Expression of angiotensin II and its receptor subtypes in endometrial hyperplasia: a possible role in dysfunctional menstruation.
Dysfunctional uterine bleeding is associated with hyperplastic endometrium, and angiotensin II may affect cyclic menstruation. Cellular distribution of angiotensin II and its receptor subtypes (AT1 and AT2) in hyperplastic endometria from patients who had dysfunctional uterine bleeding with or without progestogen treatment was investigated by immunocytochemistry and quantitative receptor autoradiography. Angiotensin II-like immunoreactivity decreased in the hyperplastic endometrial stroma and glandular epithelia compared with normal cyclic endometria. The pattern of angiotensin II immunostaining on perivascular stromal cells in hyperplastic endometria was markedly different from that detected in the normal endometrium. The angiotensin II-like immunostaining was more intense in the progestogen-treated endometria compared with normal endometria. In the progestogen-treated endometrium from patients who had regular menstrual cycles, the angiotensin II-like immunostaining was localized in the perivascular stromal cell, as seen in the normal cyclic endometrium. Both AT1 and AT2 receptor levels in the hyperplastic and progesterone-treated endometria were significantly lower than the levels detected in normal endometrium. The results suggest that the normal function of angiotensin II in endometrium may be essential for regular cyclic menstruation and that alteration in the distribution of angiotensin II and/or the levels of its receptors are likely to be involved in dysfunctional uterine bleeding associated with hyperplastic endometria.
Li
X F
XF
Department of Obstetrics and Gynaecology, Birmingham Women's Hospital, University of Birmingham, United Kingdom.
Ahmed
A
A
D000804:Angiotensin II / Q000096:biosynthesis*; D004714:Endometrial Hyperplasia / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D004717:Endometrium / Q000737:chemistry / Q000378:metabolism; D005260:Female; D006801:Humans; D008599:Menstruation Disturbances / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D011945:Receptors, Angiotensin / Q000096:biosynthesis* / Q000145:classification
D011945:Receptors, Angiotensin; D000804:Angiotensin II