Differential effects on phrenic output of two dopamine agonists, apomorphine and bromocriptine.
Effects of dopamine agonists upon phrenic output were studied in decerebrate, vagotomized, paralyzed, carotid-body denervated dogs. Intravenous administration of dopamine was without effect in these dogs. Apomorphine (APO) increased phrenic minute activity while bromocriptine (BRO) decreased phrenic minute activity following intravenous injection at doses of 100 micrograms/kg for each drug. BRO-induced decreases in phrenic minute activity were associated with decreases in phrenic amplitude; burst frequency remained unchanged. Conversely, APO-induced increases in phrenic minute activity resulted from significant increases in both frequency and amplitude. Both APO and BRO significantly prolonged inspiratory duration and shortened expiratory duration. Responses to APO and BRO were abolished with haloperidol. These results confirm previous evidence for the existence of dopaminergic receptors within the central nervous system, which are inaccessible to exogenous dopamine, and which can alter timing as well as amplitude characteristics of the integrated phrenic neurogram. Both excitation and inhibition of phrenic activity following administration of APO and BRO are mediated by mechanisms within or below the caudal brainstem.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology*; D001971:Bromocriptine / Q000494:pharmacology*; D002344:Carotid Body / Q000502:physiology; D003655:Decerebrate State; D003714:Denervation; D004285:Dogs; D006220:Haloperidol / Q000494:pharmacology; D010791:Phrenic Nerve / Q000187:drug effects / Q000502:physiology*; D011954:Receptors, Dopamine / Q000187:drug effects / Q000502:physiology*; D012119:Respiration / Q000187:drug effects*; D013997:Time Factors; D014628:Vagotomy
D011954:Receptors, Dopamine; D001971:Bromocriptine; D006220:Haloperidol; D001058:Apomorphine