Mechanism of the natriuretic effect of unilateral carotid artery traction in the rat.

Abstract

Unilateral traction on a carotid artery is known to activate the carotid baroreceptor reflex. This maneuver increases sodium excretion in a manner not completely dependent on the renal nerves, suggesting that a humoral factor(s) could be involved. We measured sodium excretion before and after unilateral carotid artery traction or sham traction in anesthetized rats and related the results to the plasma concentration of immunoreactive (IR)-gamma-melanocyte stimulating hormone (gamma-MSH), a peptide known to be natriuretic in other circumstances. In 12 rats undergoing sham traction, sodium excretion did not change and plasma IR-gamma-MSH activity at the end of the experiment was 10.5 +/- 5.4 (SD) fmol/mL. Carotid artery fraction in 20 other rats caused a transient dip in mean arterial pressure of 20.1 +/- 13.2 mm Hg, and sodium excretion increased from 746 +/- 431 to 1,739 +/- 1,436 nEq/min (P less than 0.005). Plasma IR-gamma-MSH was increased to 21.1 +/- 7.1 fmol/mL (P less than 0.001 versus sham). Prior ipsilateral carotid sinus denervation markedly attenuated the carotid artery traction-related dip in blood pressure and prevented both the natriuresis and the increase in IR-gamma-MSH activity seen after this maneuver in intact rats. Pretreatment with anti-gamma-MSH antiserum also blocked the natriuretic response to carotid artery traction, despite a similar transient dip in blood pressure of 18.3 +/- 9.9 mm Hg. These observations suggest that activation of the carotid baroreceptor reflex by unilateral carotid artery traction causes natriuresis that is mediated largely by an increase in the plasma concentration of a peptide or peptides closely related to the gamma-MSH sequence.