Renal sodium handling and haemodynamics are equally affected by hyperinsulinaemia in salt-sensitive and salt-resistant hypertensives.

ABSTRACT

OBJECTIVE: It is well-known that insulin induces renal sodium retention. It is not yet known whether insulin's renal effects are involved in the development of salt-sensitive hypertension. We assessed the effects of insulin on renal sodium handling and haemodynamics in 10 salt-sensitive (SS) and 10 salt-resistant (SR) essential hypertensives. DESIGN: After a baseline period of 90 min, all subjects underwent a euglycaemic clamp with sequential infusion of a physiological and supraphysiological dose of insulin (50 and 150 mU/kg per h) during 90 min periods each. Time-control studies were performed in the same subjects. Clearances of 131I-hippuran, 125I-iothalamate, sodium and lithium were used to evaluate renal plasma flow (RPF), CNa/glomerular filtration rate (GFR) and fractional proximal and distal sodium reabsorption. RESULTS: Plasma insulin levels and insulin-mediated glucose uptake did not differ between both groups. RPF and GFR showed similar increases during both insulin infusions in both groups. During physiological hyperinsulinaemia, fractional sodium excretion decreased 38% (P = 0.009) in the SS group and 36% (P = 0.002) in the SR group. During supraphysiological hyperinsulinaemia, fractional sodium excretion decreased 49% (P = 0.01) in the SS group and 19% (P = 0.2) in the SR group, not statistically different between both groups. Fractional proximal sodium reabsorption was unaffected and fractional distal sodium reabsorption increased to a similar magnitude in both groups. CONCLUSION: The comparable renal effects of acute exogenous hyperinsulinaemia in SS and SR hypertensives do not support a role for insulin in the development of salt-sensitive hypertension. However, the results do not yet exclude a role for chronic hyperinsulinaemia.