Electrical responses of guinea pig coronary artery to transmural stimulation.

Isolated segments of the guinea pig circumflex coronary artery were stimulated transmurally with brief duration (0.05 msec) pulses while recording intracellularly. Resting membrane potential was -60.3 +/- 4.3 mV (n = 66). Transient depolarizations (TDs) graded in amplitude with stimulus intensity were elicited with single stimuli. An action potential of 47 +/- 5 mV was superimposed upon the TD above a threshold membrane potential of -48 +/- 4 mV. Following the spike, a period of slow repolarization requiring 77 +/- 33 seconds was observed. Repetitive stimulation led to summation of TDs and a slow depolarization (less than or equal to 21 mV) that persisted for up to 90 seconds. The TD was reduced in amplitude when the membrane was depolarized with increased [K]o and enhanced when the membrane was hyperpolarized by adding potassium back to a potassium-depleted tissue. Phentolamine (10(-5) M), prazosin (10(-6) M), guanethidine (2 X 10(-5) M), alpha,beta-methylene ATP (2 X 10(-5) M), tetrodotoxin (10(-6) M), and 10-20 mM norepinephrine did not block TDs, action potentials, or slow depolarization. TDs were abolished following cold storage (4 degrees C) for 4 days and significantly reduced in a 2.25-mM CdCl2 solution with 0.25 mM CaCl2. Acetylcholine (10(-8) M to 10(-5) M) produced membrane hyperpolarization and reduced the amplitude of TDs and altered their time course. Atropine (10(-5) M) blocked the effects of acetylcholine but had no effect on the response to nerve stimulation. These observations indicate that TDs exhibit some, but not all, of the properties characteristic of excitatory junction potentials obtained with release of neurotransmitter substances in other vessels. If these TDs are neural events, they must involve a transmitter other than norepinephrine, acetylcholine, or ATP.