Human decidua is a major source of renin.
ABSTRACT Plasma prorenin levels are elevated in normal pregnant women. Current evidence suggests renin production by tissues of the uteroplacental unit contribute to this elevation. The purpose of this investigation was to define the source of renin biosynthesis within the human uteroplacental unit and to characterize the renin produced. RNA extraction and Northern blot analysis consistently demonstrated renin mRNA expression in uterine lining both in the pregnant (decidua) and nonpregnant states (endometrium) and in fetal chorion laeve, which is inseparable from the decidua. In contrast, renin mRNA expression was not detected in basal plate and intertwin chorion (which is separate from decidua), amnion, myometrium, or placental villi. The total renin content in decidual homogenates was two- to threefold greater than in endometrial homogenates, and cultured human decidual cells produced significantly more total renin than cultured human endometrial cells, suggesting that pregnancy enhanced renin production by the cells lining the uterus. Immunoblot analysis and [3H]leucine incorporation identified 47,000-mol wt prorenin as the major form of renin produced by cultured human decidual cells. These studies indicate that maternal decidua is the major source of prorenin in the uteroplacental unit.
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ABSTRACT: The renin-angiotensin system (RAS) plays an important role in the pathogenesis of hypertension. However, the role of RAS in preeclampsia is largely unknown, because the plasma concentration of renin and angiotensin (AII) is lower in preeclampsia than in normal pregnancy, whereas its cardinal sign is hypertension. A pressor response to AII infusions can predict the onset of preeclampsia, resulting in involvement of RAS in the pathogenesis of preeclampsia. It has been reported that patients with preeclampsia exhibit angiotensin type I receptor agonistic autoantibody (AT1-AA), suggesting the involvement of RAS in the pathogenesis of this condition. The physiological action of AT1-AA can explain the various clinical symptoms of preeclampsia. However, the significance of circulatory RAS, including AT1-AA, in the pathogenesis of preeclampsia remains obscure. Since many reports state that circulating RAS is thought to be suppressed in preeclampsia it is difficult to explain the onset of hypertension in preeclampsia by circulating RAS. Therefore, I propose new insights into the role of RAS in preeclampsia to resolve the contradiction as above-mentioned. The recent discovery of tissue RAS, on which prorenin and its receptor act, suggests a promising new direction in understanding the role of RAS in the pathogenesis of preeclampsia.Medical Hypotheses 01/2014; 82(3). DOI:10.1016/j.mehy.2013.12.024 · 1.15 Impact Factor
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ABSTRACT: Angiotensin synthesis at tissue sites is well-established, and interference with tissue angiotensin is now believed to underlie the beneficial effects of renin-angiotensin system blockers. At first it was thought that the renin required to synthesize angiotensin at tissue sites was also synthesized locally. Recent studies show, however, that this is not the case at important cardiovascular sites like the heart and vessel wall. Moreover, extrarenal sites that do express the renin gene release prorenin, the inactive precursor of renin, instead of renin. This chapter provides an update on the sources of (pro)renin in the body, lists the known stimulants and inhibitors of its production, and discusses the concept that prorenin rather than renin determines tissue angiotensin generation.
Reproduction Fertility and Development 09/2010; 22(9):65-65. DOI:10.1071/SRB10Abs147 · 2.58 Impact Factor