TY - JOUR
T1 - Hypotension in the chronically hypoxic chicken embryo is related to the beta-adrenergic response of chorioallantoic and femoral arteries and not to bradycardia
AU - Lindgren, Isa
AU - Crossley, Dane, II
AU - Villamor, Eduardo
AU - Altimiras, Jordi
PY - 2011/10
Y1 - 2011/10
N2 - Lindgren I, Crossley II D, Villamor E, Altimiras J. Hypotension in the chronically hypoxic chicken embryo is related to the beta-adrenergic response of chorioallantoic and femoral arteries and not to bradycardia. Am J Physiol Regul Integr Comp Physiol 301: R1161-R1168, 2011. First published July 27, 2011; doi: 10.1152/ajpregu.00458.2010.-Prolonged fetal hypoxia leads to growth restriction and can cause detrimental prenatal and postnatal alterations. The embryonic chicken is a valuable model to study the effects of prenatal hypoxia, but little is known about its long-term effects on cardiovascular regulation. We hypothesized that chicken embryos incubated under chronic hypoxia would be hypotensive due to bradycardia and beta AR-mediated relaxation of the systemic and/or the chorioallantoic (CA) arteries. We investigated heart rate, blood pressure, and plasma catecholamine levels in 19-day chicken embryos (total incubation 21 days) incubated from day 0 in normoxia or hypoxia (14-15% O(2)). Additionally, we studied alpha-adrenoceptor (alpha AR)-mediated contraction, relaxation to the beta-adrenoceptor (beta AR) agonist isoproterenol, and relaxation to the adenylate cyclase activator forskolin in systemic (femoral) and CA arteries (by wire myography). Arterial pressure showed a trend toward hypotension in embryos incubated under chronic hypoxic conditions compared with the controls (mean arterial pressure 3.19 +/- 0.18 vs. 2.59 +/- 0.13 kPa, normoxia vs. hypoxia, respectively. P = 0.056), without an accompanied bradycardia and elevation in plasma norepinephrine and lactate levels. All vessels relaxed in response to beta AR stimulation with isoproterenol, but the CA arteries completely lacked an alpha AR response. Furthermore, hypoxia increased the sensitivity of femoral arteries (but not CA arteries) to isoproterenol. Hypoxia also increased the responsiveness of femoral arteries to forskolin. In conclusion, we suggest that hypotension in chronic hypoxic chicken embryos is the consequence of elevated levels of circulating catecholamines acting in vascular beds with exclusive (CA arteries) or exacerbated (femoral arteries) beta AR-mediated relaxation, and not a consequence of bradycardia.
AB - Lindgren I, Crossley II D, Villamor E, Altimiras J. Hypotension in the chronically hypoxic chicken embryo is related to the beta-adrenergic response of chorioallantoic and femoral arteries and not to bradycardia. Am J Physiol Regul Integr Comp Physiol 301: R1161-R1168, 2011. First published July 27, 2011; doi: 10.1152/ajpregu.00458.2010.-Prolonged fetal hypoxia leads to growth restriction and can cause detrimental prenatal and postnatal alterations. The embryonic chicken is a valuable model to study the effects of prenatal hypoxia, but little is known about its long-term effects on cardiovascular regulation. We hypothesized that chicken embryos incubated under chronic hypoxia would be hypotensive due to bradycardia and beta AR-mediated relaxation of the systemic and/or the chorioallantoic (CA) arteries. We investigated heart rate, blood pressure, and plasma catecholamine levels in 19-day chicken embryos (total incubation 21 days) incubated from day 0 in normoxia or hypoxia (14-15% O(2)). Additionally, we studied alpha-adrenoceptor (alpha AR)-mediated contraction, relaxation to the beta-adrenoceptor (beta AR) agonist isoproterenol, and relaxation to the adenylate cyclase activator forskolin in systemic (femoral) and CA arteries (by wire myography). Arterial pressure showed a trend toward hypotension in embryos incubated under chronic hypoxic conditions compared with the controls (mean arterial pressure 3.19 +/- 0.18 vs. 2.59 +/- 0.13 kPa, normoxia vs. hypoxia, respectively. P = 0.056), without an accompanied bradycardia and elevation in plasma norepinephrine and lactate levels. All vessels relaxed in response to beta AR stimulation with isoproterenol, but the CA arteries completely lacked an alpha AR response. Furthermore, hypoxia increased the sensitivity of femoral arteries (but not CA arteries) to isoproterenol. Hypoxia also increased the responsiveness of femoral arteries to forskolin. In conclusion, we suggest that hypotension in chronic hypoxic chicken embryos is the consequence of elevated levels of circulating catecholamines acting in vascular beds with exclusive (CA arteries) or exacerbated (femoral arteries) beta AR-mediated relaxation, and not a consequence of bradycardia.
KW - prenatal hypoxia
KW - hypoxic hypotension
KW - chorioallantoic membrane
KW - beta-adrenoceptors
KW - alpha-adrenoceptors
U2 - 10.1152/ajpregu.00458.2010
DO - 10.1152/ajpregu.00458.2010
M3 - Article
C2 - 21795631
SN - 0363-6119
VL - 301
SP - R1161-R1168
JO - American Journal of Physiology-regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology-regulatory Integrative and Comparative Physiology
IS - 4
ER -