AJP - Heart and Circulatory Physiology, Vol 257, Issue 1 272-H279, Copyright © 1989 by American Physiological Society
Effects of ANP on venous pressures and microvascular protein permeability in dog forelimb
D. Eliades, B. Swindall, J. Johnston, M. Pamnani and F. J. Haddy
Department of Physiology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814.
Intravenous administration of alpha-atrial natriuretic peptide (ANP)
produces a decrease in arterial blood pressure due to a decrease in cardiac
output. The mechanism of the decrease in cardiac output is unknown but has
been suggested to result from transcapillary fluid efflux caused by
venoconstriction and/or increased permeability of the microvascular
membrane to plasma proteins. We investigated these possibilities in the dog
forelimb perfused at constant flow and prepared to measure 1) large and
small vessel pressures in the two parallel skin and skeletal muscle
vascular beds, and limb weight; or 2) skin lymph flow and skin lymph
protein concentration. In both preparations, human ANP was injected and
infused into the brachial artery. Bolus injections of ANP (0.1-0.4
micrograms) depressed perfusion pressure much less than acetylcholine or an
isotonic solution of potassium chloride and did not raise small vein
pressures. ANP infused at nine different rates ranging from 0.1 ng to 38.8
micrograms/min failed to influence skin and muscle small and large vein
pressures, limb weight, skin lymph flow, and skin lymph protein
concentration. It also failed to affect perfusion pressure and skin and
muscle small artery pressures until the infusion was shut off, at which
time they increased above control levels. These studies suggest that human
alpha-ANP is neither a direct venous constrictor nor a potent arteriolar
dilator and does not directly influence the permeability of the
microvascular membrane to plasma proteins in the skin and skeletal muscle
of the dog forelimb.
