[The role of angiotensin in paracrine interaction between rat anterior pituitary cells].
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.
Kubota
T
T
Department of Obstetrics and Gynecology, Faculty of Medicine, Tokyo Medical and Dental University.
Kamada
S
S
Aso
T
T
D000804:Angiotensin II / Q000494:pharmacology / Q000502:physiology*; D000818:Animals; D002478:Cells, Cultured; D007987:Gonadotropin-Releasing Hormone / Q000502:physiology*; D007986:Luteinizing Hormone / Q000378:metabolism; D008297:Male; D010903:Pituitary Gland, Anterior / Q000166:cytology / Q000378:metabolism*; D011388:Prolactin / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D012504:Saralasin / Q000494:pharmacology
D000804:Angiotensin II; D007987:Gonadotropin-Releasing Hormone; D011388:Prolactin; D007986:Luteinizing Hormone; D012504:Saralasin