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AJP - Regulatory, Integrative and Comparative Physiology, Vol 258, Issue 2 383-R387, Copyright © 1990 by American Physiological Society
ARTICLES |
S. Koyama, T. Fujita, H. Uematsu, T. Shibamoto, M. Aibiki and S. Kojima
Department of Physiology, Shinshu University School of Medicine, Nagano, Japan.
We have examined baroreceptor regulation of renal nerve activity (RNA) during anaphylactic hypotension that affects renal nerve activity. In anesthetized dogs, mean blood pressure (MBP), heart rate (HR), and RNA were simultaneously measured. To test for a normally functioning baroreceptor reflex in each animal, a transient hypotension was induced by an intravenous injection of sodium nitroprusside (4 micrograms/kg). Nitroprusside produced a reflex increase in RNA (+63 +/- 12% at -20 mmHg and +139 +/- 8% at -40 mmHg) and HR (+13 +/- 1 beats/min at -20 mmHg and +21 +/- 2 beats/min at -40 mmHg). However, intravenous administration of Ascaris suum antigen in animals with an intact neuraxis caused a decrease in RNA (-15 +/- 14% at -20 mmHg and -42 +/- 11% at -40 mmHg blood pressure during the antigen-induced hypotension) in parallel with a fall in systemic blood pressure. HR responses were -5 +/- 2 beats/min at -20 mmHg and -10 +/- 1 beats/min at -40 mmHg during the hypotension induced by the antigen. In animals with combined denervation of the carotid sinus and vagal nerves, HR did not change significantly during anaphylactic hypotension. However, a decrease in RNA remained (-60 +/- 4% at -20 mmHg and -72 +/- 4% at -40 mmHg of hypotension). The decrease in RNA after antigen administration was significantly greater after denervation than in animals with an intact neuraxis. These results indicate that systemic baroreceptor reflex control of RNA is reduced during anaphylactic hypotension. Impaired reflex control of sympathetic nerve activity may result from an impairment of sympathetic outflow through the central nervous system.
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