Potassium restriction, high protein intake, and metabolic acidosis increase expression of the glutamine transporter SNAT3 (Slc38a3) in mouse kidney.
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Effect of potassium intake on blood pressure.
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Epidemiologic, experimental, and clinical studies suggest that potassium is an important regulator of blood pressure. Surveys conducted in widely divergent geographic locations indicate higher prevalence of hypertension in populations ingesting diets low in potassium. Amelioration of hypokalemia lowers blood pressure in mineralocorticoid-induced hypertension in rats and in essential hypertensive patients receiving thiazide diuretics. We observed that in normotensive subjects ingesting normal amounts of sodium, short-term potassium depletion increases the mean arterial pressure from 90.9 +/- 2.2 mm Hg to 95.0 +/- 2.2 mm Hg (P less than 0.01). Furthermore, acute sodium loading increases blood pressure in potassium-depleted subjects but it had no effect in subjects ingesting normal amounts of potassium. Preliminary studies indicate that short-term potassium depletion also elevates blood pressure in hypertensive patients. Potassium supplementation lowers blood pressure in hypertensive patients ingesting normal amounts of sodium. Blacks appear to be more sensitive to the hypotensive effects of potassium. The mechanism of potassium-induced changes in blood pressure is not well understood. Potassium depletion consistently induces sodium retention. The hypertensive effects of potassium depletion and hypotensive effects of potassium supplementation are not observed when sodium intake is kept low. Direct vasoconstrictive effects of hypokalemia may contribute to the pressor effect of potassium depletion. The role of altered vascular sensitivity to vasoactive hormones and alterations in divalent cation metabolism in mediating the potassium-induced changes in blood pressure require further study. (+info)
Factors influencing the increase in Na-K-ATPase in compensatory renal hypertrophy.
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An increase in Na-K-ATPase in kidney homogenates usually accompanies compensatory renal hypertrophy. While it may be evident in both the cortex and medulla of the kidney, it is most marked in the outer medulla and may be present only in that region. The increase in enzyme activity does not depend on an intact adrenal cortex and can be elicited in the absence of adrenal glucocorticoids. It is not seen in the form of renal hypertrophy produced by potassium depletion, in which the transport of sodium and potassium by the kidney is not increased. When present in compensatory renal growth, the enzyme change is correlated with an increase in the reabsorption of sodium, or the excretion of potassium, or both, per unit of renal tissue. It proceeds in the presence of either, but not in the absence of both. (+info)
Dietary intake and nutritional deficiencies in patients with diabetic or idiopathic gastroparesis.
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