Actions of Nipradilol (K-351), a New α- and β-Adrenoceptor Blocker, on the Rabbit Portal Vein

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Abstract
Nipradilol but not desnitro nipradilol ((N-)nipradilol) inhibited the norepinephrine (NE)-induced rabbit portal vein depolarization and contraction. The NE-induced contraction and depolarization were also blocked by prazosin, but not blocked by yohimbine. Nipradilol possesses an .alpha.1-blocking action. The order of potency was prazosin > nipradilol > yohimbine > (N-)-nipradilol = 0. With application of field stimulations to muscle tissues, the smooth muscle membrane was depolarized with a latency of several seconds, and the action potential was generated. These phenomena were blocked by tetrodotoxin (TTX), prazosin or nipradilol, but not by yohimbine. Isoproterenol (Isop) inhibited the 30 mM K-induced contraction, and this inhibitory action was blocked by (N-)nipradilol, nipradilol or propranolol, dose-dependently. The potency of .beta.-blocking actions of nipradilol was much the same as that observed by propranolol and (N-)nipradilol. When ipradilol (10-5 M) was applied to the tissue, the amplitude of the 30 mM K contraction was slightly reduced. Such inhibitory action was not observed by application of (N-)nipradilol. The Ki values of nipradilol for blocking actions on the NE-induced contraction and Isop-induced relaxation were of the same order of 10-7 M. The potencies of .alpha.1-blocking and .beta.-blocking actions of nipradilol may be the same in the rabbit portal vein. The vasodilating action of nipradilol on the rabbit portal vein apparently is mainly due to the .alpha.1-blocking action; the nitrate action of this agent may be weak.

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