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. 2016 Mar 2;52:1–17. doi: 10.1540/jsmr.52.1

Fig. 2.

Fig. 2.

Effects of AITC on DSM contractility are not influenced by the inhibitors of efferent neurotransmission. A: The bar graph (mean ± s.e.m., n=6–8) shows no significant difference in the residual amplitude of EFS-contractions of DSM strips from control rats in the presence of atropine (1 µM) plus phentolamine (1 µM) (ATR+PHE, dark grey columns) and atropine (1 µM) plus guanethidine (3 µM) (ATR+GUA, dark grey columns) without or with 100 µM suramine (SUR, horizontal bar). B: A representative recording of the contractions of DSM strips from control rats during application of atropine (ATR, 1 µM) plus guanethidine (GUA, 3 µM) plus (SUR, 100 µM) followed by consecutive applications of 10 µM and 100 µM of AITC; note the strong inhibition of the amplitude of the EFS-contractions as a result of ATR+GUA+SUR and its transient potentiation by AITC accompanied by tone enhancement. C: The bar graph (mean ± s.e.m., n=6–8), shows the similarity of relative potentiation of the amplitude of the EFS-contractions in response to AITC (100 µM) applied in the presence of atropine (1 µM) plus phentolamine (1 µM) (ATR+PHE), atropine (1 µM) plus guanethidine (3 µM) (ATR+GUA) without or with 100 µM suramine (ATR+PHE+SUR and ATR+GUA+SUR).