Angiotensin II increases evoked release at the frog neuromuscular junction through a receptor sensitive to A779.

Receptor mediated presynaptic modulation is a ubiquitous mechanism involved in synaptic plasticity. Here we show that angiotensin II increased quantal content at the frog neuromuscular junction. This presynaptic effect of angiotensin II was insensitive to losartan and PD123319, but was antagonized by a more potent partial agonist of the amphibian angiotensin receptor, L162313. In addition, A779, a blocker of the angiotensin-[1-7] receptor, also abolished the effect of angiotensin II. These results indicate that the effect of angiotensin II on evoked release is mediated through an angiotensin receptor. L162313 alone increased quantal content, and A779 also antagonized this effect of L162313. We conclude that the neuromuscular junction possesses angiotensin receptors involved in presynaptic modulation.