Corticotropin releasing hormone (CRH) does not relax isolated human fetoplacental resistance arteries.
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文摘
Objectives The serum concentration of Corticotropin Releasing Hormone (CRH) is elevated in the second and third trimester. The functional significance is not clear, but it has been suggested that CRH may be involved in the maintenance of the feto-placental circulation through vasodilation of the placental vasculature. In this study we have determined whether CRH affects vascular tone in human fetoplacental stem villous (second order) arteries and, for comparison, in rat mesenteric small arteries. Methods Stem villous arteries were dissected from freshly delivered placentae from normal pregnancies and mesenteric small arteries from male Wistar rats. Arteries were mounted on a small vessel wire myograph, set to an approximate physiological transmural pressure and equilibrated in Physiological Saline Solution (PSS). Stem villous arteries were gassed in 5 % CO2 in N2 and mesenteric arteries in 5 % CO2, 95 % O2. Arteries were pre-constricted with U46619(10−7M) or 125mM KCl substituted PSS (stem villous arteries) and PGF2∞ (10μM) or 60mM KCl PSS (mesenteric arteries). Concentration responses to human CRH (10−9 to 3×10−7M) were then performed. Results CRH relaxed small mesenteric arteries (i.d. 323±SEM14μm, n=9) when preconstricted with PGF2∞ (Log EC50. −9.49±0.73) or with 60mMKCl (Log EC50,−8.41 ± 0.38). In contrast CRH caused no relaxation of the stem villous arteries (i.d. 282±38μm, n=8) when constricted with either agonist. Conclusions CRH has no effect on vascular tone in isolated human fetoplacental arteries but, as reported previously, is a potent vasodilator of the mesenteric circulation of the rat. These data suggest that CRH is not involved in the control of human fetoplacental blood flow.