Effect of Cortisol on Gene Expression of the Renin-Angiotensin System in Fetal Sheep

Fetal growth restriction: adaptations and consequences

“…Furthermore, blood pressure responses to increasing doses of angiotensin II, but not noradrenaline, were increased in sheep fetuses after infusion of cortisol for 48 h at about day 125 of gestation (Tangalakis et al, 1992). Intrafetal infusion of cortisol also results in an increased expression of angiotensin II type I (AT1) receptor mRNA within the fetal heart (right and left atrium and right ventricle) (Segar et al, 1995) and there is a greater hypotensive effect after blockade of AT1 receptors in sheep fetuses that have been infused with cortisol (Forhead et al, 2000). Thus, there is evidence that increased exposure to cortisol during fetal life results in an increased sensitivity to the vasoconstrictor actions of angiotensin II through either an increase in the expression of the AT1 receptor or changes in the post-receptor-mediated events within the vascular smooth muscle.…”

Effects of placental insufficiency on the ovine fetal renin-angiotensin system

“…In the present study, although PR fetuses had higher plasma cortisol levels than in controls, no significant correlation between cortisol and renal angiotensinogen mRNA or renin mRNA was found. Segar et al (1995) showed that infusions of cortisol that increased plasma levels to 113 nmol dl¢ suppressed renal renin mRNA and hepatic angiotensinogen mRNA but did not affect renal angiotensinogen mRNA levels. However, these levels of cortisol were far in excess of any levels found in the present study (< 5.0 nmol l¢).…”

Management of hypotension and low systemic blood flow in the very low birth weight neonate during the first postnatal week

“…30,31,34 The attenuated cardiovascular responsiveness to catecholamines in critical illness is, at least in part, caused by the downregulation of the cardiovascular adrenergic and type-1 angiotensin-2 receptors and their intracellular signaling systems. 31,33,35 As expression of these receptors and their signaling systems is inducible by corticosteroids, 36 steroid administration has the potential to reverse adrenergic receptor downregulation. In addition, corticosteroids inhibit prostacyclin production and the induction of nitric oxide synthase, 37 and thus limit the pathological vasodilation associated with the nonspecific or specific inflammatory response of the critically ill neonate.…”