Effects of insulin on kidney function and sodium excretion in healthy subjects

Abstract

Insulin action on kidney function was evaluated in 8 healthy subjects, (mean age 27 years) using the euglycaemic clamp technique. Insulin was infused at rates of 0, 20 and 40 mU.min-1.m-2 over consecutive periods of 120 min resulting in plasma insulin concentrations of 8 +/- 2, 29 +/- 7 and 66 +/- 14 mU/l. The renal clearance of 51Cr-EDTA, lithium, sodium and potassium was determined during the last 90 min of each period. Sodium clearance declined with increasing plasma insulin concentrations (1.3 +/- 0.4, 1.0 +/- 0.3 and 0.5 +/- 0.2 ml.min-1.1.73 m-2, p less than 0.001), while glomerular filtration rate (108 +/- 21, 104 +/- 21 and 108 +/- 20 ml.min-1. 1.73 m-2) and lithium clearance (a marker of fluid flow rate from the proximal tubules) 29 +/- 5, 29 +/- 4 and 30 +/- 4 ml.min-1.1.73 m-2) remained unchanged. Calculated proximal tubular reabsorption of sodium and water was unchanged, while calculated distal fractional sodium reabsorption increased (95.5 +/- 1.5, 96.4 +/- 1.2 and 98.1 +/- 0.7%, p less than 0.001). Potassium clearance and plasma potassium concentration declined, whereas plasma aldosterone and plasma renin concentrations were unchanged. In conclusion, elevation of plasma insulin concentration within the physiological range has a marked antinatriuretic action. This effect is located distally to the proximal renal tubules.

Effects of acetazolamide on kidney function in Type 1 (insulin-dependent) diabetic patients with diabetic nephropathy

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Prehypertension in dyslipidemic individuals; relationship to metabolic parameters and intima-media thickness

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Effects of nicotinic acid on insulin sensitivity and blood pressure in healthy subjects

“…In support of the hypothesis that insulin resistance may cause hypertension are observations that improving insulin sensitivity by weight loss or by pharmacological therapy without weight loss may reduce blood pressure. 6,7 Furthermore, insulin has a number of physiological effects such as sodium retention, 8,9 stimulation of the sympathetic nervous system 10 and increased intracellular cation concentrations 11 which could predispose to hypertension in conditions of hyperinsulinaemia. However, in human subjects neither acute hyperinsulinaemia induced 26.2 ± 4.6 mol/kg/min, P = 0.002) associated with a decrease in non-oxidative glucose disposal.…”