In this report, the respiratory and cardiovascular effects of dopamine, especially as a depressant of respiration, were re-examined using anesthetized dogs with respect to current concepts of dopamine as an inhibitory modulator in respiratory control. An intravenous inje-ction of dopamine (1μg/kg) slightly depressed respiration either in tidal volume or in respi-ratory rate. In the range of doses (1-20μg/kg) investigated, the respiratory depression induced by dopamine were transient and dose-dependent accompanied by a biphasic blood pressure change. In the doses above 30μg/kg, the depressed respiration induced by dopamine lasted for several minutes, while the rise in blood pressure was still transient. In the dose of 10 pg/kg, breathing volume and respiratory rate were depressed by dopamine in average to approximately 50% and 21% of control values, respectively. Average and minimum tidal volumes were also reduced to approximately 36% and 45% respectively. The depressed respiration induced by dopamine was not antagonized by pretreatment with phenoxybenzamine or proparnolol, while it was fully counteracted by pretreatment with chlorpromazine in tidal volume, but not antagonized in respiratory rate. The depressed respiration by dopamine can be related to its specific action on dopamine receptors. The mechanism of respiratory depression by dopamine seems to be due mainly to a reflex inhibition of the respiratory center via the carotid chemoreceptor mechanism in which dopamine is involved.
