AJP - Heart and Circulatory Physiology, Vol 253, Issue 5 1167-H1176, Copyright © 1987 by American Physiological Society
Neural, hemodynamic, and renal responses to stimulation of intestinal receptors
L. C. Weaver, S. Genovesi, A. Stella and A. Zanchetti
Department of Physiology, Michigan State University East Lansing 48824-1101.
Stimulation of visceral receptors with bradykinin has been shown to cause
reflex increases in sympathetic nerve activity and systemic arterial
pressure. In this investigation, serosal receptors of the intestine were
stimulated by bradykinin in anesthetized cats to 1) compare mesenteric and
renal sympathetic responses, 2) compare hemodynamic responses in mesenteric
and renal beds, and 3) determine changes in renal function. This
stimulation in intact animals caused pressor responses, significantly
greater excitation of mesenteric than renal nerves, significantly greater
mesenteric than renal vasoconstriction, diuresis, natriuresis, and, in
denervated kidneys, increases in fractional sodium excretion. In
vagotomized, sinoaortic-denervated cats, stimulation of intestinal
receptors caused excitation of mesenteric nerve activity greater than renal
for only 30 s. This sympathetic reflex response led to pressor responses,
equal mesenteric and renal vasoconstriction, diuresis, natriuresis, and
increased fractional excretion of sodium only in denervated kidneys. When
abdominal perfusion pressure was held constant with an aortic snare in
these same animals, the sympathetic reflexes initially caused greater
mesenteric than renal vasoconstriction and antidiuresis and antinatriuresis
only in innervated kidneys. These findings demonstrate that the intensity
of hemodynamic and renal responses to stimulation of visceral receptors
correlates well with the magnitude of sympathetic nerve responses.
