Analysis of the effects of apomorphine and bulbocapnine in relation to the proposed dopamine receptor.

Abstract

Abstract On rat isolated vas deferens, apomorphine was found to be l/5th as active as dopamine. Reserpine or cocaine pretreatment failed to reduce the response to apomorphine. Low concentrations of apomorphine which do not cause contraction of the tissue, antagonize the effects of dopamine. The effects of dopamine were antagonized equally by phentolamine or apomorphine. On rabbit aortic strips 4 × 10−4M apomorphine repeated at 45 min intervals induces pronounced tachyphylaxis. During the tachyphylactic period dopamine was not inhibited to a significantly greater extent than was phenylephrine. Bulbocapnine tested against dopamine and phenylephrine yielded identical pA2 values of 6. Only at 10−5M was bulbocapnine observed to produce a preferentially greater blockade of dopamine. Dopamine or isoprenaline-induced relaxations of aortic strips were not blocked by bulbocapnine. Dopamine and 3 times 10−6M bulbocapnine increased the chronotropic effects in atria. Apomorphine and higher doses of bulbocapnine produced rate decelerating effects. On atria low doses of apomorphine were equally effective in reducing the effects of dopamine or histamine. These results are discussed in light of the proposal that the effects of apomorphine and bulbocapnine involve dopamine receptor interactions. In all three tissues there was no clear cut evidence of specific dopamine receptors.