help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
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
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Pan, L.
Right arrow Articles by Gutkowska, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pan, L.
Right arrow Articles by Gutkowska, J.

Endocrinology, Vol 123, 1259-1263, Copyright © 1988 by Endocrine Society

ARTICLES

Is clonidine-induced diuresis mediated by atrial natriuretic factor?

L Pan and J Gutkowska
Clinical Research Institute of Montreal, Quebec, Canada.

The effect of intracerebroventricular (ICV) administration of clonidine on urine output, urinary sodium excretion, urinary cGMP, and plasma immunoreactive atrial natriuretic factor (IR-ANF) was studied in conscious, normally hydrated rats. Clonidine treatment evoked a significant dose-dependent increase in urine output. A 20-fold elevation was noted after the highest clonidine dose (2 micrograms/rat). The observed diuresis was accompanied by enhanced sodium excretion, which with the highest dose (2 micrograms) of clonidine increased from 1.6 +/- 0.36 to 39.4 +/- 10.5 meq/liter (P less than 0.001). Plasma IR-ANF rose from 30.7 +/- 8.8 to 113.3 +/- 32.3 pg/ml plasma 5 min after the 0.5 micrograms clonidine dose (P less than 0.05), and urinary cGMP excretion was augmented from 8.49 +/- 4.29 to 27.7 +/- 5.0 pmol/min 1 h after 0.5 micrograms clonidine (P less than 0.05). Pretreatment with peripherally administered anti-ANF serum abolished the diuretic effect of intracerebroventricularly administered clonidine; urine output decreased from 1.49 +/- 0.41 to 0.42 +/- 0.21 ml/h. The urinary cGMP level after anti-ANF serum treatment fell from 25.0 +/- 7.56 to 7.1 +/- 3.5 pmol/min (P less than 0.05). Peripheral pretreatment with the alpha 2-antagonist yohimbine or the opioid antagonist naloxone partially abolished clonidine's diuretic impact: urine output dropped from 1.91 +/- 0.55 to 0.42 +/- 0.18 and 0.46 +/- 0.18 ml/h (P less than 0.05), respectively. At the same time, plasma IR- ANF decreased from 113.3 +/- 32.2 to 30.3 +/- 11.4 after yohimbine and to 24.6 +/- 12.1 pg/ml after naloxone treatment (P less than 0.05). These data suggest that ANF may be involved in the mechanism of diuresis of centrally applied clonidine, which appears to enhance ANF release through its central stimulation of opiate and alpha 2- adrenergic receptors.


This article has been cited by other articles:


Home page
 J. Pharmacol. Exp. Ther.Home page
J. Gutkowska, S. Mukaddam-Daher, and J. Tremblay
The Peripheral Action of Clonidine Analog ST-91: Involvement of Atrial Natriuretic Factor
J. Pharmacol. Exp. Ther., May 1, 1997; 281(2): 670 - 676.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1988 by The Endocrine Society