Recovery of the slow action potential is hastened by the calcium slow channel agonist, Bay-K-8644

Potassium channel blockers differentially affect carbachol and (−)‐N6‐phenylisopropyladenosine on guinea‐pig atria

“…K+ 22 mm abolishes the contractility of atria by inhibiting the fast Na' current (Thyrum, 1974). Further addition of catecholamines (or of other positive inotropic agents such as Ca2", or histamine) together with suitable conditions of electrical stimulation, induces slow action potentials chiefly due to Ca2 + currents (Pappano, 1970;Thyrum, 1974;Sada et al, 1986). In our experiments, slow action potentials were evoked by adding noradrenaline 3 yM.…”

“…R-PIA is still effective in the presence of TEA or of 4-AP, implying a negative effect on Ca2+-channels. This is further supported by the effect of TEA in experimental conditions where slow Ca2+ currents through L-channels are activated: 22 mm K+ inhibits the fast Na+ current thus abolishing the contractility of atria; the addition of noradrenaline together with suitable electrical stimulation induces slow action potentials chiefly due to slow Ca2 + currents (Pappano, 1970;Thyrum, 1974;Sada et al, 1986). In such experimental conditions, carbachol is not effective, while R-PIA is still inhibitory.…”

“…An equilibration period of 60 min was allowed before experiments were started. To investigate the calciumdependent responses, the fast Na+ channels were inactivated by elevating the external potassium concentration to 22mM (Pappano, 1970;Thyrum, 1974;Sada et al, 1986); equimolar NaCl was subtracted to maintain constant osmolarity. Under these conditions, contractility disappeared.…”