The effect of insulin on renal handling of sodium, potassium, calcium, and phosphate in man.

Abstract

A B S T R A C T The effects of insulin on the renal handling of sodium, potassium, calcium, and phosphate were studied in man while maintaining the blood glucose concentration at the fasting level by negative feedback servocontrol of a variable glucose infusion. In studies on six water-loaded normal subjects in a steady state of water diuresis, insulin was administered i.v. to raise the plasma insulin concentration to between 98 and 193 PU/ml and infused at a constant rate of 2 mU/kg body weight per min over a total period of 120 min. The blood glucose concentration was not significantly altered, and there was no change in the filtered load of glucose; glomerular filtration rate (CIN) and renal plasma flow (CPAH) were unchanged. Urinary sodium excretion (UNaV) decreased from 401±46 (SEM) to 213+18 iteq/min during insulin administration, the change becoming significant (P < 0.02) within the 30-60-min collection period. Free water clearance (CH2o) increased from 10.6±0.6 to 13±0.5 ml/min (P <0.025); osmolar clearance decreased and urine flow was unchanged. There was no change in plasma aldosterone concentration, which was low throughout the studies, and a slight reduction was observed in plasma glucagon concentration. Urinary potassium (UKV) and phosphate (Ui.V) excretion were also both decreased during insulin administration; UKV decreased from 66±9 to 21±1 Meq/min (P < 0.005), and UrV decreased from 504±93 to 230 ±43 Ag/min (P <0.01). The change in UKV was associated with a significant reduction in plasma potassium concentration. There was also a statistically significant but small reduction in plasma phosphate concentration which was not considered sufficient alone to account for the large reduction in UPV. Urinary calcium excretion (UCaV) increased from 126±24 to 200±17 ug/min (P < 0.01).These studies demonstrate a reduction in UNaV associated with insulin administration that occurs in the absence of changes in the filtered load of glucose, glomerular filtration rate, renal blood flow, and plasma aldosterone concentration. The effect of insulin on CH2o suggests that insulin's effect on sodium excretion is due to enhancement of sodium reabsorption in the diluting segment of the distal nephron.

The effect of intravenous insulin infusion on kidney function in insulin-dependent diabetes mellitus

“…When blood glucose was kept constant insulin infusion resulting in plasma insulin concentrations within the physiological range (mean 110 mU/1) did not affect RPF or GFR. Similar results have been obtained in normal man when blood glucose was kept constant during insulin infusion at the same rate as presently used [13] and after an intravenous bolus injection of 20 U of insulin [14]. This lack of insulin effect on kidney function may either be due to constant blood glucose or plasma volume expansion induced by the glucose infusion (255 ml, 20 g/100 ml glucose in our study).…”

Randomized Trial of the Effects of Insulin and Metformin on Myocardial Injury and Stress in Diabetes Mellitus: A Post Hoc Exploratory Analysis

“…Alternatively, insulin therapy is known to lead to sodium and fluid retention, thus leading to increases in myocardial wall stress and NP release 30. If so, our observations may represent an early sign of cardiovascular hazard, particularly of heart failure, in susceptible patients.…”

Silent ischemia is more prevalent among hypertensive patients with microalbuminuria and salt sensitivity

“…Recent evidence indicates that several patients with essential hypertension manifest insulin resistance and/or hyperinsulinemia. 54 Acute and chronic infusion of insulin may cause sodium retention, 55 may stimulate the sympathetic nervous system, 56 may alter cation transport and stimulate hypertrophy of smooth muscle cells in the absence of changes in serum glucose. These cellular effects of insulin, if present in smooth muscle cells, could underlie the increase in total body sodium and in blood pressure in salt-sensitive hypertensives.…”