Abstract
Gut motility is modulated by adrenergic mechanisms. The aim of our study was to examine mechanisms of selective adrenergic receptors in rat jejunum. Spontaneous contractile activity of longitudinal muscle strips from rat jejunum was measured in 5-ml tissue chambers. Dose–responses (six doses, 10−7–3 × 10−5M) to norepinephrine (NE, nonspecific), phenylephrine (PH, α1), clonidine (C, α2), prenalterol (PR, β1), ritodrine (RI, β2), and ZD7714 (ZD, β3) were evaluated with and without tetrodotoxin (TTX, nerve blocker). NE(3 × 10−5M) inhibited 74 ± 5% (mean ± SEM) of spontaneous activity. This was the maximum effect. The same dose of RI(β2), PH(α1), or ZD(β3) resulted in an inhibition of only 56 ± 5, 43 ± 4, 33 ± 6, respectively. The calculated concentration to induce 50% inhibition (EC50) of ZD(β3) was similar to NE, whereas higher concentrations of PH(α1) or RI(β2) were required. C(α2) and PR(β1) had no effect. TTX changed exclusively the EC50 of RI from 4.4±0.2 to 2.7 ± 0.8% (p < 0.04). Contractility was inhibited by NE (nonspecific). PH(α1), RI(β2), and ZD(β3) mimic the effect of NE. TTX reduced the inhibition by RI. Our results suggest that muscular α1, β2, and β3 receptor mechanisms mediate adrenergic inhibition of contractility in rat jejunum. β2 mechanisms seem to involve also neural pathways.
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