The purpose of the current study was to examine where @entity5463 ( @entity1831 ) inhibits respiration by direct action on the areas of the ventrolateral medulla (VLM) in the @entity35 . The animal was anesthetized by @entity4774 (1.2 g/kg, i.p.), paralyzed with @entity9563 , and artificially ventilated. Catheterization of the femoral artery and vein, and bilateral vagotomy were performed. The @entity35 was then placed upon a stereotaxic instrument in a prone position. The phrenic nerve was separated and cut peripherally. Phrenic nerve activity (PNA) was monitored at normocapnia and @entity2944 in @entity871 . Microinjection of @entity1831 into various subregions of the VLM was then performed. In response to @entity1831 microinjection, a transient period of @entity386 and then a significant decrease in PNA amplitude were observed. Arterial blood pressure was unchanged. This inhibition of PNA with @entity1831 treatment was site-specific, attenuated by raising @entity515 concentration, and totally abolished by pretreatment with @entity1831 V1A receptor antagonist. Data of the present study indicate that endogenous resource of @entity1831 may produce an inhibitory effect upon respiration via @entity1831 receptors presented on neurons within the VLM.

Arginine vasopressin produces inhibition upon respiration without pressor effect in the XXXX .

@entity1831 :: ('CHEBI:34543', 'Chemical') :: ['AVP'] @entity2944 :: ('MESH:D006935', 'Disease') :: ['hypercapnia'] @entity5463 :: ('MESH:D001127', 'Chemical') :: ['arginine vasopressin'] @entity9563 :: ('MESH:D005703', 'Chemical') :: ['gallamine triethiodide'] @entity4774 :: ('MESH:D014520', 'Chemical') :: ['urethane'] @entity871 :: ('MESH:D018496', 'Disease') :: ['hyperoxia'] @entity515 :: ('CHEBI:29334', 'Chemical') :: ['CO2'] @entity35 :: ('10116', 'Species') :: ['rat'] @entity386 :: ('MESH:D001049', 'Disease') :: ['apnea']
@entity35 :: (10116,Species) :: ['rat']
