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. 2015 Nov 11;310(2):H188–H198. doi: 10.1152/ajpheart.00666.2015

Fig. 1.

Fig. 1.

Topical exposure to 5-HT + Nω-nitro-l-arginine methyl ester (l-NAME) maintains arteriolar constriction for 4 h and induces inward remodeling in vivo. A: normalized diameter of 1A cremaster feed arterioles (expressed as percent maximum passive diameter) in response to a 4-h exposure to the indicated vasoconstrictors. Data are expressed as means. B: mean time for arterioles exposed to 10−5.5 M norepinephrine (NE) + 10−7 M Ang II, 10−5.5 M NE + 10−7 M Ang II + 10−4 M l-NAME, or 10−5.5 M NE + 10−7 M Ang II + 5 × 10−5 M indomethacin (Indo) to return to maximum passive diameter while in the presence of the indicated vasoconstrictors. Data are expressed as means ± SE. C: normalized diameter of 1A cremaster feed arterioles (expressed as percent maximum passive diameter) in response to a 4-h exposure to 5-HT + l-NAME. Data are expressed as means ± SE. Remodeling is expressed as a percent reduction from the maximal passive diameter obtained before exposure to the vasoconstrictor agonists ± SE. For A–C, n = 4 for NE + Ang II, n = 3 for NE + Ang II + l-NAME and NE + Ang II + l-NAME + indomethacin, and n = 5 for 5-HT + l-NAME. Max, maximum; min, minutes.