Changes in extracellular potassium concentration influence arterial tone by modulating alpha- and beta-adrenergic effects and regulating neurotransmitter release from coronary nerves.
Does extracellular potassium concentration modulate adrenergic responsiveness and norepinephrine release in isolated canine coronary arteries?
Extracellular potassium concentration modulates coronary arterial tone through direct effects on adrenergic responsiveness and regulation of norepinephrine release from coronary nerves.
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 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.
Borda et al. (1977) studied this question. Extracellular potassium concentration changes was evaluated on Mechanical responsiveness and norepinephrine release. Changes in extracellular potassium concentration influence arterial tone by modulating alpha- and beta-adrenergic effects and regulating neurotransmitter release from coronary nerves.