The positive inotropic effect of sodium arachidonate on auricles from diabetic rats

Canga, Liliana; Sterin‐Borda, Leonor; Borda, Enri; Peredo, Horacio A.; Gimeno, A.L.

doi:10.1016/0014-2999(85)90027-5

Cited by 17 publications

(7 citation statements)

References 29 publications

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“…As the depressor action of prostacyclin was overshadowed by the pressor effect of thromboxane A2, this led to the weaker hypotensive response to arachidonic acid in diabetic rats. The present findings with thromboxane B2 are supported by those of other workers in dia betic animals [1,2] and patients [8,13,22]. Non-specific effects in the radioimmunoas say method, if any, although not examined for, cannot be excluded.…”

Section: Discussionsupporting

confidence: 80%

Changes in Arachidonic Acid Metabolite Patterns in Alloxan-Induced Diabetic Rats

et al. 1989

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The vasodepressor responses to intravenous injections of arachidonic acid, and the formation of its metabolites, were studied in rats made diabetic 1 or 2 weeks after a 1-dose alloxan treatment. Arachidonic acid dose-dependently decreased the diastolic blood pressure in normal animals, but this hypotensive effect was significantly weaker in 2-week postalloxan-treated rats. Indometacin abolished arachidonic-acid-induced depressor responses in both normal and diabetic animals. Hypotension induced by sodium nitroprusside was of the same magnitude in non-diabetic and insulin deficient rats. Plasma levels of thromboxane B₂ were significantly increased in both the 1- and 2-week diabetic rats, being greater in the latter group; those of 6-keto-PGF_1α remained unchanged during the 2-week diabetic period. It is concluded that the attenuation by diabetes of depressor responses to arachidonic acid could be due to changes in the thromboxane/prostacyclin balance, with thromboxane formation being elevated whereas prostacyclin generation remains unaffected.

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Section: Discussionsupporting

confidence: 80%

Changes in Arachidonic Acid Metabolite Patterns in Alloxan-Induced Diabetic Rats

et al. 1989

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“…They also found reduced formation of 6-keto-PGF1a from arachidonic acid by aortic rings from diabetic rats. Canga et al (1985) found that diabetic rat atria produced more TXB2 than PGI2 whereas in contrast the opposite was the case in normal tissue.…”

Section: Discussionmentioning

confidence: 91%

Changes in cardiovascular sensitivity of alloxan‐treated diabetic rats to arachidonic acid

Boura

Hodgson

King

1986

British J Pharmacology

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1 Arachidonic acid (AA, 0.125-2.0mgkg-') administered intravenously to male Wistar rats produced a dose-dependent fall in diastolic blood pressure. However AA (0.125 -1.0 mg kg-') injected into the autoperfused hindquarters via the aorta produced a dose-dependent increase in perfusion pressure. Both these responses to AA were inhibited by indomethacin (5 mg kg-'). 2 The thromboxane A2 receptor antagonist AH23848 (5 mg kg-', i.v.) inhibited pressor responses to AA in the autoperfused hindquarters, but potentiated depressor responses to AA (0.125-0.5 mg kg ') in the whole animal. 3 Alloxan-treated diabetic rats (14 days after a single s.c. injection of alloxan, 175mg kg-')displayed reduced sensitivity to the depressor effects of AA (1-2mgkg-1) in the whole animal, increased sensitivity to the pressor effects of AA (0.5-1.0 mg kg-1) in the perfused hindquarters, and reduced sensitivity to the pressor effects of the thromboxane A2 mimetic U46619 (0.5-8.0 fig kg-', i.a.) in the perfused hindquarters. 4 These results suggest that AA can be predominantly converted to either pressor or depressor metabolites depending on the vasculature. In the diabetic state the ratio of the metabolites formed appears to change favouring a major pressor metabolite, which is probably thromboxane A2.

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“…slowly and with greater force than tissues from control rats (Foy & Lucas 1978;Kofo-Abayomi & Lucas 1988;Karasu et al 1990). However, other workers have found no changes in basal parameters (Canga et al 1985;Canga & Sterin-Borda 1986;Austin & Chess-Williams 1991). There are also conflicting reports regarding the sensitivity of rat isolated atria to the inotropic and chronotropic action of the fl-adrenoceptor agonist isoprenaline (Foy & Lucas 1978;Kofo-Abayomi & Lucas 1988;Durante et al 1989;Karasu et al 1990;Austin & Chess-Williams 1991;Yu & McNeill 199 1).…”

mentioning

confidence: 98%

Effects of Aldose Reductase Inhibition With Epalrestat on Diabetes‐induced Changes in Rat Isolated Atria

Booth

Hodgson

1993

Clin Exp Pharma Physio

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1. Isoprenaline and cardiac responsiveness of isolated atria from 2 and 6 week streptozotocin-diabetic rats, and their age-matched controls, was examined. The effects of chronic administration of epalrestat (40 mg/kg orally, by gavage) on diabetes-induced changes were also investigated. 2. Spontaneously beating atria, bathed in either normal or high glucose (30 mmol/L) Krebs' solution, from both 2 and 6 week diabetic rats beat more slowly and with greater force than atria from control rats. These changes in basal parameters were normalized by 2 weeks of insulin (5 U/day s.c.) treatment but not by 2 or 6 weeks of chronic treatment with epalrestat. 3. Isoprenaline (0.1 nmol-0.1 mumol/L) produced concentration-dependent increases in inotropy and chronotropy in atria from both control and diabetic rats. 4. Atria from 2 week diabetic rats displayed decreased sensitivity to the positive inotropic effects of isoprenaline. This change was normalized by chronic insulin treatment but not by chronic epalrestat treatment. 5. Atria from 6 week diabetic rats displayed increased sensitivity to the positive chronotropic effects of isoprenaline which was normalized by epalrestat. 6. These results suggest that changes observed in atria from 2 week diabetic rats may be due to hyperglycaemia per se whereas in atria from 6 week diabetic rats abnormal activity of the polyol pathway may be a contributing factor.

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The positive inotropic effect of sodium arachidonate on auricles from diabetic rats

Cited by 17 publications

References 29 publications

Changes in Arachidonic Acid Metabolite Patterns in Alloxan-Induced Diabetic Rats

Changes in Arachidonic Acid Metabolite Patterns in Alloxan-Induced Diabetic Rats

Changes in cardiovascular sensitivity of alloxan‐treated diabetic rats to arachidonic acid

Effects of Aldose Reductase Inhibition With Epalrestat on Diabetes‐induced Changes in Rat Isolated Atria

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