|Effects of ACE inhibition and angiotensin II type 1 receptor blockade on cardiac function and G proteins in rats with chronic heart failure.|
|PMID: 11522607 Owner: NLM Status: MEDLINE|
|1. Inhibition of the renin-angiotensin system (RAS) improves symptoms and prognosis in heart failure. The experimental basis for these benefits remains unclear. We examined the effects of inhibition of ACE or blockade of angiotensin II type 1 (AT1) receptor on the haemodynamics, cardiac G-proteins, and collagen synthesis of rats with coronary artery ligation (CAL), a model in which chronic heart failure (CHF) is induced. 2. Rats were orally treated with the ACE inhibitor trandolapril (3 mg kg(-1) day(-1)) or the AT1 receptor blocker L-158809 (1 mg kg(-1) day(-1)) from the 2nd to 8th week after CAL. CAL resulted in decreases in the left ventricular systolic pressure and its positive and negative dP/dt, an increase in the left ventricular end-diastolic pressure, and the rightward shift of the left ventricular pressure-volume curve. Long-term treatment with either drug improved these signs of CHF to a similar degree. 3. Cardiac Gsalpha and Gqalpha protein levels decreased, whereas the level of Gialpha protein increased in the animals with CHF. Long-term treatment with trandolapril or L-158809 attenuated the increase in the level of cardiac Gialpha protein of the animals with CHF without affecting Gsalpha and Gqalpha protein levels. Cardiac collagen content of the failing heart increased, whose increase was blocked by treatment with either drug. 4. Exogenous angiotensin I stimulated collagen synthesis in cultured cardiac fibroblasts, whose stimulation was attenuated by either drug. 5. These results suggest that blockade of the RAS, at either the receptor level or the synthetic enzyme level, may attenuate the cardiac fibrosis that occurs after CAL and thus affect the remodelling of the failing heart.|
|H Yoshida; M Takahashi; K Tanonaka; T Maki; Y Nasa; S Takeo|
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|Type: Journal Article|
|Title: British journal of pharmacology Volume: 134 ISSN: 0007-1188 ISO Abbreviation: Br. J. Pharmacol. Publication Date: 2001 Sep|
|Created Date: 2001-08-27 Completed Date: 2001-10-11 Revised Date: 2009-11-18|
Medline Journal Info:
|Nlm Unique ID: 7502536 Medline TA: Br J Pharmacol Country: England|
|Languages: eng Pagination: 150-60 Citation Subset: IM|
|Department of Pharmacology, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi, Hachioji 192-0392, Japan.|
|APA/MLA Format Download EndNote Download BibTex|
Angiotensin II / pharmacology
Angiotensin-Converting Enzyme Inhibitors / pharmacology
Body Weight / drug effects
Collagen / drug effects, metabolism
Dose-Response Relationship, Drug
Fibroblasts / drug effects, metabolism
GTP-Binding Proteins / drug effects*, metabolism
Heart / drug effects*, physiopathology
Heart Failure / metabolism, pathology, prevention & control*
Heart Septum / drug effects, metabolism, physiopathology
Heart Ventricles / drug effects, pathology, physiopathology
Hemodynamics / drug effects
Imidazoles / pharmacology
Indoles / pharmacology
Lung / growth & development
Organ Size / drug effects
Peptidyl-Dipeptidase A / drug effects*
Receptor, Angiotensin, Type 1
Receptor, Angiotensin, Type 2
Receptors, Angiotensin / antagonists & inhibitors*
Tetrazoles / pharmacology
|0/Angiotensin-Converting Enzyme Inhibitors; 0/Imidazoles; 0/Indoles; 0/Receptor, Angiotensin, Type 1; 0/Receptor, Angiotensin, Type 2; 0/Receptors, Angiotensin; 0/Tetrazoles; 11128-99-7/Angiotensin II; 135145-96-9/L 158809; 87679-37-6/trandolapril; 9007-34-5/Collagen; 9041-90-1/Angiotensin I; EC 184.108.40.206/Peptidyl-Dipeptidase A; EC 3.6.1.-/GTP-Binding Proteins|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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