Effects of caffeine and procaine on the membrane and mechanical properties of the smooth muscle cells of the rabbit main pulmonary artery.

Effects of caffeine and procaine on the membrane and mechanical properties of the smooth muscles of the rabbit main pulmonary artery were investigated using microelectrode and voltage clamp methods. Caffeine (greater than 0.5 mM) depolarized the membrane and increased ionic conductance. On the other hand, procaine (greater than 2.5 mM) depolarized the membrane, generated spikes and reduced the ionic conductance of the membrane. When depolarization-contraction relations were observed, the threshold depolarization to evoke contraction and the amplitude of the contraction were not affected by 5 mM procaine. However, the mechanical threshold was raised and the mechanical response was suppressed by treatment with 5 and 10 mM caffeine or 10 mM procaine. Procaine and caffeine accelerated the depletion of Ca++ from the stored sites of Ca-free (EGTA) solution, and suppressed the mechanical responses induced by chemical stimulation. Caffeine and procaine suppressed the increase in ionic conductance and depolarization produced by noradrenaline or prostaglandin F2alpha. Caffeine also suppressed the mechanical response induced by the above agents. Procaine suppressed the noradrenaline induced contraction, but accelerated the prostaglandin F2alpha induced contraction. From the above results, it is concluded that caffeine and procaine act not only on Ca-stored sites in the cell but also on the surface membrane. The actions of these agents were not competitive with each other, thus suggesting that the properties of the internal membrane structures, which is assumed to be a main Ca-storage site, are not exactly the same as those in striated muscles.