Vascular angiotensin II and atrial natriuretic peptide receptors in normal and growth-retarded human placentae

• Published in: Journal of endocrinology Vol. 126; no. 2; pp. 341 - 347
• Main Authors: MCQUEEN, J, KINGDOM, J. C. P, JARDINE, A. G, CONNELL, J. M. C, WHITTLE, M. J
• Format: Journal Article
• Language: English
• Published: Colchester BioScientifica 01.08.1990; Portland Press
• Subjects: angiotensin II; Angiotensin II - metabolism; Arteries - analysis; Atrial Natriuretic Factor - metabolism; atrial natriuretic hormone; Biological and medical sciences; comparison; Female; Fetal Growth Retardation - metabolism; Fundamental and applied biological sciences. Psychology; growth; Humans; man; Mother. Fetoplacental unit. Mammary gland. Milk; placenta; Placenta - analysis; Pregnancy; Pregnancy. Parturition. Lactation; Radioligand Assay; receptors; Receptors, Angiotensin - analysis; Receptors, Atrial Natriuretic Factor; Receptors, Cell Surface - analysis; Vertebrates: reproduction; Human; Placenta; Blood vessel; Angiotensin; Peptide hormone; Scatchard plot; Atrial natriuretic peptide; Circulatory system; Angiotensin II; Somatic growth; Hormonal receptor
• ISSN: 0022-0795; 1479-6805
• DOI: 10.1677/joe.0.1260341

ABSTRACT Receptors for angiotensin II (AII) and atrial natriuretic peptide (ANP) were characterized in a membrane fraction from resistance-type artery from human placentae. Placentae from normal pregnancies and pregnancies complicated by intrauterine growth retardation (IUGR) were studied. High- and low-affinity receptors for AII (dissociation equilibrium constant (Kd) 1 ·7 and 15·7 nmol/l respectively) and ANP (Kd 0·2 and 55·5 nmol/l respectively) were identified; these parameters were unchanged in IUGR, but there was a reduction in high-affinity receptor number by approximately 50% for AII and 80% for ANP in this condition. Both peptides may have a role in the regulation of fetoplacental blood flow. The alterations in IUGR are consistent with sustained activation of the fetal reninangiotensin system and suggest altered vascular responsiveness to ANP. Journal of Endocrinology (1990) 126, 341–347