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. 2019 Jul 31;317(4):R576–R587. doi: 10.1152/ajpregu.00174.2019

Table 2.

Effect of vehicle controls for TRPV1 antagonists on the peak pressor and cardioaccelerator responses to injecting chemicals into superficial epigastric artery

10% Ethanol/10% Tween 80
0.5% DMSO
100% Saline
0.1% Ethanol
Chemicals Before After Before After Before After Before After
Capsaicin
    MAP 36 ± 11 42 ± 25 63 ± 29 70 ± 26 35 ± 8 38 ± 10 34 ± 20 43 ± 25
    HR 10 ± 9 13 ± 11 4 ± 2 4 ± 2 2 ± 3 3 ± 2 3 ± 1 2 ± 1
    n 6 4 4 4
Bradykinin
    MAP 23 ± 8 29 ± 14 Not tested Not tested 21 ± 12 19 ± 8
    HR 2 ± 1 3 ± 2 1 ± 1 2 ± 2
    n 5 3
α-β-Methylene ATP
    MAP 22 ± 12 21 ± 9 Not tested Not tested Not tested
    HR 3 ± 1 2 ± 1
    n 9
Diprotonated phosphate
    MAP 33 ± 24 37 ± 26 Not tested Not tested Not tested
    HR 4 ± 4 4 ± 2
    n 5

Results are presented as means ± SD increase in mean arterial blood pressure (MAP, in mmHg) or heart rate (HR, in beats/min), evoked by each chemical; n = sample size. Note that no significant difference in the pressor or cardioaccelerator response was found for any of the vehicles that were injected into the superficial epigastric artery. TRPV1, transient receptor potential vanilloid-1.