Effects of quinagolide (CV 205-502), a selective D2-agonist, on vascular reactivity in patients with a prolactin-secreting adenoma

C. W. Bodmer, Stephen Atkin, M. W. Savage, E. A. Masson, M. C. White

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Abstract

Background - Quinagolide (CV 205 502) is a dopamine D2-receptor agonist which has proved effective in the treatment of prolactinomas, reducing both serum PRL and tumour size. Some of its D2-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: log10 dose estimated to cause 50% vasoconstriction (ED50) 1.37 (0.12) vs 0.85 (0.12) ng/min (P = 0.003; a lower ED50 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.

Original languageEnglish
Pages (from-to)49-53
Number of pages5
JournalClinical Endocrinology
Volume43
Issue number1
Publication statusPublished - 1995
Externally publishedYes

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Prolactin
Adenoma
Blood Vessels
Prolactinoma
Norepinephrine
Veins
Bromocriptine
Vasoconstrictor Agents
Adrenergic Receptors
Hand
Therapeutics
Neoplasms
Dopamine D2 Receptors
quinagolide
Dopamine Agonists
Vasoconstriction
Estradiol
Arterial Pressure
Body Mass Index
Blood Pressure

ASJC Scopus subject areas

  • Endocrinology

Cite this

Effects of quinagolide (CV 205-502), a selective D2-agonist, on vascular reactivity in patients with a prolactin-secreting adenoma. / Bodmer, C. W.; Atkin, Stephen; Savage, M. W.; Masson, E. A.; White, M. C.

In: Clinical Endocrinology, Vol. 43, No. 1, 1995, p. 49-53.

Research output: Contribution to journalArticle

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abstract = "Background - Quinagolide (CV 205 502) is a dopamine D2-receptor agonist which has proved effective in the treatment of prolactinomas, reducing both serum PRL and tumour size. Some of its D2-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: log10 dose estimated to cause 50{\%} vasoconstriction (ED50) 1.37 (0.12) vs 0.85 (0.12) ng/min (P = 0.003; a lower ED50 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.",
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T1 - Effects of quinagolide (CV 205-502), a selective D2-agonist, on vascular reactivity in patients with a prolactin-secreting adenoma

AU - Bodmer, C. W.

AU - Atkin, Stephen

AU - Savage, M. W.

AU - Masson, E. A.

AU - White, M. C.

PY - 1995

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N2 - Background - Quinagolide (CV 205 502) is a dopamine D2-receptor agonist which has proved effective in the treatment of prolactinomas, reducing both serum PRL and tumour size. Some of its D2-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: log10 dose estimated to cause 50% vasoconstriction (ED50) 1.37 (0.12) vs 0.85 (0.12) ng/min (P = 0.003; a lower ED50 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.

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