Reduced renal sodium excretion in primary hypertensive patients after an oral glucose load

ABSTRACT

This study was designed to determine urinary sodium excretion in response to an oral glucose load in hypertensive patients. Fifteen hypertensive patients and eighteen normotensive subjects were studied after an overnight fast and for 4 h after the ingestion of 100 g glucose. A subgroup of intreated, nonobese, primary hypertensive patients (five of the 15 hypertensive patients) became hyperinsulinemic (total area under the insulin curve[TAUC]33,080 + 3349 muU ml(-1) 120 min(-1) in response to an oral glucose load compared to normotensive subjects (TAUC 3670<13.731<23,693 muU ml(-1) 120 min(-1) or to the other subgroup of normoinsulinemic hypertensive individuals (TAUC10,221 + 1615 muU ml(-1) 120 min(-1) despite a similar serum glucose concentration in both groups. A significant decrease in renal sodium excretion in the entire hypertensive group (47.1 + 4.7 per cent, P<0.019) compared to the normotensive (20.0 + 10.5 per cent) subjects was also observed during the oral glucose tolerance test. Decreased renal sodium excretion was followed by a transient increase in urinary acid excretion. We speculate that the increase in insulin secretion may be responsible for the sodium-dependent increase in intracellular Ca2+, cellular H+ output and blood pressure in a subgroup of salt-sensitive patients with hypertension. New studies should be designed to identify the precise mechanisms involved in the interaction between hypertension, serum insulin-glucose levels and the magnitude of the renal tubule reabsorption abnormality.