On the basis of a study of the activity of five sympathomimetic amines, Ahlquist in 1948 classified adrenoceptive receptors into two main types, which he designated alpha and beta. This classification has been vindicated by the development of drugs which specifically block the effects of stimulation of one type of receptor but not the other. Classical adrenergic blocking drugs such as phenoxybenzamine, dibenamine, phentolamine, tolazoline and dihydroergotamine block the effects of stimulation of alpha receptors but not beta receptors (Nickerson, 1949;Levy & Ahlquist, 1961 ;Moran & Perkins, 1961). These drugs are now described as adrenergic alpha receptor blocking agents. Recently several compounds have been described which block beta receptors but not alpha receptors. These, adrenergic beta receptor blocking agents, include dichloroisoprenaline (Powell & Slater, 1958) (Shanks, Wood, Dornhorst &Clark, 1966) and H 56/28 (Johnsson, Norrby, Solvell &Ablad, 1966). Structurally these compounds are closely related to each other and may be considered as derivatives of isoprenaline; in each case the side chain is identical with that of isoprenaline, or as in the last three compounds differs by the addition of an -OCH2 group. The blocking activity of these compounds is similar qualitatively, in that they block all beta receptors, but differs quantitatively. Another group of compounds, which block some but not all beta receptors, has recently emerged. These compounds include N-isopropylmethoxamine (Levy, 1964) which blocks beta receptors in the rat uterus; N tertiary butylmethoxamine (Levy, 1966a), and dimethyl isopropylmethoxamine (Levy, 1966b) which block beta receptors in the rat uterus, canine intestine and peripheral blood vessels. None of these compounds blocks the cardiac inotropic or chronotropic actions of catecholamines. Structurally these compounds are characterized by having a methyl group attached to the alpha carbon atom of the side chain. These observations suggest that beta receptors are not a homogenous group and may be capable of division into sub-groups. This hypothesis is further substantiated by the present paper in which

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PIlar,uac'uh'ic'. Di)ivisioii, Imipcrial Chlemiical Inidustrie.s Limitedl, A lderlev Park, MaCcle,.fiw/1dl1. The changes in heart rate and arterial pressure produced by the intravenous injection of isoprenaline (05 [rg/kg), noradrenaline (10 jg/kg), phenylethylamine (0.5 mg/kg), amphetamine (0 5 mg/kg) and by bilateral occlusion of the carotid arteries and by stimulation of the central ends of both vagus nerves have been recorded in groups of dogs anaesthetized with pentobarbitone.2. The acute intravenous injection of propranolol (1 mg/kg) reduced the increases in heart rate produced by the six procedures, the increases in arterial pressure in response to the last five procedures and the decrease in pressure produced by isoprenaline. 3. This decrease produced by propranolol in the pressor responses resulted from a reduction in the increases in cardiac output elicited by the five procedures and has been attributed to blockade of cardiac adrenergic ,0-receptors. 4. Three groups of dogs were pretreated for 6 weeks by the oral administration of either placebo, propranolol 50 mg/kg daily or propranolol 10 mg/kg twice daily. The responses to the six test procedures were obtained 17 24 hr after the last dose of propranolol, when only minimal blockade of adrenergic /99-receptors was present. In the propranolol-treated groups, the pressor response to carotid occlusion but not to the other test procedures was significantly reduced. 5. The pressor response to carotid occlusion was not reduced in a fourth group ot dogs given a single dose of propranolol (50 mg/kg) 24 hr before the test procedures. 6. The mechanism of this selective reduction in the pressor response to occlusion of the carotid arteries is not clear. It is suggested that it may contribute to the hypotensive action of propranolol in man during prolonged oral administration.Several reports have shown that the intravenous injection of propranolol (5 15 mg) under resting conditions in patients with normal or raised arterial pressure

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