Renal Sodium Handling in Hypertensive Rats

Spontaneously hypertensive rats have reduced peripheral insulin sensitivity. To determine whether hypertensive rats demonstrate reduced response to the antinatriuretic effect of insulin, urinary sodium excretion was determined in hypertensive and normotensive rats (n=7 per group) before and during euglycemic insulin administration at two infusion rates (21 milliunits/kg load and 4 milliunits/kg/min or 85 milliunits/kg load and 8 milliunits/kg/min). Hypertensive and normotensive time controls received the vehicle for insulin administration. Mean arterial pressure was greater (/?<0.05) and inulin clearance was less (/?<0.05) in hypertensive than normotensive rats before insulin infusion. Baseline fractional sodium excretion was not different between groups. Low dose insulin infusion reduced (p<0.05) fractional sodium excretion from 0.81 ±0.43% to 0.31 ±0.07% in hypertensive rats and from 1.05±0.37% to 0.47±0.18% in normotensive rats. High dose insulin infusion reduced (/><0.05) fractional sodium excretion from 0.67±0.22% to 0.21 ±0.08% in hypertensive rats and from 0.81 ±0.15% to 0.30±0.09% in normotensive rats. Sodium excretion was unchanged in time controls. The reduction in sodium excretion was similar in both rat groups during low dose and high dose insulin infusions. Mean arterial pressure and inulin clearance were unchanged from baseline values during insulin infusion in all rat groups. Glucose requirement to maintain euglycemia was greater (p<0.05) in normotensive than hypertensive rats at both insulin infusion rates. Thus, while hypertensive rats have reduced sensitivity to the hypoglycemic effects of insulin, the antinatriuretic response to insulin is not different from that of normotensive rats. Furthermore, the presence of hypertension does not modulate the antinatriuretic activity of insulin. (Hypertension 1990;15:514-518)