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AJP - Heart and Circulatory Physiology, Vol 261, Issue 6 1945-H1950, Copyright © 1991 by American Physiological Society
ARTICLES |
D. Rampe, A. E. Lacerda, R. C. Dage and A. M. Brown
Marion Merrell Dow Research Institute, Cincinnati, Ohio 45215.
We have tested the effects of the active 1-34 amino acid sequence of rat parathyroid hormone (PTH) on Ca2+ channel activity in neonatal rat ventricular cells. Rat PTH (30 pM to 10 nM) increased depolarization-induced Ca2+ influx into these cells, an effect that was abolished by 1 microM nifedipine. The 1-34 amino acid sequence of bovine PTH also stimulated Ca2+ influx in control cells but not in cells pretreated with cholera toxin. Rat PTH also elevated adenosine 3',5'-cyclic monophosphate accumulation in these ventricular myocytes. Whole cell voltage-clamp recordings confirmed a stimulatory effect of rat PTH on cardiac L-type Ca2+ channels. Cell-attached single channel recordings revealed an increase in the probability of channel opening as the primary mechanism for the enhancement of Ca2+ current. Taken together these results suggest an important role for PTH as an endogenous modulator of cardiac L-type Ca2+ channels.
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R. Meyer, R. Schreckenberg, F. Kretschmer, A. Bittig, C. Conzelmann, C. Grohe, and K.-D. Schluter Parathyroid hormone-related protein (PTHrP) signal cascade modulates myocardial dysfunction in the pressure overloaded heart Eur J Heart Fail, December 1, 2007; 9(12): 1156 - 1162. [Abstract] [Full Text] [PDF] |
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