Post-hypoxic frequency decline does not depend on alpha2-adrenergic receptors in the adult rat.

The aim of this study was to determine whether post-hypoxic frequency decline (PHFD) requires central activation of alpha2-adrenergic receptors. PHFD is defined as the undershoot in respiratory frequency that occurs immediately following brief hypoxic periods. Adult anesthetized, vagotomized rats were exposed to hypoxia (8% O2, mean=45 s) before and after intracerebroventricular (i.c.v.) infusion of vehicle or alpha2-antagonist. The efficacy of the i.c.v. antagonist was assessed by recording the response to intravenous injection of alpha2-agonist before and after the infusion. We compared breathing frequencies before, during, and after hypoxia, both before and after treatments. The decline in breathing frequency after hypoxia was not prevented by the alpha2-antagonists, RX 821002 or SK&F-86466. Guanabenz, an alpha2-agonist, prolonged baseline expiration and potentiated PHFD. Prior treatment with SK&F-86466 blocked the agonist-evoked response which was also reversed by subsequent administration of SK&F-86466. We conclude that PHFD does not require the activation of alpha2-adrenergic receptors, but that alpha2-adrenergic receptors can modulate resting and post-hypoxic respiratory frequency.