Abstract
The pharmacological effects of norathyriol on isolated rat thoracic aorta were examined. In the high-K + (60 mM) medium, Ca 2+ (0.03 to 3 mM)-induced vasocontraction was inhibited concentration dependently by norathyriol. Given as pretreatment norathyriol (20 to 200 μM) also inhibited the norepinephrine (NE, 3 μM)-induced tonic contraction. However, the phasic contraction was inhibited only by high concentrations of norathyriol (200 and 400 μM). The tonic contraction elicited by NE was also relaxed by the addition of norathyriol. This relaxing effect of norathyriol was not antagonized by methylene blue (50 μM) or indomethacin (20 μM) and was still seen in denuded rat aorta. Although the cAMP level was not changed by norathyriol, the cGMP level was increased by a high concentration of norathyriol (400 μM). [ 3H]Inositol monophosphate formation caused by NE was not affected by norathyriol at concentration of either 100 or 400 μM. The 45Ca 2+ influx caused by either NE or high K + was inhibited by norathyriol in a concentration-dependent manner. It is concluded that norathyriol relaxed the rat thoracic aorta mainly by suppressing the Ca 2+ influx through both voltage-dependent and receptor-operated calcium channels.
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