Adrenergic receptors and sodium reabsorption in normotensive subjects as related to salt sensitivity.
We have studied proximal tubular sodium reabsorption as measured by lithium clearance, alpha-2 and beta-2 adrenergic receptors on circulating platelets and lymphocytes, respectively, and urinary aldosterone after variations of sodium intake in 24 normotensive volunteers. Fractional lithium clearance was 14.8% +/- 2.64 under a high salt diet of 200 mmol per day. After a low salt diet of 50 mmol/d for two weeks fractional lithium clearance did not change significantly (13.3% +/- 3.35). There were no correlations between alpha-2 adrenergic receptors, beta-2 adrenergic receptors or the alpha-2/beta-2 ratio and fractional lithium clearance, irrespective of the high or low salt diet. In contrast, a significant correlation was found between urinary aldosterone excretion and alpha-2 receptor densities under low salt diet (r = -0.55, n = 17, p less than 0.02). There were no correlations between beta-2 adrenoceptor density, alpha-2/beta-2 ratio and urinary aldosterone during high or low salt diet. Whereas our results are inconclusive about the value of lithium clearance determinations as a measure of proximal tubular sodium reabsorption during variations of sodium intake, we conclude, that alpha-adrenoceptor density, as measured on circulating blood cells, may possibly be representative for alpha-adrenergic equipment of the kidney. The inverse correlation between urinary aldosterone excretion in subjects equilibrated on a low salt diet of 50 mmol/d and alpha-2 adrenoceptor densities could be interpreted as an indirect evidence, that those subjects with a high alpha-2 adrenoceptor equipment show a high proximal tubular sodium reabsorption and thus can afford a low rate of aldosterone mediated distal tubular sodium reabsorption to maintain sodium balance. Our results are thus in accord with our previous hypothesis, that different receptor equipment of individual subjects may cause marked differences in sodium handling by the kidney. These differences may be responsible, at least in part, for the degree of salt sensitivity in individual subjects.
Kotanko
P
P
Department of Internal Medicine, University of Innsbruck, Austria.
Skrabal
F
F
Gruber
G
G
Doll
P
P
Meister
B
B
D000042:Absorption; D000328:Adult; D000450:Aldosterone / Q000652:urine; D004039:Diet, Sodium-Restricted; D006801:Humans; D007687:Kidney Tubules, Proximal / Q000378:metabolism; D008094:Lithium; D008297:Male; D011941:Receptors, Adrenergic / Q000378:metabolism*; D012016:Reference Values; D012964:Sodium / Q000378:metabolism*; D012965:Sodium Chloride / Q000494:pharmacology*
D011941:Receptors, Adrenergic; D012965:Sodium Chloride; D000450:Aldosterone; D008094:Lithium; D012964:Sodium