AJP - Heart Calcium Transients and Cell-Sarcomere
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 265: H15-H21, 1993;
0363-6135/93 $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 Bockman, C. S.
Right arrow Articles by Abel, P. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bockman, C. S.
Right arrow Articles by Abel, P. W.

AJP - Heart and Circulatory Physiology, Vol 265, Issue 1 15-H21, Copyright © 1993 by American Physiological Society

ARTICLES

Endothelium, vasopressin receptors, and resistance to DOCA-salt hypertension

C. S. Bockman, W. B. Jeffries, W. A. Pettinger and P. W. Abel
Department of Pharmacology, Creighton University School of Medicine, Omaha, Nebraska 68178.

Mesenteric artery rings from Wistar and Wistar-Furth rats subcutaneously treated with deoxycorticosterone acetate (DOCA) and 1% NaCl drinking water were used to measure endothelial modulation of contractile sensitivity and vasopressin receptor function and affinity. DOCA-salt hypertension reduced contractile sensitivity to arginine vasopressin (AVP) and did not affect contractile sensitivity to norepinephrine in arteries from Wistar rats. Endothelial removal caused a threefold increase in contractile sensitivity to AVP and norepinephrine in DOCA-salt hypertensive Wistar rats. In Wistar-Furth rats, DOCA-salt treatment did not affect contractile sensitivity to AVP, lysine vasopressin, oxytocin, and norepinephrine or the affinity of the vasopressin receptor for agonists or antagonists. Removal of endothelium did not affect vasopressin contractile sensitivity but caused a 15-fold increase in contractile sensitivity to norepinephrine in untreated or DOCA-salt-treated Wistar-Furth rats. These data show that reduced vasopressin receptor function and increased endothelial function that compensate for increased contractile sensitivity in arteries from DOCA-salt hypertensive Wistar rats are not the cause of resistance of DOCA-salt-treated Wistar-Furth rats to the development of enhanced contractile sensitivity and hypertension.


This article has been cited by other articles:


Home page
 HypertensionHome page
M. E. Ullian, C. J. Robinson, C. T. B. Evans, J. Z. Melnick, and W. R. Fitzgibbon
Role of Citrate Synthase in Aldosterone-Mediated Sodium Reabsorption
Hypertension, April 1, 2000; 35(4): 875 - 879.
[Abstract] [Full Text] [PDF]

Home page
 J. Am. Soc. Nephrol.Home page
W. R. FITZGIBBON, E. L. GREENE, J. S. GREWAL, F. N. HUTCHISON, S. E. SELF, S. Y. LATTEN, and M. E. ULLIAN
Resistance to Remnant Nephropathy in the Wistar-Furth Rat
J. Am. Soc. Nephrol., April 1, 1999; 10(4): 814 - 821.
[Abstract] [Full Text]


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