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[The role of angiotensin in paracrine interaction between rat anterior pituitary cells].

Tetsuo Kubota, Shinji Kamada, T. Aso

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Abstract

The present study was undertaken to investigate the role of angiotensin II (AII) in GnRH-induced prolactin (PRL) release from anterior pituitary cells of young male rats. The anterior pituitary glands were enzymatically dispersed, and subsequently the cells were allowed to reaggregate for 48 hours. Twenty-min perifusion with 100 nM GnRH increased PRL release (p less than 0.01) from the anterior pituitary cell aggregates. The integrated value for PRL release was 9.1 +/- 2.9 ng/10(7) cells. The release of angiotensin I (AI) from these perifused pituitary aggregates was significantly increased by GnRH. In contrast, GnRH-stimulated release of PRL was significantly suppressed by saralasin, a specific AII antagonist, whereas saralasin did not attenuate GnRH-induced LH release from these aggregates. These data demonstrate that GnRH is capable of stimulating PRL release through a mechanism that may involve the release of angiotensin.

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What this paper is about

The present study was undertaken to investigate the role of angiotensin II (AII) in GnRH-induced prolactin (PRL) release from anterior pituitary cells of young male rats. The anterior pituitary glands were enzymatically dispersed, and subsequently the cells were allowed to reaggregate for 48 hours. Twenty-min perifusion with 100 nM GnRH increased PRL release (p less than 0.01) from the anterior pituitary cell aggregates. The integrated value for PRL release was 9.1 +/- 2.9 ng/10(7) cells. The release of angiotensin I (AI) from these perifused pituitary aggregates was significantly increased by GnRH. In contrast, GnRH-stimulated release of PRL was significantly suppressed by saralasin, a specific AII antagonist, whereas saralasin did not attenuate GnRH-induced LH release from these aggregates. These data demonstrate that GnRH is capable of stimulating PRL release through a mechanism that may involve the release of angiotensin.

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Available abstract

The present study was undertaken to investigate the role of angiotensin II (AII) in GnRH-induced prolactin (PRL) release from anterior pituitary cells of young male rats. The anterior pituitary glands were enzymatically dispersed, and subsequently the cells were allowed to reaggregate for 48 hours. Twenty-min perifusion with 100 nM GnRH increased PRL release (p less than 0.01) from the anterior pituitary cell aggregates. The integrated value for PRL release was 9.1 +/- 2.9 ng/10(7) cells. The release of angiotensin I (AI) from these perifused pituitary aggregates was significantly increased by GnRH. In contrast, GnRH-stimulated release of PRL was significantly suppressed by saralasin, a specific AII antagonist, whereas saralasin did not attenuate GnRH-induced LH release from these aggregates. These data demonstrate that GnRH is capable of stimulating PRL release through a mechanism that may involve the release of angiotensin.

Key concepts: Saralasin, Anterior pituitary, Prolactin, Internal medicine, Endocrinology, Angiotensin II, Chemistry, Renin–angiotensin system

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