A comparison of the ability of various α‐adrenoreceptor agonists to induce EGTA‐resistant contractions of rat aorta

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Abstract
Phenylephrine (PE) and Guanfacine (GU) produced maximum contractions of rat isolated aorta which were 96.8 .+-. 1.3% and 96.0 .+-. 2.8% respectively of the maximum responses induced by noradrenaline (NA). The responses produced by maximum concentrations of NA following 2 min incubation of the preparations with 3.0 mM EGTA were 38.1 .+-. 1.2% of the maxima achieved in normal Krebs. PE produced maximum EGTA-resistant responses which were significantly less than those seen with NA; GU produced EGTA-resistant responses which were significantly less than those to PE. The concentration response curves to NA and PE were shifted to the right by incubation with EGTA. The curve for PE was shifted by a significantly greater degree than that for NA. Amidephrine, UK-14,304 and St-587 produced only nominal EGTA-resistant responses even though one of these (UK-14,304) produced contractions in normal Krebs which were almost 70% of the maximum achieved by NA. The log dose ratio for all agonists (except amidephrine) were similar following the addition of 5 nM prazosin. Amidephrine had no effect in the presence of this concentration of prazosin. It is concluded that all agonists tested were acting on .alpha.1-adrenoreceptors. Prazosin (5 nM) but not corynanthine (2.5 .mu.M) slowed the rate of rise of contraction of all agonists tested. It is proposed that the rate of rise of agonist/receptor combinations is an important determinant of .alpha.-adrenoreceptor agonist induced EGTA-resistant responses in rat aorta.

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