Effects of some ergot alkaloids on dopamine receptors of molluscan smooth muscle.
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Abstract:
Some ergot alkaloids relaxed catch contraction of an isolated molluscan smooth muscle (anterior byssus retractor muscle of Mytilus edulis). Haloperidol, a competitive dopamine antagonist, shifted the dose response curves of ergot alkaloids, but methysergide did not. Bromocriptine, a potent dopaminergic ergot alkaloid, did not relax catch contraction. These results suggest that relaxation of catch contraction by some ergot alkaloids is mediated through dopamine receptors of this muscle, but dopamine receptors of this muscle seem to be somewhat different from those of mammalian brain.Keywords:
Methysergide
The interaction between bromocriptine and metoclopramide on intraocular pressure (IOP), pupil diameter, and other parameters were studied in healthy volunteers. Pupil diameter was not affected by both treatments and only bromocriptine lowered IOP. Prior treatment with metoclopramide blocked the IOP-lowering effect of bromocriptine. It is concluded that bromocriptine lowers IOP by stimulation of dopamine-2 receptors.
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In experimental Parkinson9s disease, we studied the effects of chronic administration (30 days), withdrawal, and reinstitution of bromocriptine. Dopamine (DA) receptor supersensitivity was produced by 6-hydroxydopamine and reversed by chronic bromocriptine administration. Drug holiday reestablished sensitivity of DA receptors, but reinstitution of bromocriptine again downregulated receptors. The effects of a drug holiday on DA receptors are shortlived, and long-term clinical improvement cannot be expected. Apomorphine-induced contralateral turning produced by the lesion was unaffected by any drug regimen.
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The bromocriptine-TRH test was performed in 11 patients with advanced Parkinson's disease and in 10 control subjects. Seven patients were receiving treatment with Levo-DOPA, which was discontinued 12 h prior to the test. Basal prolactin levels were 5.88 ng/ml in treated and 18.22 ng/ml in untreated patients as compared to 9.68 mg/ml in controls. Bromocriptine induced a similar reduction of about 60% in prolactin levels in all groups (3.28, 11.5 and 5.95 ng/ml, respectively). After TRH, prolactin levels increased to 13.8 ng/ml in controls and 15.2 ng/ml in patients treated with levo-DOPA. Untreated patients remained with prolactin below basal levels (11.6 ng/ml). We postulate that low basal levels of prolactin in patients treated with levo-DOPA reveal a residual suppressing effect of the drug. The sharp increase after TRH is related to a significant dopaminergic hypofunction as evidenced by clinical findings. A high sensitivity of dopaminergic receptors in the anterior hypofisis is suggested as an explanation for the findings of the test in the untreated patients.
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