AJP - Regulatory, Integrative and Comparative Physiology, Vol 266, Issue 2 572-R577, Copyright © 1994 by American Physiological Society
Atrial natriuretic peptide and glomerular hyperfiltration during onset of spontaneous diabetes mellitus
M. I. Okwueze, T. J. Opgenorth, T. W. von Geldern and R. C. Vari
Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana 70112.
The mechanisms responsible for the elevation of glomerular filtration rate
(GFR) in early stages of insulin-dependent diabetes mellitus (IDDM) are
undefined. The objectives of this study were to define the temporal pattern
of onset of glomerular hyperfiltration in the spontaneously diabetes-prone
(BB/DP) rat and to evaluate the possible role of atrial natriuretic peptide
(ANP) as the primary mediator of the observed alterations in renal
hemodynamics. GFR was significantly higher (1.38 +/- 0.07 ml.min-1 x g-1; n
= 5) in moderately hyperglycemic BB/DP rats (blood glucose > 270 mg/dl)
14 days after the onset of IDDM compared with age-matched
diabetes-resistant rats (BB/DR), which averaged 1.03 +/- 0.07 ml.min-1 x
g-1 (n = 7). Circulating ANP levels in moderately hyperglycemic BB/DP rats
1, 7, and 14 days after onset of IDDM were within the normal range,
averaging 100 +/- 21, 57 +/- 12, and 65 +/- 6 pg/ml, respectively, and were
not significantly different (P > 0.05) from ANP levels in age-matched
normoglycemic BB/DR rats. To further test the role of ANP in glomerular
hyperfiltration, an ANP receptor antagonist was infused into anesthetized
BB/DP rats (n = 10) 14 days after onset of IDDM, after baseline
measurements of mean arterial pressure, renal hemodynamics, and renal fluid
and electrolyte excretions. ANP receptor antagonism caused a significant
reduction in mean arterial pressure from 120 +/- 3 to 103 +/- 2 mmHg;
however, there were no significant effects of ANP receptor blockade on
GFR.(ABSTRACT TRUNCATED AT 250 WORDS)
