Effect of PACAP1–27, PACAP1–38, and VIP on contraction to ACh in vitro measured as amplitude of response
| Treatment | 10−8M | 10−6 M | ||
|---|---|---|---|---|
| Before S1 | After S3 | Before S1 | After S3 | |
| Control (n = 4) | 21.8 ± 5.5 | 17.0 ± 7.0 | ||
| PACAP1–27 (n = 4) | 12.5 ± 2.8 | 8.8 ± 3.3 | ||
| Control (n = 4, 6)b | 24.5 ± 6.6 | 16.5 ± 4.1 | 12.5 ± 2.6 | 13.0 ± 3.1 |
| PACAP1–38 (n = 4, 6)b | 14.3 ± 1.3 | 18.5 ± 4.5 | 9.3 ± 1.9 | 5.7 ± 1.17-150 |
| Control (n = 8, 6)b | 8.9 ± 2.5 | 10.9 ± 2.8 | 32.2 ± 12 | 40.5 ± 16.1 |
| VIP (n = 8, 6)b | 8.9 ± 4.1 | 10.3 ± 3.7 | 26.3 ± 8.7 | 27.7 ± 9.8 |
Contractions measured in mm (5 mm = 1 g) and presented as mean ± S.E.M.
7-a Refers to the number of animals studied at the two higher concentrations. The first n value represents the number of animals studied at the two lower concentrations.
↵7-150 p > .05 significantly different from control. Note that because the release of [3H]ACh response shown in Table 4was increased by PACAP1–27 at 10−* M and by 10−6 M VIP, as were responses to EFS (although insignificantly; data not shown), the ACh response was decreased (also insignificantly); this suggests that PACAP1–27 and VIP released sufficient extra ACh to overcome their inhibitory myogenic actions, but PACAP1–38 did not.