Table 1 |
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|
Vasodilator responses after organ culture |
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|
n |
pEC50 (-log M) |
P |
Rmax (%) |
P |
||
|
|
||||||
|
ACh |
Control |
10 |
7.5 ± 0.2 |
} n.s. |
93 ± 1 |
} n.s. |
|
Cultured |
10 |
7.1 ± 0.1 |
93 ± 3 |
|||
|
ACh, NO-mediated |
Control |
10 |
7.2 ± 0.2 |
} n.s. |
84 ± 6 |
} <0.0001 |
|
Cultured |
10 |
7.1 ± 0.2 |
36 ± 6 |
|||
|
ACh, prostaglandin-mediated |
Control |
10 |
6.1 ± 0.4 |
} n.s. |
48 ± 7 |
} <0.001 |
|
Cultured |
10 |
6.6 ± 0.4 |
16 ± 4 |
|||
|
ACh, EDHF-mediated |
Control |
10 |
7.1 ± 0.2 |
} n.s. |
83 ± 3 |
} n.s. |
|
Cultured |
10 |
6.1 ± 0.5 |
80 ± 3 |
|||
|
Forskolin |
Control |
7 |
7.1 ± 0.2 |
} n.s. |
95 ± 1 |
} n.s. |
|
Cultured |
7 |
7.3 ± 0.2 |
97 ± 2 |
|||
|
SNP |
Control |
9 |
8.8 ± 0.1 |
} n.s. |
96 ± 1 |
} n.s. |
|
Cultured |
9 |
8.9 ± 0.2 |
93 ± 4 |
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|
|
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|
Vasodilatation was assessed by cumulative addition of ACh, forskolin or SNP in the precontracted mesenteric artery branch, before and after organ culture for 20 h. NO-dilatation was studied in the presence of indomethacin (10 μM), charybdotoxin (50 nM) and apamin (1 μM); prostaglandin-dilatation in the presence of L-NOARG (0.1 mM), charybdotoxin and apamin; and EDHF-dilatation in the presence of indomethacin and L-NOARG. Dilatory responses are expressed as percentage of a precontraction induced by U46619. n denotes the number of experiments (animals). Statistical significance is expressed as P. Data are given as mean values ± S.E.M. |
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|
Alm et al. BMC Cardiovascular Disorders 2002 2:8 doi:10.1186/1471-2261-2-8 |
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