Skip to main content
. 2013 May 24;305(3):H321–H329. doi: 10.1152/ajpheart.00099.2013

Fig. 1.

Fig. 1.

Regulation of carotid arterial dilation in the immediate postnatal period. Arteries were isolated from postnatal day 1 (P1, newborn), P7, and P21 mice, and analyzed in a microperfusion system at a transmural pressure of 20 mmHg. Functional responses are expressed as a percentage of the baseline diameter of the arteries (B) and presented as means ± SE. To observe dilation, arteries were initially constricted to ∼80% of baseline diameter with the thromboxane receptor agonist U46619 (U4). For statistical analysis, * symbols indicate significant difference compared with P1; # symbols indicate significant difference between P7 and P21. In each case, 1 symbol = P < 0.05; 2 symbols = P < 0.01; 3 symbols = P < 0.001. A: under control conditions in P1 arteries, acetylcholine caused significant dilation only at the highest dose tested (10−6 M) but caused markedly increased dilation in P7 and P21 arteries [n = 6 (P21), 8(P7), or 11(P1)]. In B, the NO donor DEA-NONOate caused dilation that was similar in P1, P7, and P21 arteries [n = 5 (P1), 7 (P21), or 9 (P7)]. In C, in the presence of the NO synthase inhibitor l-NAME (10−4 M), acetylcholine did not cause significant dilation in P1 or P7 arteries but continued to cause marked dilation in P21 arteries [n = 5 (P21, P1) or 6 (P7)].