Mechanism of hydralazine-induced relaxation of arterial smooth muscle

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Abstract
The effect of hydralazine on contractile responses by various agents has been studied in isolated rat tail artery strips. Hydralazine caused dose-dependent relaxation of contractions produced by 10−7mol·litre−1 noradrenaline (N); 10−7mol·litre−15-HT or 100 mmol·litre−1KCl, suggesting that the relaxation response is non-specific. CaCl2 dose-response (in the presence of 10−5mol·litre−1N; 10−5mol·litre−15-HT or 100 mmol·litre−1 KCl) was significantly inhibited by 5 × 10−4mol·litre−1 hydralazine in the order: KCl >5-HT>N. Hydralazine also inhibited BaCl2 dose-response curve (in K+-depolarised strips); maximal contraction to BaCl2 was depressed by 87%. In other experiments, hydralazine significantly depressed (by 20%) the phasic contractile response to N due to mobilisation of calcium from a membrane-bound pool. D 600, a calcium entry blocker, also caused dose-dependent relaxation of contractile responses to all three agents studied; and inhibited CaCl2 and BaCl2 dose-response curves in K+-depolarised media, as well as depressed the phasic contractile response to N in Ca-free media by 17%. These results suggest that in the rat tail artery, hydralazine interferes with Ca2+ influx, as well as release from a membrane-bound pool.

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