Role of Gαq or Gαo Proteins in α1-Adrenoceptor Subtype-Mediated Responses in Fischer 344 Rat Aorta

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Abstract
Previous studies showed that α-adrenoceptor (AR) stimulation with norepinephrine is more potent at eliciting contraction in aortas from 1-month-old Fischer 344 rats than from older rats and that this response is mediated by α1b- and α1d-AR subtypes in 1-month-old rats. We examined the G proteins responsible for α1-AR-mediated contractile response and inositol phosphate accumulation in the aortas of 1-month-old Fischer 344 rats. Pertussis toxin (PTX) treatment (2.5 μg/ml for 4 hr) of aortic rings partially inhibited phenylephrine (PHE)-stimulated contraction and inositol phosphate accumulation, suggesting the involvement of PTX-sensitive and -insensitive G proteins. Specific antisera directed against Gαq and Gαo but not Gαs and Gαi precipitated specific α1-AR binding sites labeled with 2-[β-(4-hydroxy-3-[125I]iodophenyl)ethylaminomethyl]tetralone. The number of 2-[β-(4-hydroxy-3-[125I]iodophenyl)ethylaminomethyl]tetralone binding sites precipitated by Gα proteins was increased by activating membrane α1-ARs with PHE. Moreover, PHE stimulated the palmitoylation of Gαq and Gαo, and this response was blocked by the α1-AR antagonist prazosin. Characterization of the α1-AR subtypes that couple to G proteins indicates that although aortic α1a-, α1b-, and α1d-ARs were associated with Gαq, α1b-AR was also linked to Gαo. These results suggest that α1-ARs mediate the contractile response in rat aorta by coupling to both Gq protein and the PTX-sensitive Go protein.