There was no significant difference between Tyrode and DMSO, and their effect did not differ from the baseline (p>0.999). ATG decreased the frequency of contractions in a dose-dependent manner, manifested by the increased period time [Fig. 4].; 20 µM ATG and 40 µM ATG showed an observable increased period time characterised by an alteration in spontaneous contraction [Fig. 2]. After 15 and 30 min, 40 µM ATG had higher activity than Tyrode, DMSO, 10 µM ATG, 20 µM ATG and 10 µM TGN (p˂ 0.0001). ButHowever, increasing the concentration of ATG from 1 µM to 10 µM did not lead to a significant increase in activity (p> 0.999) [ Fig. 4].
Likewise, (TGN) increased the contraction period in a dose-dependent manner. After 15 and 30 min, 20 µM TGN had higher activity than Tyrode, DMSO, 10 µM ATG, 20 µM ATG and 10 µM TGN (p˂ 0.05)
.; 20 µM TGN was also marked by an alteration of spontaneous contraction that becomebecame clear after 30 min [Fig. 2]. Though there was an observable increase after treatment with 10 µM TGN, it was not significantly different from 0.5 µM TGN and 1 µM TGN and (p> 0.999).
Comparatively, there was no difference between 10 µM ATG and 10 µM TGN (p>0.05).
ButHowever, 20 µM TGN, had higher activity than 20 µM ATG (p˂0.05) and was comparable to 40 µM ATG over the same period (p> 0.05) [Fig.4].
CNQX, AP5, propranol plus phentolamine and LNAME had no effect (p>0.999). The activity of 0.5 µM nifedipine was higher than 1 µM ATG, 10 µM ATG, 0.5 µM TGN, 1 µM TGN and 10 µM TGN, (p˂0.05) [ Fig. 4]
.; 1 µM nifedipine abolished the phasic contractions, which waswere reversed after 15 min of washout with Tyrode’s solution [Fig. 2].

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