Nitric oxide and sodium nitroprusside (3 x 10(-5) M) attenuated isolated guinea pig cardiac myocyte contraction amplitude by 23%, acting via cyclic GMP production.
Does nitric oxide attenuate cardiac myocyte contraction in isolated guinea pig cardiac myocytes?
Nitric oxide attenuates cardiac myocyte contraction, likely via cGMP production, suggesting endothelial products may play an important role in myocardial function.
Cardiac muscle fibers have microvessels in close proximity, the distance from the nearest capillary being no greater than 8 microns. We performed experiments on isolated, electrically stimulated, contracting guinea pig cardiac myocytes to test whether NO from endothelium or nitrovasodilators or directly superfused in solution might affect myocyte contractility. In endothelium-myocyte coculture experiments, 10(-7) M bradykinin reduced myocyte shortening by 11 +/- 3.5%. This effect was abolished in the presence of NG-nitro-L-arginine methyl ester and was unaffected by indomethacin. Sodium nitroprusside, but not organic nitrovasodilators, reduced myocyte contraction amplitude by 23% at 3 x 10(-5) M. This effect was reversed by methylene blue. Superfusion with NO solution had an effect similar to sodium nitroprusside, as did exposure to 8-bromoguanosine 3',5'-cyclic monophosphate. Thus the present study shows that cardiac myocyte contraction is attenuated by NO, which appears to act via production of guanosine 3',5'-cyclic monophosphate within the myocytes. Because cardiac myocytes in vivo are in such close proximity to endothelium, the effects of endothelial products on cardiac myocyte contractility may be important in myocardial function.
Brady et al. (Thu,) conducted a other in Cardiac myocyte contractility. Nitric oxide (NO) and nitrovasodilators was evaluated on Myocyte shortening and contraction amplitude. Nitric oxide and sodium nitroprusside (3 x 10(-5) M) attenuated isolated guinea pig cardiac myocyte contraction amplitude by 23%, acting via cyclic GMP production.