Possible increases in potassium conductance by apamin in mammalian ventricular papillary muscles: a comparison with the effects on enzymatically isolated ventricular cells.
Apamin, a bee venom polypeptide, is reported to block the Ca2+-dependent K+ channel in smooth muscle, hepatocyte, and neuroblastoma cells. In embryonic chick hearts, it was found to block the Ca2+ channel. We report here that apamin (10(-9)-10(-7) M) hyperpolarizes the resting membrane potential and shortens the duration of the action potential (AP) in the fast response of adult guinea pig ventricular papillary muscles. This peptide also depresses the isoproterenol or Ba2+-induced slow response APs in the presence of high K+ (21.6 mM) Tyrode solution, without affecting the resting potential. The most striking effect of apamin on the slow response was to shorten the duration of AP with only slight decreases in the maximal rate of increase (Vmax) of the AP, a nonlinear measure of Ca2+ currents. These findings suggest that apamin increases membrane K+ conductance in the mammalian ventricular myocardium. However, in enzymatically isolated single ventricular cells and at wide range of concentrations (10(-7)-10(-11) M), apamin did not affect the AP configuration and did not alter the membrane Ca2+ or K+ current, perhaps because of a loss of apamin sensitivity secondary to enzymatic digestion of the tissue with collagenase.[1]References
- Possible increases in potassium conductance by apamin in mammalian ventricular papillary muscles: a comparison with the effects on enzymatically isolated ventricular cells. Nakagawa, A., Nakamura, S., Arita, M. J. Cardiovasc. Pharmacol. (1989) [Pubmed]
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