMID:Hypertension in the elderly. 354 29

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

This study investigated the effect of sodium pump activity on vascular smooth muscle responsiveness to norepinephrine (NE) in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Dose-response curves to NE were generated in normal (5.9 mM), high (10 mM) or 0 mM potassium (K) Krebs physiological solution. Inhibition of the sodium pump (0 mM K) in femoral arterial smooth muscle from control rats resulted in an increased response to NE which was similar to the DOCA-salt rat, while increasing sodium pump activity (10 mM K) in femoral arterial smooth muscle from DOCA-salt rats resulted in a decreased response which was similar to controls. These results show that altering sodium pump activity in vitro by changing extracellular K concentration can affect femoral arterial smooth muscle responsiveness to NE in both control and DOCA-salt rats. Alterations in sodium pump activity observed in vascular smooth muscle from DOCA-salt hypertensive rats may contribute to the increased NE responsiveness and increased vascular resistance seen in this model of hypertension.
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PMID:Sodium pump activity and norepinephrine responsiveness of femoral arterial smooth muscle from DOCA-salt rats. 358 54

Erythrocyte cation transport was measured in vitro using 22Na+ and 86Rb+ uptake techniques in Caucasian men with newly-detected hypertension and in male control groups. The Na+, K+ cotransport [determined by ouabain-resistant frusemide-sensitive (ORFS) components of Na+ or Rb+ influx], sodium pump activity (determined by ouabain-sensitive Rb+ influx) and erythrocyte Na+ and K+ concentrations were not significantly altered in hypertensive men. The total Na+ influx in hypertensives (n = 59) was significantly greater (P less than 0.001) than in controls. The difference was mainly attributable to an increase in the ouabain-resistant frusemide-resistant component of this flux. The total Rb+ influx in hypertensives (n = 39) was also greater (P less than 0.005) than in controls. Overall, both total Na+ influx and total Rb+ influx were positively correlated (P less than 0.01) with diastolic blood pressure and with habitual dietary intake of alcohol. Multivariate analyses after controlling for the effect of blood pressure showed that mean corpuscular volume (MCV) and alcohol intake were statistically significant predictor variables for total Rb+ influx, although not for total Na+ influx. The results are compatible with increased diffusion of cations across the erythrocyte membrane in hypertension, but raise the question of a possible role of alcohol intake in mediating this effect.
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PMID:Erythrocyte cation fluxes in the normotensive and hypertensive clients of a health screening clinic. 361 77

To investigate the effects of changes in sodium balance on blood pressure and leucocyte sodium transport, normotensive first-degree relatives of hypertensive patients and control subjects were randomized to receive low- and high-salt diets for 2 weeks, separated by a wash-out period of 2 weeks. High-salt intake failed to alter blood pressure, whereas the low-salt diet produced significant falls in standing pressures in both groups. In the control subjects leucocyte sodium efflux was not changed by either manoeuvre, but in the relatives low-salt diet stimulated ouabain-insensitive sodium efflux rate constant. There was a significant qualitative difference in the pattern of response of total efflux rate constant to the two dietary periods between the two groups of subjects. These data are not compatible with the release of a humoral sodium pump inhibitor in response to sodium-induced volume expansion, and lend support to a disturbance of membrane permeability to sodium in subjects genetically prone to hypertension.
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PMID:Effects of changes in sodium balance on leucocyte sodium transport: qualitative differences in normotensive offspring of hypertensives and matched controls. 373 50


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