Mechanism of diuresis following acute modest hyperglycemia in the rat.

In paired micropuncture studies in the Munich-Wistar rat we examined the mechanism of diuresis after acute induction of modest hyperglycemia (430-460 mg/dl) in the absence of an increase in total body water. The major reasons for the diuresis were an increase in nephron filtration rate (SNGFR) (from 30.3 +/- 1.8 to 35.3 +/- 1.6 nl/min) and a reduction in absolute proximal reabsorption (APR) (from 14.0 +/- 0.6 to 9.8 +/- 1.2 nl/min). All determinants of SNGFR were measured and a reduction in systemic oncotic pressure was the sole reason for the increase in SNGFR; vascular resistances did not change. Late proximal tubular fluid-to-plasma glucose concentration ratio was 0.96 +/- 0.04; therefore, the osmotic effects of unreabsorbed glucose could not account for the reduction in APR. Directly measured net renal interstitial pressure increased by 5 mmHg and the peritubular capillary effective reabsorptive pressure decreased (from 15.5 to 10.9 mmHg) in direct proportion to the reduction in APR, changes that could contribute to the reduction in APR. Equal elevations in glucose concentration in tubule and plasma may have also eliminated effective osmotic pressure gradients for water movement and influenced APR. As a result of increases in late proximal tubular flow rate, loop of Henle tubular reabsorption and absolute tubular reabsorption beyond the distal tubule both increased with hyperglycemia. The major reduction in APR was secondary to altered "physical factors" and osmotic effects of glucose that are not dependent on creation of unfavorable chemical gradients for Na+ reabsorption.