RELATIONSHIP BETWEEN INSULIN RELEASE, ANTINATRIURESIS AND HYPOKALEMIAAFTER GLUCOSE-INGESTION IN NORMAL AND HYPERTENSIVE MAN

1. Insulin simultaneously causes hypokalaemia and antinatriuresis, and it has been suggested that the two effects are tightly coupled. Wheth er these actions are preserved in patients with essential hypertension is not known. 2. Eight hypertensive patients and eight normotensive c ontrol subjects were studied before and after the ingestion of 75 g of glucose. Despite similar glycaemic profiles, the patients showed a hy perinsulinaemic response incremental area 49 +/- 8 versus 27 +/- 6 nmo l l-1 3h, P<0.04) but a blunted hypokalaemic response (-7 +/- 1 versus - 16 +/- 1%, P < 0.001). Both absolute and fractional urinary excreti on of sodium and potassium were significantly decreased during glucose -induced hyperinsulinaemia in hypertensive patients as well as in norm otensive subjects (P<0.05 for all changes). 3. To test whether hypokal aemia is required for insulin-induced antinatriuresis, each hypertensi ve patient received another oral glucose load during which enough pota ssium chloride was given to clamp the plasma potassium concentration a t baseline. Under these conditions, significant insulin-induced antina triuresis still occurred. In addition, whereas the glycaemic profile w as superimposable, the response of the plasma insulin concentration wa s significantly greater with than without maintenance of the plasma po tassium concentration (total area 79 +/- 14 versus 63 +/- 8 nmol l-1 3 h, P<0.04). 4. We conclude that (a) insulin causes antinatriuresis, an tikaliuresis and hypokalaemia under phys anticonditions; (b) in hyperi nsulinaemic (insulin-resistant) patients with essential hypertension, the antinatriuretic action of insulin is quantitatively preserved; and (c) clamping plasma potassium levels prevents insulin-induced antikal iuresis but not antinatriuresis, and potentiates the insulin secretory response to glucose.