Contractile and relaxing reactivity in carotid and femoral arteries of chicken embryos

Abstract

Contractile and relaxing reactivity in carotid and femoral arteries of chicken embryos. Am J Physiol Heart Circ Physiol 278: H1261-H1268, 2000.-In the embryo, hypoxemia causes redistribution of cardiac output from the periphery toward the heart and the brain. In view of this, we investigated developmental changes in the contractile and relaxing properties of the peripheral femoral artery (Fem) and the more central carotid artery (Car) at 0.7, 0.8, and 0.9 of the chicken embryo incubation time. Isolated arteries were studied in myographs and were exposed to norepinephrine or phenylephrine. High K ϩ (125 mM) and electrical field stimulation (0.25-16 Hz) were used to induce receptor-independent and neurogenic contractions. Relaxing responses to ACh were evaluated in the absence and presence of the nitric oxide (NO) synthase inhibitor N G -nitro-L-arginine methyl ester (L-NAME) and before and after endothelium removal. ␣ 1 -Adrenergic contractile responses increased in a time-dependent manner and were significantly larger in Fem than in Car. Neurogenic contractions and adrenergic nerves could only be demonstrated in Fem at 0.9 incubation. ACh caused relaxation in both Fem and Car at 0.7, 0.8, and 0.9 incubation. The NO-independent part of the relaxation was more pronounced in Car than in Fem at all developmental stages. We conclude that the chicken embryo is a useful model to investigate the development of vasomotor control and vascular heterogeneity. The observed regional vascular differences may contribute to cardiac output redistribution during hypoxia in the embryo and might result from endothelial and neurogenic influences on vascular smooth muscle differentiation.

Chronic Moderate Hypoxia and Protein Malnutrition Both Induce Growth Retardation, But Have Distinct Effects on Arterial Endothelium-Dependent Reactivity in the Chicken Embryo

“…Our group previously showed that the response to ACH in the femoral artery of the chicken embryo at the end of incubation is entirely endothelium-dependent (19). Precontraction with high K ϩ , blockade of NO synthase with L-NAME, and inhibition of cyclooxygenase with indomethacin are not sufficient to entirely block ACH-induced relaxation in the chicken embryo [this study and (19)] and adult chicken (24,25).…”

“…Precontraction with high K ϩ , blockade of NO synthase with L-NAME, and inhibition of cyclooxygenase with indomethacin are not sufficient to entirely block ACH-induced relaxation in the chicken embryo [this study and (19)] and adult chicken (24,25). This indicates that besides NO, prostaglandins, and EDHF, an additional unknown factor contributes to the endotheliumdependent response in this species.…”

“…In children and young adults with low birth weight, endothelial function is reduced (16 -18). Endothelium-dependent relaxation involves mediators such as NO and EDHFs (15), which have also been demonstrated to participate in the response to ACH in chicken embryo arteries (19). As acute and prolonged exposure to hypoxia can interfere with NO production and release (16,20,21), endothelial dysfunction resulting from chronic in utero exposure to hypoxia could be an interesting mechanism to link intrauterine stress and the programming of cardiovascular disease in the adult.…”

Flow regulates arterial-venous differentiation in the chick embryo yolk sac

“…It is furthermore possible that protein cannot elicit a proper signal transduction cascade in the yolk sac, perhaps because a member of the downstream cascade is absent. This occurs in other receptor/ligand systems during embryonic development (LeNoble et al, 2000). It may also be that ephrin/Eph signaling in the yolk sac is already maximally active, and the added proteins, which were previously described as agonists in both neural and endothelial cells (Wang and Anderson, 1997;Füller et al, 2003) do not increase signal transduction.…”

Dll4-Notch signaling determines the formation of native arterial collateral networks and arterial function in mouse ischemia models

“…To examine arteriolar contractility and relaxation behavior, resistance sized arterioles were isolated and mounted in a wire myograph as described previously (le Noble et al, 2000). To examine vasoconstriction, arterioles were challenged with norepinephrine (NE), phenylephrine (Phe) and angiotensin II (AngII).…”