Potentiation of the Contractile Response of Isolated Aortae to Transmural Stimulation by Angiotensin

Electrical transmural stimulation (0.3 msec duration at frequencies of 5, 20 and 100/sec) was given to spirally-cut strips of the ascending aorta from rabbits. Angiotensin (5 × 10−11 to 10−9 M) significantly potentiated the contractile response to transmural stimulation but did not influence the response to exogenously-applied noradrenaline. In response to angiotensin, percent increase in the duration of contraction induced by transmural stimulation was approx. proportional to that in the developed tension, whereas a prolongation of the duration by cocaine greatly exceeded the increase in the tension. The contractile response to transmural stimulation was suppressed by 5 × 10−6M bretylium. The inhibitory1 effect of bretylium was not antagonized by angiotensin when administered prior to bretylium and after the bretylium-induced inhibition had been established. Cocaine reversed the inhibition by bretylium to a potentiation. The Mg++-induced inhibition of the response to transmural stimulation was not reversed by angiotensin but by excess Ca++. It appears that the angiotensin-induced potentiation of the contractile response to transmural neural stimulation is due mainly to a facilitation of the release of noradrenaline and that angiotensin does not participate in Ca++-Mg++ interactions relating to the release of sympathetic transmitters.