SUMMARYBromocriptine is currently and successfully used for the treatment of pituitary prolactinomas. However, bromocriptine appears unable to normalize plasma prolactin levels in about 10|X% and to reduce tumour size in one‐third of cases. The lack of normalization of plasma prolactin levels in spite of a daily dose of bromocriptine equal to or higher than 15 mg suggests a bromocriptine resistance. We compared the long‐term effects of bromocriptine and CV 205–502 (a non‐ergot derivative D2dopamine agonist) on plasma prolactin levels and tumour size in seven bromocriptine‐resistant prolactinomas. Bromocriptine reduced significantly (P>0.001) plasma prolactln levels (from 2307 |Mp 518 to 568 |Mp 279 μg/I) (conversion to SI units: 1 μg/I = 20 mU/I). Visual field defects observed in five patients Improved in four. However, CT scan analysis showed a decrease in tumour size in only three patients. Except for transient and minor side‐effects at the beginning of the treatment, CV 205–502 was well tolerated In five of seven patients. In the remaining two patients nausea and vertigo occurred with high dosages of CV 205–502 and it was necessary to reduce the daily dose. CV 205–502 lowered plasma prolactin to levels similar to those obtained after bromocriptine therapy in four cases. In the three remaining patients, CV 205–502 was more potent than bromocriptine as demonstrated by the further 90|X% reduction in plasma levels obtained in one case and by the normalization of plasma prolactin levels in the two other cases. One woman became pregnant during CV 205–502 treatment. However, no further change in visual disturbance or in tumour size was observed during the treatment with CV 205–502. These results show that CV 205–502 appears to be more potent than bromocriptine in reducing plasma prolactin levels in some bromocriptine‐resistant prolactinomas and suggest that different mechanisms may be