Changes induced by angiotensins and prostaglandin E2 on the release of transmitter from isolated perfused rabbit kidney during periarterial stimulation.

The influence of A II and PGE2 on the rise of perfusion pressure induced by periarterial stimulation and NA were studied in the rabbit isolated perfused kidney. Periarterial stimulation produced an increase in perfusion pressure and the venous outflow superfusing the rabbit aortic strip caused the muscle to contract. Both effects were found to be frequency dependent. NA induced similar effect when given into the renal artery. A II and its N-terminal analogs produced equal potentiation to periarterial stimulation without altering the effect of exogenous NA when added to the perfusion medium. DMGIA II which is a competitive inhibitor of A II inhibited the potentiating affect of A II. PGE2 also inhibited the effect of A II without altering the effect of exogenous NA. Addition of aspirin to the perfusion medium caused a potentiation to periarteral stimulation but did not change the effect of NA. A II added to the perfusion fluid containing aspirin still caused potentiation. From these results it was concluded that: (i) A II-induced potentiation to periarterial stimulation is mediated via specific receptors and probably due to facilitation of the release of transmitter from sympathetic nerve ending. (ii) PGE2 inhibited the release of transmitter. The effect of A II and PGE2 seemed to be mediated by independent mechanisms.