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Early clinical experience with propranolol indicated that it could precipitate severe bronchospasm in patients with bronchial asthma (McNeill, 1964; McNeill & Ingram, 1966), presumably due to its effect on /i-adrenoceptors in the bronchi. Subsequently, Lands, Luduena & Buzzo (1967) suggested that /-adrenoceptors could be subclassified into those mediating cardiac effects (J1) and those responsible
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DG McDevitt (1978) studied this question.
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