AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 272: H2616-H2621, 1997;
0363-6135/97 $5.00
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AJP - Heart and Circulatory Physiology, Vol 272, Issue 6 2616-H2621, Copyright © 1997 by American Physiological Society

ARTICLES

Possible role of T-type Ca2+ channels in L-NNA vasoconstriction of hypertensive rat lungs

M. Muramatsu, R. C. Tyler, D. M. Rodman and I. F. McMurtry
Department of Medicine, University of Colorado Health Sciences Center, Denver 80262, USA.

Acute inhibition of endothelium-derived nitric oxide (NO) synthesis by L-arginine analogs such as N omega-nitro-L-arginine (L-NNA) has little effect on basal vascular tone in normal rat lungs but elicits marked vasoconstriction in hypertensive lungs. The NO-suppressible vasoconstriction is dependent on extracellular Ca2+ but is not mediated by L-type Ca2+ channels. This study tested whether the response was mediated by Ca2+ influx through receptor-operated channels, reverse Na+/Ca2+ exchange, or low-threshold voltage-gated (T-type) Ca2+ channels. We first examined whether SKF-96365, a blocker of receptor-operated Ca2+ channels, inhibited L-NNA-induced vasoconstriction in salt solution-perfused hypertensive lungs isolated from chronically hypoxic male rats (exposed to hypobaria of 410 mmHg for 3-5 wk). Whereas 50 microM SKF-96365 inhibited pressor responses to angiotensin II and acute hypoxia, it did not reduce vasoconstriction in response to 100 microM L-NNA. We next examined effects of pretreatment with Na+/Ca2+ exchange blockers and observed that L-NNA vasoconstriction was reduced by both 100 microM amiloride and 50 microM ethylisopropyl amiloride (EIPA). The third experiment showed that each of two different blockers of T-type Ca2+ channels, 10 microM Ro-40-5967 and 300 microM nordihydroguariaretic acid, inhibited L-NNA vasoconstriction and that the combination of EIPA and Ro-40-5967 did not cause more inhibition than did Ro-40-5967 alone. These results suggest that, whereas receptor-operated Ca2+ channels are not significantly involved in the mechanism of NO-suppressible vasoconstriction in hypertensive rat lungs, Ca2+ influx through reverse Na+/Ca2+ exchange and/or T-type Ca2+ channels may play a role. Because both amiloride and EIPA also inhibit T-type Ca2+ channels, we speculate that Ca2+ influx through these channels rather than through reverse Na+/Ca2+ exchange is an important mediator of the vasoconstriction.


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K.-X. Li, B. Fouty, I. F. McMurtry, and D. M. Rodman
Enhanced ETA-receptor-mediated inhibition of Kv channels in hypoxic hypertensive rat pulmonary artery myocytes
Am J Physiol Heart Circ Physiol, July 1, 1999; 277(1): H363 - H370.
[Abstract] [Full Text] [PDF]


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