Renal and Systemic Hemodynamic Effects of Synthetic Atrial Natriuretic Peptide in the Anesthetized Rat

• Published in: Circulation research Vol. 59; no. 3; pp. 237 - 246
• Main Authors: DUNN, B RENTZ, ICHIKAWA, IEKUNI, PFEFFER, JANICE M, TROY, JULIA L, BRENNER, BARRY M
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD American Heart Association, Inc 01.09.1986; Lippincott
• Subjects: Anesthesia, General; Animals; Atrial Natriuretic Factor - pharmacology; Biological and medical sciences; Blood Pressure - drug effects; Fundamental and applied biological sciences. Psychology; Glomerular Filtration Rate - drug effects; Hemodynamics - drug effects; Hemodynamics. Rheology; Hormones - pharmacology; Kidney Glomerulus - blood supply; Male; Natriuresis - drug effects; Rats; Renal Circulation - drug effects; Vascular Resistance - drug effects; Vertebrates: cardiovascular system; Excretion; Glomerular filtration; Rat; Rodentia; Peptide hormone; Kidney; Vertebrata; Mammalia; Synthetic product; Urinary system; Sodium; Circulatory system; Hemodynamics; Atrial natriuretic factor
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/01.res.59.3.237

To characterize the hemodynamic events responsible for alterations in renal function during administration of atrial natriuretic peptide, we studied the systemic, renal, and glomerular circulatory effects of intravenous rANP[126–149], administered as a 4 μg/kg prime and 0.5 μg/kg per minute continuous infusion in anesthetized, euvolemic rats. With this protocol, a small decline in mean systemic arterial blood pressure occurred in the context of markedly enhanced urinary sodium excretion, hemoconcentration, and reduced left ventricular end-diastolic pressure and +dP/dt. However, despite a significant decrement in renal vascular resistance, total peripheral resistance remained constant, thereby denoting a preferential renal vasodilatory effect of this peptide in vivo. Whole kidney and single nephron GFR increased by approximately 20%, while effective renal and glomerular plasma flow rates remained stable, resulting in a substantial rise in filtration fraction. Of all the parameters potentially capable of augmenting single nephron GFR, only glomerular capillary hydraulic pressure increased significantly and therefore accounted entirely for the hyperfiltration observed during ANP infusion. This rise in glomerular capillary pressure, in turn, resulted from afferent arteriolar vasodilatation and concurrent efferent arteriolar vasoconstriction, findings that proved independent of both endogenous angiotensin II activity and ANP-induced reductions in renal perfusion pressure. These renal hemodynamic effects are unique when compared with actions of previously studied renal vasodilatory agents.