Patterns of sympathetically mediated acute pressor responsesThe classical work of Goldenberg et al. (1948) and Barcroft & Starr (1952) in healthy volunteers, demonstrated that intravenous (i.v.) infusion of adrenaline (over 5-35 minutes) reduced diastolic blood pressure and peripheral resistance (a,-receptor mediated vasoconstriction being more than balanced out by R2-receptor mediated vasodilatation), but increased systolic pressure and heart rate (fl-receptor mediated and reflex effects). By contrast, noradrenaline infusion increased peripheral resistance, diastolic and systolic pressure (a-receptor mediated vasoconstriction) and reduced heart rate (reflexly). During prolonged (1 hour) catecholamine infusions, however, feedback through presynaptic P (facilitatory) and a2 (inhibitory) receptors may become evident (Brown et al., 1985) and greatly complicate the resultant haemodynamic response.Theoretical concerns, that antagonism ofP-receptor mediated vasodilatation might elevate blood pressure in sustained hypertension, were eventually refuted. However, Prichard & Ross (1966) demonstrated, in phaeochromocytoma patients pretreated with phenoxybenzamine, increases in lying and standing systolic and diastolic blood pressure lasting about 8 hours after single 80 mg doses of oral propranolol. Presumably, P-receptor mediated vasodilatation due to circulating adrenaline was antagonized, thus unmasking a-receptor mediated vasoconstriction leading to increased peripheral resistance and venoconstriction.