JPET Assistant Professor of Medicine (Clinician-Educator)

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
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 Narita, H.
Right arrow Articles by Yamaguchi, I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Narita, H.
Right arrow Articles by Yamaguchi, I.

Hypotensive and diuretic actions of diltiazem in spontaneously hypertensive and Wistar Kyoto rats

H Narita, T Nagao, H Yabana and I Yamaguchi

We investigated the hypotensive and diuretic effects of diltiazem and hydralazine in conscious, spontaneously hypertensive rats (SHR) and their counterpart, Wistar Kyoto rats (WKY). Orally administered diltiazem induced dose-dependent hypotension both in SHR (10-60 mg/kg) and in WKY (30-100 mg/kg) and the effects were more pronounced in SHR than in WKY. Diltiazem did not cause tachycardia in either strain. Moreover, hypotensive doses of diltiazem acutely increased urinary excretion of sodium as well as urine volume in saline-loaded SHR and WKY. Chronic administration of diltiazem (30 mg/kg/day for 8 weeks) to young SHR caused no changes in body fluid distribution or in plasma sodium concentration. On the other hand, hydralazine not only showed almost the same hypotensive potency in SHR and WKY but also resulted reflex tachycardia in both strains. In addition, hydralazine (5 mg/kg) decreased urinary sodium excretion in saline-loaded SHR. In conclusion, it was suggested that diltiazem is an antihypertensive agent with an enhanced hypotensive action in the hypertensive state and without tachycardia and sodium retention effects.

Volume 227, Issue 2, pp. 472-477, 11/01/1983
Copyright © 1983 by American Society for Pharmacology and Experimental Therapeutics




This article has been cited by other articles:


Home page
Mol. Interv.Home page
S. Sonkusare, M. Fraer, J. D. Marsh, and N. J. Rusch
Disrupting Calcium Channel Expression To Lower Blood Pressure: New Targeting of a Well-Known Channel
Mol. Interv., December 1, 2006; 6(6): 304 - 310.
[Abstract] [Full Text] [PDF]


Home page
HypertensionHome page
P. F. Pratt, S. Bonnet, L. M. Ludwig, P. Bonnet, and N. J. Rusch
Upregulation of L-Type Ca2+ Channels in Mesenteric and Skeletal Arteries of SHR
Hypertension, August 1, 2002; 40(2): 214 - 219.
[Abstract] [Full Text] [PDF]


Home page
HypertensionHome page
S.I. Garcia, S.M. Dabsys, V.N. Martinez, A. Delorenzi, D. Santajuliana, V.E. Nahmod, S. Finkielman, and C.J. Pirola
Thyrotropin-Releasing Hormone Hyperactivity in the Preoptic Area of Spontaneously Hypertensive Rats
Hypertension, December 1, 1995; 26(6): 1105 - 1110.
[Abstract] [Full Text]


Home page
JAMAHome page
M. R. Flicker, M. A. Quigley, and E. G. Caldwell
Diltiazem and Hyperkalemia
JAMA, October 9, 1987; 258(14): 1891 - 1891.
[Abstract] [PDF]




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
 Molecular Interventions Drug Metabolism and Disposition

Copyright © 1983 by the American Society for Pharmacology and Experimental Therapeutics.