Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The gut may be a site of early diabetic neuropathy in humans and rats. The latter may provide appropriate models of these conditions. Therefore, cholinergic function was examined in two gut smooth muscle preparations from control, 30-day, and 6-month streptozotocin-diabetic and similarly diabetic rats that had received continuous treatment with an aldose reductase inhibitor, ponalrestat. Responses of terminal ileum longitudinal muscle to transmural nerve stimulation were depressed in preparations from untreated 30-day diabetic animals. Responses to exogenous acetylcholine were also depressed, by at least the same extent, in preparations from both 30-day and 6-month diabetic groups. Ponalrestat treatment prevented both changes in the 30-day study but did not prevent a depression of responses to acetylcholine in the 6-month study. Neither diabetes nor ponalrestat affected responses of esophageal muscularis mucosa to electrical stimulation or to exogenous acetylcholine. These observations suggest a change in the smooth muscle and/or noncholinergic innervation rather than in the cholinergic nerves of the ileal preparation. Cholinergic function in the ileum did not, therefore, seem to be an appropriate model of diabetic neuropathy.
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PMID:Effects of diabetes on cholinergic transmission in two rat gut preparations. 189 95

1. The responses of rat isolated aortae to vasoconstrictor and vasodilator agents have been studied in 14-day streptozotocin-diabetic rats. The effects of treatment with the aldose reductase inhibitor, ponalrestat, on these responses have also been investigated. 2. Maximum contractile responses and aortic sensitivity to phenylephrine were significantly enhanced in 14-day diabetic aortae. 3. In contrast, endothelium-dependent relaxations to carbachol were depressed in diabetic rats, whilst endothelium-independent relaxations to forskolin and sodium nitroprusside were unchanged. 4. Pretreatment with ponalrestat (25 mg kg-1, daily) prevented both the enhanced maximum contractile responses to phenylephrine and the depressed endothelium-dependent relaxations to carbachol in aortae from 14-day diabetic rats. Ponalrestat however, had no effect on the reduced phenylephrine EC50 values observed in tissues from diabetic animals. 5. It is concluded that ponalrestat prevents the depression of endothelium-dependent aortic relaxations induced by diabetes of 14 days duration, suggesting that the polyol pathway is involved in these vascular changes. Ponalrestat does not prevent the increase in aortic sensitivity to alpha 1-adrenoceptor agonists.
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PMID:The effects of aldose reductase inhibition with ponalrestat on changes in vascular function in streptozotocin diabetic rats. 783 10