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Effects of quinagolide (CV 205‐502), a selective D 2 ‐agonist, on vascular reactivity in patients with a prolactin‐secreting adenoma
Author(s) -
Bodmer C. W.,
Atkln S. L.,
Savage M. W.,
Masson E. A.,
White M. C.
Publication year - 1995
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1995.tb01893.x
Subject(s) - medicine , endocrinology , bromocriptine , prolactinoma , agonist , prolactin , dopamine agonist , blood pressure , receptor , hormone
Summary BACKGROUND Quinagolide (CV 205 502) Is a dopamine D 2 ‐receptor agonist which has proved effective In the treatment of prolactinomas, reducing both serum PRL and tumour size. Some of Its D 2 ‐receptor effects are mediated via α‐adrenoceptors, which have a major influence on the control of vascular tone. The aim of this study was to examine the influence of quinagolide on In‐vivo dorsal hand vein vascular responses to noradrenaline In patients with a prolactinoma. DESIGN AND PATIENTS Seven female patients with prolactinomas (age 37 (28‐46) years), Intolerant of bromocriptine, were studied before and after 3 months treatment with quinagolide (0.75‐1.5 mg/day). Patients were otherwise disease free, were taking no other medication, and had been on no other medication (Including bromocriptine) for at least 3 months prior to enrolment into the study. MEASUREMENTS Vascular responses to locally infused noradrenaline were measured In dorsal hand veins using an established technique. PRL, oestradiol, FSH, LH, blood pressure and body mass Index were also measured before and after 3 months treatment. RESULTS Quinagolide significantly reduced PRL in all 7 patients (1795 (696‐4680) (mean (range)) vs 488 (290‐868) mU/l, P =0.001), with no effect on the other parameters, including mean arterial pressure (88 (2) vs 87 (4) mmHg, P =0.6). Vascular reactivity to noradrenaline was significantly increased after 3 months therapy: log 10 dose estimated to cause 50% vasoconstriction (ED 50 ) 1.37 (0.12) vs 0.85 (0.12) ng/mln ( P =0.003; a lower ED 50 indicates less noradrenaline Is required to constrict the vein by 50%). CONCLUSIONS Vasoconstrictor responses to noradrenaline were increased in all patients after 3 months treatment with quinagolide. Peripheral veins carry α‐adrenoceptors analogous to those of systemic resistance vessels. If this increased vasoconstrictor response In patients with prolactinomas was occurring in hypophyseal vessels, It would lead to reduced tumour blood supply. Quinagolide may therefore reduce tumour blood flow, which may be one factor responsible for its effectiveness In these patients.