Spontaneous rhythmic contractions in isolated rat thoracic aorta depend on temperature and calcium entry, demonstrating inherent contractile capabilities of large elastic arteries.
The mechanism of spontaneous contraction of vascular smooth muscles in the elastic artery was studied in a ring-shaped preparation isolated from the rat aorta. The observation of small changes in vascular tension with a high gain AC amplification of tension signal provided a reliable detection of spontaneous contractions. The spontaneous rhythmic contraction (RC) occurred consistently in the preparation taken from the thoracic aorta without external stimuli. The RC (frequency, 5-20 cycle/min; amplitude, 10-100 mg) was accompanied with small oscillatory changes in the membrane potential (2-5 mV, peak to peak). A reduction in temperature (below 30 degrees C) or superfusing the preparation with Ca-free solution inhibited the generation of RC. Ca-entry blockers (verapamil and nifedipine) also inhibited the RC. The cessation of RC by these procedures reduced the vascular tension by about 40% of control baseline tension. The application of adrenergic blockers had little effect on the pattern of RC and on the vascular tension. The results suggest that the RC is generated by a synchronization of electrical and mechanical activities in relatively small groups of smooth muscle cells, which depends upon the temperature and requires the Ca-entry into the cells. The process of initiation of spontaneous RC in the rat aorta was discussed.
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Hayashida et al. (1986) studied this question.
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