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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Nitric oxide-mediated neurotransmission is attenuated in the anococcygeus muscle from diabetic rats.

The effect of STZ-induced diabetes of 8-weeks duration was examined on nitric oxide-mediated neurotransmission in the rat anococcygeus muscle. In the presence of noradrenergic blockade and raised tissue tone, relaxant response to nerve stimulation (0.5-5 Hz, for 10 s), sodium nitroprusside (5 and 10 nmol/l) and nitric oxide (1 and 3 mumol/l) were significantly reduced in anococcygeus muscles from diabetic rats compared to responses from control rats (p < 0.05). In contrast, relaxations to papaverine (3 and 10 mumol/l) were not reduced in tissues from diabetic rats. The nitric oxide synthesis inhibitor NOLA (100 mumol/l) abolished relaxant responses to nerve stimulation but had no effect on responses to any of the relaxant agents used. Exposure to NOLA at 10 mumol/l reduced stimulation-induced relaxations; this reduction was significantly greater in tissues from the diabetic group than from the control group (p < 0.05), probably as a consequence of the smaller relaxant responses in muscles from diabetic rats. Contractile responses to nerve stimulation (1-10 Hz, for 10 s), but not noradrenaline (0.03-30 mumol/l), were significantly greater in anococcygeus muscles from diabetic rats than from control rats (p < 0.05). NOLA (100 mumol/l) significantly enhanced stimulation-induced contractions (p < 0.05), however the enhancement was significantly less in tissues from diabetic rats (p < 0.05). The results suggest that STZ-induced diabetes impairs smooth muscle reactivity to nitric oxide in the rat anococcygeus muscle.[1]


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