Effects of potassium on isolated canine coronary arteries. Modulation of adrenergic responsiveness and release of norepinephrine.

We studied effects of changes in the extracellular potassium concentration (|K* ]") on the mechanical responsiveness of canine coronary artery preparations. Four different contractile behaviors were delineated between | K *),, = 0 and 40 HIM: (1) at [K + ] o < 1 mu, a contracture developed which was augmented by /3-adrenergic stimulation and inhibited by propranolol, 1 x 10~7M; (2) at |K*| (I between 1 and 2.5 mti, arterial tone was minimum and propranolol acted as a potent constrictor. Within this range of [K + ],,, arteries exhibited calciuminduced relaxations and verapamil-induced contractions; (3) at |K* |,, between 5 and 15 mM there was a steep rise in force which was increased by isoproterenol (/3-adrenergic contraction), almost completely blocked by L-propranolol, but not attenuated by a-adrenergic blockade with phentolamine; (4) at |K' ] > 30 mM, effects of /3-adrenergic stimulation and blockade became very small. Steady increases in force elicited by isoproterenol and by sudden increases in [K + ] o were preceded by transient relaxations. Effects of exogenous and endogenous (tyramine, nerve stimulation) norepinephrine paralleled those of isoproterenol and were blocked by propranolol but not attenuated by phentolamine. In contrast, modulation of the effects of phenylephrine by potassium consisted of monotonicaUy increasing constrictor responses over the whole range of |K'| 0 tested. Arteries labeled with ( 3 H)-norepinephrine showed substantial changes in ( 3 H)-efTlux with relatively small changes in [K + ] o . Maximum releases were observed with |K* I,, ranging between 10 and 25 mM. The smallest releases were observed at the highest (K + | o (40 mM). Thus, changes in [K + ] o influence arterial tone by modulating or-and /3-adrenergic effects and by regulating the release of neurotransmitter from the coronary nerves.