AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 257: H2001-H2005, 1989;
0363-6135/89 $5.00
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AJP - Heart and Circulatory Physiology, Vol 257, Issue 6 2001-H2005, Copyright © 1989 by American Physiological Society

ARTICLES

Role of calcium in U 46619 and PGF2 alpha pulmonary vasoconstriction in rat lungs

E. C. Santoian, A. D. Angerio, M. J. Schneidkraut, P. W. Ramwell and P. A. Kot
Department of Physiology and Biophysics, Georgetown University Medical Center, Washington, DC 20007.

The role of calcium and calmodulin during U 46619 and PGF2 alpha-induced pulmonary vasoconstriction was studied in isolated rat lungs perfused with Krebs-Ringer bicarbonate (KRB) or calcium-free KRB. In lungs perfused with KRB, bolus injections of U 46619 (0.2 microgram) and PGF2 alpha (40.0 micrograms) resulted in a 48.0 +/- 4.0 and 23.9 +/- 2.5% increase in mean pulmonary artery pressure, respectively. During lung perfusion with KRB without calcium, the U 46619 response decreased to 31.1 +/- 7.5% whereas the PGF2 alpha response increased to 34.6 +/- 4.1%. Repeated challenges with PGF2 alpha in the KRB without calcium resulted in reduction of the response to 11.8 +/- 1.2%; the U 46619 response was unaltered. The intracellular calcium blocker, 8-(N,N-diethylamino)-octyl-3,4,5, trimethoxybenzoate HCL (TMB-8) significantly attenuated the pressor response to U 46619 at low doses and PGF2 alpha at high doses. The calmodulin inhibitor trifluoperazine (TFP 100 microM) attenuated the vasoconstrictor response to U 46619 by 54%, whereas the PGF2 alpha was unchanged. However, in the calcium-free KRB, TFP attenuated the pressor response to both U 46619 and PGF2 alpha. The U 46619 pressor response depends on intracellular and extracellular calcium to achieve calmodulin-dependent vasoconstriction. PGF2 alpha requires extracellular calcium to replenish depletable intracellular calcium pools and is independent of calmodulin activation.


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J. K. Wright, L. T. Kim, T. E. Rogers, and R. H. Turnage
Prostaglandins potentiate U-46619-induced pulmonary microvascular dysfunction
J Appl Physiol, April 1, 2000; 88(4): 1167 - 1174.
[Abstract] [Full Text] [PDF]


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