Abstract
Superfusion of rat anterior pituitary cell aggregates with 10-min pulses of 0.1–10 nM angiotensin II (AII) resulted in a prompt and concentration-dependent rise of PRLrelease. The effect could be blocked by saralasin, an AII receptor antagonist. The response to AII, but not that to TRH, was rapidly desensitized:a 10 nM AII pulse caused an 80% depression of the response to a subsequent 10 nM pulse given 50 min later. The data provide a possible functional significance for the renin-angiotensin system recently demonstrated in the anterior pituitary.