Increase in atrial contractility induced by PGE2 in diabetic rats
Contractile response to exogenous prostaglandin E2 (PGE2) was studied in auricles from normal and acutely-diabetic (streptozotocin-treated) rats. In normal atria, PGE2 induced a biphasic inotropic effect negative at low concentrations and positive at higher ones. In diabetic, PGE2 only elicited a po...
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1986
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00316989_v18_n4_p371_Canga http://hdl.handle.net/20.500.12110/paper_00316989_v18_n4_p371_Canga |
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paper:paper_00316989_v18_n4_p371_Canga2023-06-08T14:57:11Z Increase in atrial contractility induced by PGE2 in diabetic rats acetylsalicylic acid alpha adrenergic receptor dithizone indometacin nordihydroguaiaretic acid phenoxybenzamine phentolamine prazosin propranolol prostaglandin e2 streptozocin animal cell animal experiment arachidonic acid metabolism drug efficacy endocrine system heart heart atrium heart muscle heart muscle contractility intravenous drug administration nonhuman priority journal rat streptozocin diabetes Adrenergic alpha-Antagonists Adrenergic beta-Antagonists Animal Arachidonic Acid Arachidonic Acids Cyclooxygenase Inhibitors Diabetes Mellitus, Experimental Dinoprostone In Vitro Lipoxygenase Inhibitors Male Myocardial Contraction Prostaglandins E Rats Rats, Inbred Strains Support, Non-U.S. Gov't Thromboxane-A Synthase Contractile response to exogenous prostaglandin E2 (PGE2) was studied in auricles from normal and acutely-diabetic (streptozotocin-treated) rats. In normal atria, PGE2 induced a biphasic inotropic effect negative at low concentrations and positive at higher ones. In diabetic, PGE2 only elicited a positive inotropic action which was greater in efficacy and potency than in normal controls. Incubation of diabetic atrial preparations with α-adrenoceptor antagonists (phentolamine, phenoxybenzamine or Prazosin) diminished the prostaglandin effect. However, blockade of β-adrenoceptors with propranolol did not modify the response. Blockers of arachidonic acid metabolism via cyclo-oxygenase (indomethacin and acetylsalicylic acid) or via lipoxygenase(s) (nordihydroguaiaretic acid and dithizone) were able to reduce the positive inotropism of PGE2. A significant blockade of the stimulant action of PGE2 was seen in the presence of inhibitors of thromboxane synthesis (L-8027 and imidazole). These results suggest that in diabetic atria PGE2 effect could be associated to an involvement of cardiac α-adrenergic stimulation which promotes endogenous arachidonic acid release with diversification of its metabolism towards cyclo- and lipoxygenase(s)- pathway and direct to an increased thromboxane formation which could account for the positive inotropic effect induced by PGE2. © 1986. 1986 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00316989_v18_n4_p371_Canga http://hdl.handle.net/20.500.12110/paper_00316989_v18_n4_p371_Canga |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
acetylsalicylic acid alpha adrenergic receptor dithizone indometacin nordihydroguaiaretic acid phenoxybenzamine phentolamine prazosin propranolol prostaglandin e2 streptozocin animal cell animal experiment arachidonic acid metabolism drug efficacy endocrine system heart heart atrium heart muscle heart muscle contractility intravenous drug administration nonhuman priority journal rat streptozocin diabetes Adrenergic alpha-Antagonists Adrenergic beta-Antagonists Animal Arachidonic Acid Arachidonic Acids Cyclooxygenase Inhibitors Diabetes Mellitus, Experimental Dinoprostone In Vitro Lipoxygenase Inhibitors Male Myocardial Contraction Prostaglandins E Rats Rats, Inbred Strains Support, Non-U.S. Gov't Thromboxane-A Synthase |
| spellingShingle |
acetylsalicylic acid alpha adrenergic receptor dithizone indometacin nordihydroguaiaretic acid phenoxybenzamine phentolamine prazosin propranolol prostaglandin e2 streptozocin animal cell animal experiment arachidonic acid metabolism drug efficacy endocrine system heart heart atrium heart muscle heart muscle contractility intravenous drug administration nonhuman priority journal rat streptozocin diabetes Adrenergic alpha-Antagonists Adrenergic beta-Antagonists Animal Arachidonic Acid Arachidonic Acids Cyclooxygenase Inhibitors Diabetes Mellitus, Experimental Dinoprostone In Vitro Lipoxygenase Inhibitors Male Myocardial Contraction Prostaglandins E Rats Rats, Inbred Strains Support, Non-U.S. Gov't Thromboxane-A Synthase Increase in atrial contractility induced by PGE2 in diabetic rats |
| topic_facet |
acetylsalicylic acid alpha adrenergic receptor dithizone indometacin nordihydroguaiaretic acid phenoxybenzamine phentolamine prazosin propranolol prostaglandin e2 streptozocin animal cell animal experiment arachidonic acid metabolism drug efficacy endocrine system heart heart atrium heart muscle heart muscle contractility intravenous drug administration nonhuman priority journal rat streptozocin diabetes Adrenergic alpha-Antagonists Adrenergic beta-Antagonists Animal Arachidonic Acid Arachidonic Acids Cyclooxygenase Inhibitors Diabetes Mellitus, Experimental Dinoprostone In Vitro Lipoxygenase Inhibitors Male Myocardial Contraction Prostaglandins E Rats Rats, Inbred Strains Support, Non-U.S. Gov't Thromboxane-A Synthase |
| description |
Contractile response to exogenous prostaglandin E2 (PGE2) was studied in auricles from normal and acutely-diabetic (streptozotocin-treated) rats. In normal atria, PGE2 induced a biphasic inotropic effect negative at low concentrations and positive at higher ones. In diabetic, PGE2 only elicited a positive inotropic action which was greater in efficacy and potency than in normal controls. Incubation of diabetic atrial preparations with α-adrenoceptor antagonists (phentolamine, phenoxybenzamine or Prazosin) diminished the prostaglandin effect. However, blockade of β-adrenoceptors with propranolol did not modify the response. Blockers of arachidonic acid metabolism via cyclo-oxygenase (indomethacin and acetylsalicylic acid) or via lipoxygenase(s) (nordihydroguaiaretic acid and dithizone) were able to reduce the positive inotropism of PGE2. A significant blockade of the stimulant action of PGE2 was seen in the presence of inhibitors of thromboxane synthesis (L-8027 and imidazole). These results suggest that in diabetic atria PGE2 effect could be associated to an involvement of cardiac α-adrenergic stimulation which promotes endogenous arachidonic acid release with diversification of its metabolism towards cyclo- and lipoxygenase(s)- pathway and direct to an increased thromboxane formation which could account for the positive inotropic effect induced by PGE2. © 1986. |
| title |
Increase in atrial contractility induced by PGE2 in diabetic rats |
| title_short |
Increase in atrial contractility induced by PGE2 in diabetic rats |
| title_full |
Increase in atrial contractility induced by PGE2 in diabetic rats |
| title_fullStr |
Increase in atrial contractility induced by PGE2 in diabetic rats |
| title_full_unstemmed |
Increase in atrial contractility induced by PGE2 in diabetic rats |
| title_sort |
increase in atrial contractility induced by pge2 in diabetic rats |
| publishDate |
1986 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00316989_v18_n4_p371_Canga http://hdl.handle.net/20.500.12110/paper_00316989_v18_n4_p371_Canga |
| _version_ |
1768542163783647232 |