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Original Article

Adrenergic Receptors and Sodium Reabsorption in Normotensive Subjects as Related to Salt Sensitivity

, , , &
Pages 307-318 | Published online: 03 Jul 2009
 

Abstract

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 α-2 adrenergic receptors, β-2 adrenergic receptors or the α-2/β- 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 α-2 receptor densities under low salt diet (r = -0.55, n = 17, p < 0.02). There were no correlations between β-2 adrenoceptor density, α-2/β-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 α-adrenoceptor density, as measured on circulating blood cells, may possibly be representative for α-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 α-2 adrenocsptor densities could be interpreted as an indirect evidence, that those subjects with a high α-2 adrenoceptor equipment show a high proximal tubular sodium reabsorption and thus can efford 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.

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