Effect of sodium depletion on plasma renin concentration before and during adrenergic beta-receptor blockade with propranolol in normotensive man.
Plasma renin levels have been used to discriminate between different forms of hypertension, but how to define the normal range of plasma renin levels has not been agreed upon. Sodium depletion stimulates renin release. Evaluation of plasma renin would, therefore seem possible only in relation to sodium balance. Plasma renin concentration and concurrent daily sodium excretion were determined in 33 healthy normotensive subjects (control group) ingesting high, normal and low sodium diets. A well-defined hyperbolic relationship was found between the two variables indicating that the physiologic level of plasma renin concentration depends on the state of sodium balance. An increase in plasma potassium concentration may reduce plasma renin concentration, but this appeared to be overruled by the stimulating effect of sodium depletion. To examine whether beta-adrenergic stimulation contributes to the increase in plasma renin concentration during sodium depletion, the relationship between plasma renin concentration and concurrent sodium excretion was studied during beta-receptor blockade with propranolol. In 20 healthy normotensive subjects in whom beta-receptor blockade was verified by a significant reduction in pulse rate, the same hyperbolic relationship was found between plasma renin concentration and sodium excretion as in the control group showing that sodium depletion stimulates renin release independent of sympathetic nervous activity.
D000319:Adrenergic beta-Antagonists; D000328:Adult; D004032:Diet; D005260:Female; D006801:Humans; D008297:Male; D011188:Potassium / Q000097:blood / Q000652:urine; D011433:Propranolol / Q000494:pharmacology*; D012083:Renin / Q000097:blood*; D012964:Sodium / Q000494:pharmacology* / Q000652:urine; D013268:Stimulation, Chemical
D000319:Adrenergic beta-Antagonists; D012964:Sodium; D011433:Propranolol; D012083:Renin; D011188:Potassium