The reaction to noradrenaline (NA) (10 microM) and electrical field stimulation (EFS) was studied in rat mesenteric artery segments at different magnitude of stretch and the solution pH. Alkaline solution (pH 7.8) potentiated and acidic solution (pH 7.0 or 6.6) inhibited the EFS-evoked response of segments stretched to values corresponding to arterial pressure of 5-200 mmHg. These pH changes failed to alter resting tension at any magnitude of stretch. Acedic solution of pH 6.6 caused 2-fold decrease in noradrenaline- and 5-15-fold decrease in the EFS-evoked response of segments stretched to values corresponding to arterial pressure of 50, 125, and 200 mmHg. In segments pre-contracted with noradrenaline (10 microM) acidification caused the decrease of the dilation and appearance of the constriction induced by the EFS. The effect of acidosis on the EFS-evoked response was diminished and the effect on noradrenaline-evoked response was abolished in the presence of nitric oxide synthase blocker, NG-nitro-L-arginine (100 microM). These results suggest that acidosis effectively impairs reactivity of the rat mesenteric artery in a wide range of its stretch, and the inhibition of the response to noradrenaline occurs completely, while to EFS only partially due to nitric oxide (NO) release, presumably by the endothelium. In addition, it was shown that acidosis is able to act not only as the commonly known dilator agent, but also as an agent potentiating constriction in case of the high noradrenaline-induced tone.
The effect of dynamic stretch on the reactivity of the rat tail and mesenteric artery segments was studied. Segments mounted on a myograph were stretched by a computer-controlled motorized micromanipulator. Dynamic stretch (1, 5 or 7 Hz) inhibited the artery constriction induced by noradrenaline (10 microM), 5-hydroxytryptamine (0.7 microM), or electrical field stimulation of intramural nerves. In contrast, dynamic stretch enhanced the tetrodotoxin-insensitive dilation induced by electrical field stimulation of noradrenaline-contracted arteries. Maximal increase of dilation evoked by electrical field stimulation (24.5 +/- 5.0% in mesenteric and 50.3 +/- 15.6% in the tail artery) was observed at a dynamic stretch-frequency of 5 Hz. An inhibitor of nitric oxide synthesis, NG-nitro-L-arginine (100 microM), abolished the difference in reactivity between static and dynamic conditions. The results indicate that dynamic stretch of the arteries activates nitric oxide synthesis/secretion, thus reducing constrictor and increasing dilator responses to the stimuli used.
These data suggest that melatonin can restore an attenuated neurogenic reactivity of the juvenile rat tail artery. The effect is more pronounced with further decrease in reactivity and might be due to a change in sensitivity of the post-junctional membrane to noradrenaline.
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