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001-es BibID:BIBFORM020340
Első szerző:Sári Réka (farmakológus)
Cím:Cyclic GMP-mediated activation of a glibenclamide-sensitive mechanism in the rabbit sphincter of Oddi / Reka Sari, Barna Peitl, Peter Kovacs, Janos Lonovics, Attila Palvolgyi, Peter Hegyi, Istvan Nagy, Jozsef Nemeth, Zoltan Szilvassy, Robert Porszasz
Dátum:2004
Megjegyzések:AbstractWe investigated whether glibenclamide-sensitive potassium channels are involved in cyclic GMP (cGMP)-mediated relaxation of the rabbit Oddi's sphincter. Changes in isometric tension were measured in the presence of atropine (1 microM) and guanethidine (4 microM). Concentration-response curves for nitroglycerin, vasoactive intestinal polypeptide (VIP), and sodium nitroprusside (SNP) were shifted to the right in the presence of (p-chloro-D-Phe6, Leu17)-VIP (VIPa), a VIP receptor antagonist. Glibenclamide (1 microM) attenuated the relaxations to VIP, nitroglycerin, or 8-bromo cGMP. In the presence of tetrodotoxin (TTX), glibenclamide attenuated relaxations to VIP without effect on those to nitroglycerin. Furthermore, nitroglycerin increased both cAMP and cGMP concentrations, however, it failed to increase the tissue cAMP concentration in the presence of TTX. VIPa also blocked the increase in content of either cyclic nucleotide. VIP increased cAMP with a TTX-sensitive increase in cGMP content. 8-Bromo cGMP (1 microM) significantly increased the tissue cAMP content. This was blocked by either TTX or VIPa (both 1 microM). We conclude that ATP-sensitive potassium channel (KATP) activation contributes to cGMP-mediated relaxation of the Oddi's sphincter of the rabbit. Activation of KATP results from a cyclic AMP-mediated process due to cGMP-dependent VIP release from neurons.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Cyclic GMP
GMP-Mediated Activation
Glibenclamide-Sensitive
Megjelenés:Digestive Diseases and Sciences. - 49 : 3 (2004), p. 514-520. -
További szerzők:Peitl Barna (1972-) (orvos, farmakológus) Kovács Péter (1947-) (belgyógyász, kardiológus, klinikai farmakológus) Lonovics János (Szeged) Pálvölgyi Attila Hegyi Péter Jenő (belgyógyász) Nagy István (orvos) Németh József (Pécs) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus)
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DOI
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2.

001-es BibID:BIBFORM028449
Első szerző:Szilvássy Zoltán (belgyógyász, farmakológus, klinikai farmakológus)
Cím:Insulin resistance occurs in parallel with sensory neuropathy in streptozotocin-induced diabetes in rats : differential response to early vs late insulin supplementation / Szilvássy Z., Németh J., Kovács P., Paragh G., Sári R., Vígh L., Peitl B.
Dátum:2012
Megjegyzések:We investigated whether progressive sensory neuropathy was accompanied by changes in whole-body insulin sensitivity (WBIS) in rats made diabetic by streptozotocin (STZ). The effects of early and late insulin supplementation were also studied. The STZ-treated rats failed to gain weight and exhibited stable hyperglycemia and low plasma insulin levels with a decrease in nerve conduction velocity (NCV) measured in A and C fibers of the saphenous nerve. A decreased sensory neuropeptide (SNP) release such as that of substance P, somatostatin, and calcitonin gene-related peptide determined from organ fluid of tracheal preparations subjected to electrical field stimulation also occurred in diabetic animals. These features were accompanied by a decrease in WBIS measured by hyperinsulinemic-euglycemic glucose clamping and a decrease in insulin-stimulated glucose uptake in cardiac and gastrocnemius muscle. When insulin supplementation with slow-release implants (2 IU/d) was started 4 weeks after STZ injection, blood glucose level normalized. Both insulin sensitivity and sensory nerve function reflected in either NCV or SNP release completely recovered by the 12th post-STZ week. When the insulin implants were applied from the eighth post-STZ week, both WBIS and glucose uptake remained significantly decreased, with a seriously impaired NCV and SNP release with strong hyperglycemia. Late insulin supplementation, however, even by using double implantation from the 10th post-STZ week, was unable to restore blood glucose, WBIS, NCV, and SNP release by the 12th week. Insulin resistance occurs in parallel with sensory neuropathy in STZ-diabetic rats. Both can be improved by early but not late insulin supplementation.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Metabolism. - 61 : 6 (2012), p. 776-786. -
További szerzők:Németh József (1954-) (vegyész, analitikus) Kovács Péter (1947-) (belgyógyász, kardiológus, klinikai farmakológus) Paragh György (1953-) (belgyógyász) Sári Réka (farmakológus) Vígh László (orvos Szeged) Peitl Barna (1972-) (orvos, farmakológus)
Pályázati támogatás:TÁMOP-4.2.2.-08/1-2008-0014
TÁMOP
75965
OTKA
NKFP_07-A2-2008-0260
Egyéb
GOP-1.1.207/1-2008-0004
Egyéb
OM00174/2008
Egyéb
GOP-1.1.1-07/1-2008-0032
Egyéb
GOP-1.2.1-082009-0023
Egyéb
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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