Key result
Adenosine had no direct inhibitory effect on either the contractile apparatus or calcium release from sarcoplasmic reticulum in skinned bovine coronary arteries.
Adenosine does not directly inhibit the contractile apparatus or calcium release from the sarcoplasmic reticulum in bovine coronary arteries.
In vitro adenosine relaxation data in bovine coronaries warrant clinical caution against extrapolation; leaves open mechanistic insights pending human in vivo validation.
We have investigated the mechanism of adenosine-induced relaxation in relation to its effects on intracellular organelles in Triton X-100- and saponin-skinned bovine coronary arteries. In intact coronary arteries, high K+ and prostaglandin F2 alpha caused sustained contractions, whereas caffeine produced transient contractions. Triton X-100 treatment abolished these contractions. However, Triton X-100-skinned coronary arteries were responsive to added free calcium. There was no significant difference between calcium concentration-response curves obtained in the absence and presence of adenosine (50 microM). Unlike Triton X-100, in saponin-skinned arteries, caffeine produced transient contractions but high K+ and prostaglandin F2 alpha did not. Adenosine had no effect on caffeine-induced contractions in saponin-skinned coronary arteries. These data suggest that adenosine had no direct inhibitory effect on either the contractile apparatus or calcium release from sarcoplasmic reticulum in coronary arteries.
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Ramagopal et al. (1992) studied this question. Adenosine vs. Absence of adenosine was evaluated on Calcium concentration-response curves and caffeine-induced contractions. Adenosine had no direct inhibitory effect on either the contractile apparatus or calcium release from sarcoplasmic reticulum in skinned bovine coronary arteries.
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