Contraction of vascular muscle as related to membrane potential and calcium fluxes.

Using the rabbit main pulmonary artery (RMPA) as an example of vascular smooth muscle, the processes underlying contraction to high potassium as well as to alpha 1- and alpha 2-adrenoceptor agonists have been analyzed in terms of changes in membrane potential and availability of calcium. In strips of RMPA, contraction to high potassium depends strictly on the presence of external calcium and evidence is provided that the overwhelming part of the activator calcium enters the cells through voltage-dependent calcium channels. The majority of these calcium channels opens in the potential range between -45 and -33 mV (resting membrane potential of RMPA close to -60 mV) and is highly susceptible to blockade by calcium antagonists. Depolarization by noradrenaline and alpha 1-adrenoceptor agonists appears to be too small to open voltage-dependent calcium channels and the same holds true for alpha 2-agonists. Calcium antagonists and omission of calcium from the bath fluid have a relatively minor inhibitory effect on alpha 1-agonist-induced contraction. This suggests that the major part of the activator calcium is released in this case from cellular storage sites. Under the same experimental conditions, alpha 2-agonist-induced contractions are highly susceptible to inhibition by calcium antagonists and by calcium withdrawal. It is hypothesized that alpha 2-agonists open receptor-operated calcium channels. This explanation is complicated by the absence of clearcut evidence for two different types of alpha-adrenoceptor in the RMPA.