Activation of renal sympathetic outflow by intracisternal hypertonic NaCl in dogs.

Abstract

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.