Evidence nitric oxide mediates the vasodepressor response to hypoxia in sino-denervated rats.
Systemic hypoxia, produced in deeply anesthetized, paralyzed rats in which arterial chemoreceptors were denervated, elicited a decrease in arterial pressure (AP) averaging -47 mmHg. Systemic administration of NG-nitro-L-arginine (L-NO2Arg), an inhibitor of nitric oxide (NO) synthase, attenuated the hypoxic depressor response by 79% and elevated AP by 21 mmHg. The effects of L-NO2Arg on the hypoxic depressor response and arterial pressure were reversed by systemic administration of L- but not D-arginine. Elevation of AP with arginine-vasopressin or reduction of AP with nitroprusside to the pre-L-NO2Arg levels did not modify the fall of AP to hypoxia. Endogenous NO synthesized in vivo from L-arginine, mediates most of the hypoxic depressor response.
Sun
M K
MK
Department of Neurology and Neuroscience, Cornell University Medical College, New York, NY 10021.
Reis
D J
DJ
D000768:Anesthesia, General; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D001127:Arginine Vasopressin / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D002346:Carotid Sinus / Q000294:innervation*; D003714:Denervation; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D019335:Nitroarginine; D009599:Nitroprusside / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains
D001127:Arginine Vasopressin; D009599:Nitroprusside; D019335:Nitroarginine; D009569:Nitric Oxide; D001120:Arginine