Abstract |
The cardiac cellular effects of endothelin-1 (ET-1) on intracellular free Ca2+ concentration ([Ca2+]i) were investigated in deoxycorticosterone acetate ( DOCA)- salt rats with severe cardiac hypertrophy. [Ca2+]i was measured by fura-2 methodology in ventricular cardiomyocytes and fibroblasts of DOCA- salt hypertensive and control unilaterally nephrectomized rats (Uni-Nx). Blood pressure and heart weight were increased (p < 0.01) in DOCA- salt rats compared to control rats. ET-1 (10(-12)-10(-6) M) increased [Ca2+]i in a dose-dependent manner in both cell types from control and hypertensive rats. However, ET-1-induced [Ca2+]i responses were significantly attenuated (p < 0.01) in cardiomyocytes and fibroblasts of DOCA- salt rats. Sarafotoxin S6c (S6c) increased [Ca2+]i in fibroblasts but not in cardiomyocytes. In conclusion, ET-1 dose-dependently increased [Ca2+]i in cardiomyocytes (primarily via ETA receptors) and fibroblasts (via ETA and ETB receptors). Cardiac cell ET-1 signaling pathways are blunted in DOCA- salt hypertensive rats. ET-1 may not play a critical role in the pathophysiology of the severe concentric cardiac hypertrophy present in DOCA- salt hypertensive rats.
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Authors | R M Touyz, J Fareh, G Thibault, E L Schiffrin |
Journal | Journal of cardiovascular pharmacology
(J Cardiovasc Pharmacol)
Vol. 31 Suppl 1
Pg. S179-81
( 1998)
ISSN: 0160-2446 [Print] United States |
PMID | 9595432
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Endothelin-1
- Desoxycorticosterone
- Sodium Chloride
- Calcium
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Topics |
- Animals
- Blood Pressure
(drug effects)
- Calcium
(metabolism)
- Cardiomegaly
(etiology, physiopathology)
- Cells, Cultured
- Desoxycorticosterone
- Endothelin-1
(physiology)
- Fibroblasts
(metabolism)
- Heart
(drug effects, physiopathology)
- Hypertension
(chemically induced, complications, physiopathology)
- Male
- Myocardium
(cytology)
- Rats
- Rats, Sprague-Dawley
- Signal Transduction
(physiology)
- Sodium Chloride
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