LM-MPLongitudinal Muscle with Myenteric Plexus
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Blockade of smooth muscle contractions with the [Ca.sub.v]1 (L-type) voltage-sensitive calcium channel inhibitor, nifedipine (1-5 [micro]M), did not affect the accumulation of adenine nucleosides in bath samples collected immediately before and after electric field stimulation to the LM-MP from healthy animals [19].
These results suggest that, under the present experimental conditions, the cAMP-adenosine pathway does not account significantly for endogenous adenosine formation in the LM-MP of the rat ileum.
It is, therefore, possible that disruption of ATP catabolism into adenosine via ecto-NTPDases may occur in the inflamed LM-MP of the ileum.
The activity of ecto-5'nucleotidase/CD73 was significantly (P < 0.05) impaired in the LM-MP of the ileum following an inflammatory insult, particularly when ADP (30 [micro]M) was used as substrate.
Figure 8 shows that in control LM-MP preparations the immunoreactivity against NTPDase2 is restricted to ganglion cell bodies and large ramifications (primary meshwork) of the myenteric plexus (compared to [48]).
The bath concentrations of adenosine (30 [micro]M) decrease progressively with time yielding to the formation of inosine and hypoxanthine in the LM-MP of the rat ileum (see [19]).
Figure 9(a), also shows that the activity of the soluble form of ADA retained in the incubation fluid is highest during the first 5 min after removing the LM-MP preparation from the bath.