Taurine depletion was induced by either incubation of isolated myocytes with 5 mM β-alanine or feeding rats with water containing 3% β-alanine. Hearts of taurine depleted rats exhibited an impairment in myocardial relaxation, associated with a decrease in Na+- Ca2+ exchanger activity. Exposure of the heart to angiotensin II, an activator of the Na+- Ca2+ exchanger, eliminated the relaxation defect. In agreement with the contractile results, taurine depletion prolonged the calcium transient, an effect which was partially eliminated by exposure to angiotensin II. Although peak systolic [Ca2+](i) was modestly depressed in the taurine depleted myocyte, peak ventricular pressure was normal. This may be related to an elevation in pH, induced by taurine depletion. Angiotensin II had little effect on contractility of the taurine depleted heart, presumably because of two opposing effects, a reduction in pH(i) and an increase in [Ca2+](i). Thus, taurine depletion alters contractile function and ion transport and both of these effects are modulated by exposure of the heart to angiotensin II.
|Number of pages||8|
|Journal||Advances in Experimental Medicine and Biology|
|State||Published - 1998|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology (all)