Neural mechanisms affecting pressor responses to angiotensins in the Pekin duck, Anas platyrhynchos.
1. Administration of SQ20881 diminished pressor responses to intravenous (i.v.) injections of angiotensin I (AI), but not those to injections of angiotensin II (AII), in Pekin ducks, indicating the occurrence of a mechanism similar to the mammalian angiotensin-converting enzyme reaction. 2. Pressor responses to AII were enhanced by general anaesthesia with phenobarbital, pentobarbital, or a combination of both phenobarbital and pentobarbital. 3. Ganglionic blockade with mecamylamine enhanced the pressor responses to AII and NE, but not those to tyramine, in anaesthetized ducks. 4. It is proposed that the potentiating effects of general anaesthesia and ganglionic blockade on pressor responses were due both to a lowering of baseline blood pressure (BP) and an inhibition of the neural reflexes which normally buffer BP. Furthermore, it is suggested that the augmented responsiveness of anaesthetized, ganglion-blocked ducks shows that the pressor effect of AII is predominantly of peripheral, rather than central nervous system (CNS), origin.
D000803:Angiotensin I / Q000494:pharmacology*; D000804:Angiotensin II / Q000494:pharmacology*; D000809:Angiotensins / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D004372:Ducks; D007700:Kinetics; D008297:Male; D010424:Pentobarbital / Q000494:pharmacology; D010634:Phenobarbital / Q000494:pharmacology; D013722:Teprotide / Q000494:pharmacology
D000809:Angiotensins; D000804:Angiotensin II; D000803:Angiotensin I; D013722:Teprotide; D010424:Pentobarbital; D010634:Phenobarbital