Development of vasomotor responses in fetal mesenteric arteries

Changes in mesenteric arterial diameters were studied using intravital micr oscopy in chick fetuses at days 13 and 17 of incubation, corresponding to 0 .6 and 0.8 fetal incubation time, both during 5 min of hypoxia followed by 5 min of reoxygenation and after topical administration of increasing conce ntrations (10(-6)-10(-2) M) of norepinephrine (NE) and acetylcholine (ACh). Baseline diameters of second-order mesenteric arteries increased from 56 m u m at 0.6 incubation to 75 mu m at 0.8 incubation. Acute hypoxia induced a reduction in arterial diameter to 87 +/- 4.4% of baseline at 0.6 incubatio n and to 44 +/- 6.7% at 0.8 incubation (P < 0.01). During reoxygenation, me senteric arteries dilated to 118 +/- 6.5% and 121 +/- 7.5% of baseline at 0 .6 and 0.8 fetal incubation time, respectively. Phentolamine did not affect the vasoconstriction during hypoxia at 0.6 incubation, whereas this alpha- adrenergic antagonist significantly attenuated the vasoconstrictor response at 0.8 incubation (to 93 +/- 2.7% of baseline, P < 0.01). Topical NE induc ed maximal vasoconstriction to 71 +/- 3% of baseline at 0.6 incubation and to 35 +/- 3.8% at 0.8 incubation (P < 0.01). Maximal vasodilation to topica l ACh was 113 +/- 4.4% and 122 +/- 4.8% of baseline at 0.6 and 0.8 incubati on, respectively. These in vivo findings show that fetal mesenteric arterie s constrict in response to acute hypoxia and that the increase in magnitude of this vasoconstrictor response from 0.6 to 0.8 of fetal development resu lts from an increase in adrenergic constrictor capacity.