AJP - Heart and Circulatory Physiology, Vol 256, Issue 2 411-H416, Copyright © 1989 by American Physiological Society
Activation of renal sympathetic outflow by intracisternal hypertonic NaCl in dogs
I. Abe, D. B. Averill and C. M. Ferrario
Department of Brain and Vascular Research, Research Institute of the Cleveland Clinic Foundation, Ohio 44195.
The neurohormonal and sympathetic nervous system responses to injection of
hypertonic NaCl (1.5 M) into the cisterna magna were investigated in
morphine-pentobarbital-anesthetized dogs (n = 8). Mean arterial blood
pressure (MAP), heart rate (HR), and integrated efferent renal sympathetic
nerve activity (ERSNA) were recorded, and blood samples were taken for the
determination of plasma concentrations of epinephrine (Epi), norepinephrine
(NE), arginine vasopressin (AVP), osmolality, plasma renin activity (PRA),
and serum sodium and potassium. By 2 min after injection of hypertonic NaCl
into the cisterna magna, significant increases were observed for MAP (+47
+/- 5 mmHg, P less than 0.01), HR (+59 +/- 11 beats/min, P less than 0.01),
and ERSNA (+47 +/- 16%, P less than 0.01) above base line. The increased
activity of the sympathetic nervous system was not accompanied by changes
in PRA, Epi, NE, or AVP. Hypertonic NaCl was injected into the cisterna
magna of six dogs before and after intravenous administration of the AVP
antagonist [d(CH2)5Tyr(Me)]AVP. The time course for increases in MAP, HR,
and ERSNA was not affected by AVP blockade. Subsequent administration of
hexamethonium chloride abolished the pressor, tachycardic, and ERSNA
responses elicited by cisterna magna injection of hypertonic NaCl. These
experiments indicate that hypertonic NaCl acts at the lower brain stem to
activate the sympathetic nervous system. Further, the pressor and
tachycardic responses evoked by hypertonic NaCl acting at the lower brain
stem do not appear to involve the hypothalamic-hypophysial-adrenal axis.
