There are a number of reports describing that not only in visceral (1-3) but also vascular smooth muscles (4-6) Ca
++ may be the agent linking membrane excitation to contraction. Increasing [Ca
++]
0 may either stimulate (7, 8) or inhibit (9) vascular smooth muscles. Adrenaline and K
+ elicit contraction and an increase in the Ca
++ influx into smooth muscle cells (4, 10). Elevation of [Ca
++]
0 depresses the first part of the contractile response of aortic muscles to adrenaline but potentiates the second part (11). Excitation of nervous elements in vascular tissues by electrical transmural stimulation results in contraction and a sharp rise in the output of noradrenaline (12). Contractile responses of isolated vessels to stimulation of periarterial sympathetic nerves are shown to relate directly to [Ca
++]
0 ranging from 0 to 4.4 mM (13).
It seems likely that Sr
++ can substitute for Ca
++ in the contractile mechanism of skeletal, cardiac and smooth muscles (14-18) and in the release of the neurohumoral transmitter from sympathetic nerve terminals (18). It appears that Na
+ acts through an antagonism to Ca
++ on muscular contractility (4, 19) and uptake of noradrenaline by sympathetic nerves (20). Ouabain is known to increase the exchangeable Ca
++ fraction (21, 22), which would be expected to participate in increased contractility.
The present study was an investigation into the effects of ions and drugs that interact with Ca
++ on the resting tension of the vascular smooth muscle and on its contractile response to electrical transmural stimulation and exogenous noradrenaline.
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