Effects of cooling on depolarized smooth muscle were studied using guinea-pig was deferens.
Cooling treatment of high-K-depolarized preparation caused tesion development. The maximum tension was observed by coolin the preparations from 35°C to 20°C. Lowering the temperature below 10°C caused relaxation of the preparations. No change or only a small change in membrane potential was observed by cooling, whereas the membrane resistance increased. Rapid cooling caused a phasic contraction followed by sustained tonic contraction.
The tension development was sensitive to extracellular Ca and no tension development was observed by cooling the preparation in Ca-free solution. The increase in Ca concentration of K-Tyrode solution caused further increase in tension development by cooling, whereas it caused only a small increase in tension at 35°C
It was suggested that the tension development would be caused by the inhibition of Ca extrusion through cell membrane (Ca pump), but not by the increase in Ca influx.

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The terminal of the guinea pig bile duct separates into two parts: the terminal cavity connects to the bile duct proper through the sphincter area, and the ampulla connects to the duodenum. These parts exhibit differences which are discussed in this report.
Four different results were produced by transmural stimulation. Type I was contraction during stimulation. This type and Type IV, absence of any response, were observed about equally in both parts. Type II, relaxation during stimulation, followed by contraction after stimulation, was seen much more in the terminal cavity than in the ampulla. Type III, inhibition of spontaneous contracitons during stimulation plus poststimulus contraction, occurred exclusively in the ampulla.
Type I was considered to be elicited by ACh released from cholinergic neurons. The relaxation of Type II may have been due to non-adrenergic inhibitory neurons.
In the terminal cavity, activation of α receptors caused contraction, and β receptors caused relaxation. In the ampulla, both α and β receptors caused relaxation.
Norepinephrine inhibited the contractions caused by endogenous ACh, but did not affect response to exogenous ACh. Inhibition by norepinephrine was blocked by phentolamine. Presynaptic inhibition of cholinergic excitation thus seemed to be present in both parts.
Caerulein elicited contractions in both parts: in the terminal cavity, by direct action on the muscle, and, in the ampulla by intramural cholinergic neurons.

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