HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 90/6/847    most recent expphysiol.2005.030619v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sjöquist, M. Articles by Hansell, P. Search for Related Content PubMed PubMed Citation Articles by Sjöquist, M. Articles by Hansell, P. Related Collections Renal

¹ Section of Integrative Physiology, Department of Medical Cell Biology, Biomedical Centre, University of Uppsala, Sweden

To identify defects in the salt-sensitive Dahl rat (Dahl-S), the natriuretic, catecholaminergic and pressor responses to 60-min elevation of the cerebroventricular sodium concentration (CNS-induced natriuresis) were compared between prehypertensive salt-sensitive Dahl-S and salt-resistant Dahl rats (Dahl-R). The plasma concentrations of the rat natriuretic hormone oxytocin, which has 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 and response to CNS stimulation were similar, suggesting a comparable sympathetic nervous activity between the strains. MAP increased comparably in Dahl-R and Dahl-S. Plasma AVP concentration was similar in both strains while plasma oxytocin concentration 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 in some hypertensive animal models, the findings warrant further investigation.

(Received 13 April 2005; accepted after revision 8 August 2005; first published online 9 August 2005)
Corresponding author P. Hansell: Section of Integrative Physiology, Department of Medical Cell Biology, University of Uppsala, Biomedical Center, PO Box 571, S-751 23 Uppsala, Sweden. Email: peter.hansell{at}medcellbiol.uu.se

This article has been cited by other articles:

				U. C. Kopp, M. Z. Cicha, L. A. Smith, J. Mulder, and T. Hokfelt Renal sympathetic nerve activity modulates afferent renal nerve activity by PGE2-dependent activation of {alpha}1- and {alpha}2-adrenoceptors on renal sensory nerve fibers Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2007; 293(4): R1561 - R1572. [Abstract] [Full Text] [PDF]