When rabbit aortic strips were incubated for 1 hour in Ringer's solution containing 10 −5 M chlorpromazine, 10 −4 M Dibenamine, or 10 −4 M phenoxybenzamine, or 2 hours in calcium-free Ringer's solution, they failed to respond to high potassium (10–80 mM). With increasing external calcium this inhibitory action on the potassium-induced contraction decreased. Incubation in solutions containing 10 −4 M phentolamine, dihydroergotamine, yohimbine, azapetine, pronethanol, dichloroisoproterenol, or MJ 1998 did not inhibit the response to potassium. The responses to angiotensin (5 × 10 −7 M) were not antagonized by any of the blocking agents. It was found that the three agents blocking the potassium-induced contraction inhibited calcium-45 uptake during these contractions; however, they did not inhibit the calcium-45 uptake of unstimulated muscle. The other agents tested failed to decrease the calcium-45 influx during potassium contraction. There were no tissue electrolyte changes found after treatment of the aortas with any of the agents. The results suggest that the inhibition observed was mediated by a decrease in calcium movement rather than a decrease in potassium movement into the intracellular space.
No takes yet. Share an insight, caveat, or question.
Shibata et al. (1967) studied this question.