Angiotensin II (ANG II) increases blood pressure (MAP) via specific ANG II receptors (AT) and is considered important in regulating MAP after birth. In adult animals, AT1 receptors predominate in vascular smooth muscle (VSM) and mediate vasoconstriction. In newborn sheep, AT2 receptors, which do not mediate vasoconstriction, predominate in vascular smooth muscle until 2 wk postnatal when they are replaced by AT1. Thus, the mechanisms whereby ANG II increases MAP after birth are unclear. We examined the effects of ANG II on femoral vascular resistance (FmVR) and blood flow (FmBF) in serial studies of newborn sheep (n = 7) at 7–14 d, 15–21 d, and 22–35 d. Animals had femoral catheters implanted for systemic ANG II infusions and cardiovascular monitoring, and a flow probe was implanted on the contralateral artery proximal to the superficial saphenous artery, which contained a catheter for intra-arterial ANG II infusions. Studies were performed using a range of systemic and intra-arterial ANG II doses. Systemic ANG II increased MAP dose-dependently at all ages (p p p 1 expression, stimulation of local ANG II antagonists, or ANG II-mediated release of another vasoconstrictor.Abbreviations: ANG II, angiotensin II; AT, angiotensin II receptor; AT1, angiotensin II receptor subtype 1; AT2, angiotensin II receptor subtype 2; FmBF, femoral blood flow; FmVR, femoral vascular resistance; HR, heart rate; PVR, peripheral vascular resistance; VSM, vascular smooth muscle; %Δ, percent change
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