Mechanism of Reversal of the Vasomotor Effect of Isoprenaline

Abstract

IT is interesting to see in the preceding communication that Gutman and Beyth have obtained, using isoprenaline or adrenaline as reversing agents in the spinal cat, similar results to Walz, Koppanyi and Maengwyn-Davies¹. However, several points seem to require clarification. As I have said previously^2a, I do not consider that the effects obtained by these workers are produced by the same mechanism as are obtained when larger doses of isoprenaline are given. I have suggested^2b that, when larger doses are given, the first dose produces β-adrenergic blockage and this then reveals the weak α-adrenergic activity of isoprenaline, thus causing a rise in blood pressure. It is probable that when smaller doses of isoprenaline are given they are insufficient to produce a β-blockade.