Impairment of GABA-Mediated Contractions of Rat Isolated Ileum by Experimental Diabetes

Özdem, Sadi S.; Sadan, Gulay

doi:10.1159/000028317

Cited by 4 publications

(4 citation statements)

References 24 publications

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“…Some studies have shown that GABA could decrease basal tone and phenylephrine-induced contraction in normal isolated aortic rings (Gimeno et al 1994), and GABA has a direct effect on vascular smooth muscle (Ozdem and Sadan 1999). Ozdem and co-workers have shown that besides the direct modulatory action that GABA exerts on normal vascular smooth muscle, it also modulates endothelial function (Ozdem 1997). In our previous study, we showed that GABA can induce endothelial vasorelaxation in control and diabetic groups and this effect was mediated by same pathway in both groups.…”

Section: Introductionmentioning

confidence: 63%

GABA-induced vasorelaxation mediated by nitric oxide and GABAA receptor in non diabetic and streptozotocin-induced diabetic rat vessels

Kamran¹,

Bahrami²,

Soltani³

et al. 2013

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Diabetes has profound, negative effects on the function of arteries and arterioles. Hypertension is considered an independent risk factor for cardiovascular mortality in diabetic patients. The present study was designed to determine whether GABA-induced vasorelaxation in normal and streptozotocin-induced diabetic rat vessels is mediated by nitric oxide and the GABAA receptor. Diabetes was induced by a single intraperitoneal injection of streptozotocin (STZ) (60 mg/kg). Eight weeks later, superior mesenteric arteries of all groups were isolated and perfused according to the McGregor method. Baseline perfusion pressure of STZ diabetic rats was significantly higher than non-diabetic rats in both intact and denuded endothelium. In the presence of bicuculline, a selective GABAA receptor blocker, GABA-induced relaxation in intact and denuded endothelium mesenteric beds of non-diabetic and STZ diabetic rats was suppressed. But in the presence of L-NAME, a nitric oxide synthesis inhibitor, although GABA- induced vasorelaxation was not suppressed at a dose of 1 µM of GABA in all groups, this response was suppressed with the other doses of GABA. From the results of this study it may be concluded that the vasorelaxatory effect of GABA is mediated by the GABAA receptor and nitric oxide in both STZ diabetic and non-diabetic vessels.

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Section: Introductionmentioning

confidence: 63%

GABA-induced vasorelaxation mediated by nitric oxide and GABAA receptor in non diabetic and streptozotocin-induced diabetic rat vessels

Kamran¹,

Bahrami²,

Soltani³

et al. 2013

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“…In addition, the relaxations induced by GABA were not significantly changed in hyperhomocysteinemic duodenal tissues compared with control. The finding that relaxation responses to GABA, EFS, and ATP were not different between hyperhomocysteinemic and control rats suggests that hyperhomocysteinemia does not cause an important impairment on NANC innervation of the rat duodenum such as previously shown in diabetic models [34,57]. So possible gastrointestinal symptoms or gastroenteropaties that could be associated with hyperhomocysteinemia may be a result of other mechanisms.…”

Section: Discussionmentioning

confidence: 56%

Effects of Hyperhomocysteinemia on Non-Adrenergic Non-Cholinergic Relaxation in Isolated Rat Duodenum

2008

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The effect of hyperhomocysteinemia induced by pretreatment with methionine 12 weeks prior to the study on the responses induced by gamma-aminobutyric acid (GABA), electrical field stimulation (EFS), and ATP have been evaluated in isolated rat duodenum. In the presence of adrenergic and cholinergic blockade, EFS (60 V, 1 ms, 1-3 Hz) induced frequency-dependent relaxations of the preparation. GABA and ATP also caused submaximal relaxation of the rat duodenum. The relaxations induced by GABA, EFS, and ATP were not significantly changed in duodenal tissues from hyperhomocysteinemic rats compared with control rats. GABA- and EFS-induced relaxations were inhibited by N-nitro-L-arginine methyl ester (L-NAME; 3 x 10(-4) M) in both hyperhomocysteinemic and control rats. On the other hand, L-NAME incubation did not affect ATP-induced relaxation. These results suggest that hyperhomocysteinemia does not cause an important impairment on non-adrenergic non-cholinergic innervation of the rat duodenum.

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“…8,14 Results suggest that GABA decreases the contractile responses of airway smooth muscles to cholinergic nerve stimulation by inhibiting the release of ACh from post-ganglionic parasympathetic nerves in the guinea-pig trachea. 26,27 It is also possible that the inhibitory effect of GABA and GABA analogues on contractions of tracheal smooth muscle is impaired in diabetes. 15 The GABA-producing enzyme glutamate decarboxylase (GAD) is a prominent auto-antigen in insulin-dependent diabetes mellitus (IDDM).…”

Section: Introductionmentioning

confidence: 99%

“…15,20,24,25 Recently, we have shown that induction of diabetes impairs the responsiveness of various smooth muscle tissues to GABA and its analogues in rats. 26,27 It is also possible that the inhibitory effect of GABA and GABA analogues on contractions of tracheal smooth muscle is impaired in diabetes. Thus, in the present study, we investigated the effect of GABA and selective GABA agonists and antagonists on neurally induced airway contractions in STZ-diabetic rats.…”

Section: Introductionmentioning

confidence: 99%

Effect Of Experimental Diabetes On Gaba‐Mediated Inhibition Of Neurally Induced Contractions In Rat Isolated Trachea

Özdem

Sadan

Usta

et al. 2000

Clin Exp Pharma Physio

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1. In the present study, we investigated the effect of GABA and selective GABA agonists and antagonists on neurally induced tracheal contractions in streptozotocin (STZ) diabetic rats. 2. Contractile responses to electrical field stimulation (EFS) in rat tracheal rings were completely abolished by atropine and tetrodotoxin, but were unaffected by the ganglion blocker hexamethonium, indicating that they were mediated via neuronal release of acetylcholine (ACh). 3. Contractions induced by EFS, but not by exogenous ACh, were inhibited by GABA and the selective GABA(B) receptor agonist baclofen, but not by the selective GABA(A) receptor agonist 3-aminopropane sulphonic acid. The inhibitory effects of GABA or baclofen were not affected by the GABA(A) antagonist bicuculline, but were significantly reversed by the GABA(B) antagonist phaclofen. 4. The inhibitory effects of both GABA and baclofen were found to be significantly greater in trachea from control rats compared with tissues from diabetic rats. 5. Non-adrenergic, non-cholinergic relaxation responses elicited by EFS in precontracted tracheal rings from diabetic and control rats were similar in magnitude and were unaffected by GABA or GABA analogues. 6. These results suggest that GABA decreases the response to EFS by directly inhibiting the evoked release of ACh through GABA(B) receptors in rat trachea and that STZ-induced diabetes causes an impairment in the inhibitory effect of GABA on neurally induced contractions in this tissue.

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Impairment of GABA-Mediated Contractions of Rat Isolated Ileum by Experimental Diabetes

Cited by 4 publications

References 24 publications

GABA-induced vasorelaxation mediated by nitric oxide and GABAA receptor in non diabetic and streptozotocin-induced diabetic rat vessels

GABA-induced vasorelaxation mediated by nitric oxide and GABAA receptor in non diabetic and streptozotocin-induced diabetic rat vessels

Effects of Hyperhomocysteinemia on Non-Adrenergic Non-Cholinergic Relaxation in Isolated Rat Duodenum

Effect Of Experimental Diabetes On Gaba‐Mediated Inhibition Of Neurally Induced Contractions In Rat Isolated Trachea

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