Received April 13, 2005
Revised June 8, 2005
Accepted after revision August 8, 2005

¹ Uppsala University

^* To whom correspondence should be addressed. E-mail: peter.hansell{at}medcellbiol.uu.se.

	Abstract

To identify defects in the salt-sensitive Dahl-rat, the natriuretic, catecholaminergic and pressor responses to 60 min elevation of the cerebroventricular sodium concentration (CNS-induced natriuresis) were compared between prehypertensive salt-sensitive and salt-resistant Dahl rats. The plasma concentrations of the rat natriuretic hormone oxytocin, with implications for the development of hypertension, and vasopressin (AVP) were also measured. Basal sodium and catecholamine excretion and mean arterial blood pressure (MAP) were similar in both strains. Sodium excretion during CNS-stimulation increased more than 15-fold in Dahl-R but only 10-fold in Dahl-S. Dopamine excretion increased only transiently and similarly in both strains. Noradrenaline excretion was similar suggesting a comparable sympathetic nervous activity. MAP increased comparably in Dahl-R and Dahl-S. Plasma AVP was similar in both strains while plasma oxytocin after CNS-stimulation was more than 2-fold higher in Dahl-S than in Dahl-R. In conclusion, the prehypertensive Dahl-S has an attenuated natriuretic response to elevations of the cerebroventricular fluid sodium concentration and a higher plasma level of the natriuretic hormone oxytocin. Dopamine is not a mediator of CNS-induced natriuresis in neither strain. The attenuated natriuretic response may partly explain the salt-sensitivity in Dahl-S, and the higher plasma oxytocin value may either represent an effort to compensate for the deficient natriuretic response or reflect a primary defect in this system. Due to the known involvement of oxytocin in central MAP regulation and some hypertensive animal models the findings warrants further investigation.

Key Words: Kidney, Natriuresis, Oxytocin