AJP - Renal Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Renal Physiol 253: F976-F981, 1987;
0363-6127/87 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Osborn, J. L.
Right arrow Articles by Kinstetter, D. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Osborn, J. L.
Right arrow Articles by Kinstetter, D. D.

AJP - Renal Physiology, Vol 253, Issue 5 976-F981, Copyright © 1987 by American Physiological Society

ARTICLES

Effects of altered NaCl intake on renal hemodynamic and renin release responses to RNS

J. L. Osborn and D. D. Kinstetter
Department of Physiology, Medical College of Wisconsin, Milwaukee 53226.

Relationships between frequency of renal nerve stimulation (RNS) and renal blood flow (RBF), glomerular filtration rate (GFR), and plasma renin activities (PRA) were evaluated in anesthetized dogs placed on low (5 meq/day)-, normal (40 meq/day)-, and high (200 meq/day)-sodium chloride diets. Arterial pressure, RBF, GFR, and renal venous and arterial PRA were determined before and during direct electrical RNS at 0.5, 1.0, and 2.0 Hz (15 V, 1.0 ms). Dogs on low sodium intakes increased renal venous PRA at 0.5, 1.0-, and 2.0-Hz RNS, whereas dogs on normal sodium intakes did not increase renal venous PRA until RNS reached 2.0 Hz. High sodium dogs did not increase PRA at any frequency of RNS tested. RNS at 0.5 Hz was not associated with any changes in GFR or RBF in any of the groups. Dogs on normal sodium and high sodium intakes decreased both GFR and RBF during 1.0- and 2.0-Hz RNS. Low-sodium dogs, however, only decreased GFR and RBF during 2.0-Hz RNS, and these hemodynamic responses were significantly less than 2.0-Hz GFR and RBF responses of high sodium dogs. These data indicate that renal vasoconstrictor responses to RNS are potentiated, and renin release responses to RNS are reduced by elevation of sodium chloride intake. We suggest that during low sodium intake, activation of sympathetic nerve activity elicits an enhanced renin release response, whereas the renal vasculature may be protected against neurogenic vasoconstriction.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
E. Seeliger, K. Lohmann, B. Nafz, P. B. Persson, and H. W. Reinhardt
Pressure-dependent renin release: effects of sodium intake and changes of total body sodium
Am J Physiol Regulatory Integrative Comp Physiol, August 1, 1999; 277(2): R548 - R555.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online