DIABETES‐INDUCED CHANGES IN 5‐HYDROXYTRYPTAMINE MODULATION OF VAGALLY INDUCED BRADYCARDIA IN RAT HEART (Englisch)

Clinical and Experimental Pharmacology and Physiology

In the present study, we investigated how alloxan‐induced diabetes affects the ability of 5‐hydroxytryptamine (5‐HT) to modulate bradycardia induced in vivoby electrical stimulation of the vagus nerve in pithed rats. We also analysed the type and/or subtype of 5‐HT receptors involved.

Diabetes was induced in male Wistar rats with a single injection of alloxan (150 mg/kg, s.c.). Four weeks later, rats were anaesthetized, pretreated with atenolol and pithed. Electrical stimulation (3, 6 and 9 Hz) of the vagus nerve resulted in frequency dependent decreases in heart rate (HR).

In diabetic rats, intravenous bolus administration of high doses of 5‐HT (100 and 200 µg/kg) increased the bradycardia induced by vagal electrical stimulation. Similarly, low doses (10 µg/kg) of the 5‐HT1/7 receptor agonist 5‐carboxamidotryptamine (5‐CT), increased vagally induced bradycardia. However, at high doses (50, 100 and 150 µg/kg), 5‐CT reduced the bradycardia. Attenuation of the vagally induced bradycardia evoked by the higher doses of 5‐CT was reproduced by L‐694,247 (50 µg/kg), a selective agonist for the non‐rodent 5‐HT1B and 5‐HT1D receptors. Enhancement of the vagally induced bradycardia elicited by low doses of 5‐CT was reproduced by the selective 5‐HT1A receptor agonist 8‐hydroxydipropylaminotretalin hydrobromide (8‐OH‐DPAT; 50 µg/kg). These stimulatory and inhibitory actions on vagal stimulation‐induced bradycardia in diabetic rats were also observed after administration of exogenous acetylcholine.

Vagally induced bradycardia in diabetic rats was not affected by administration of the selective 5‐HT2 receptor agonist α‐methyl‐5‐HT (150 µg/kg), the selective 5‐HT3 receptor agonist 1‐phenylbiguanide (150 µg/kg) or the selective 5‐HT1B receptor agonist CGS‐12066B (50 µg/kg).

Enhancement of the electrical stimulation‐induced bradycardia in diabetic rats caused by 5‐CT (10 µg/kg) or 8‐OH‐DPAT (50 µg/kg) was abolished by the selective 5‐HT2/7 receptor antagonist mesulergine (1 mg/kg) and the selective 5‐HT1A receptor antagonist WAY‐100,635 (100 µg/kg), respectively. Similarly, pretreatment with the non‐selective 5‐HT1 receptor antagonist methiothepin (0.1 mg/kg) blocked the inhibitory effect of 5‐CT (50 µg/kg) on the bradycardia induced by vagal electrical stimulation in diabetic rats. BRL‐15572 (2 µg/kg), a selective 5‐HT1D receptor antagonist, inhibited the action of L‐694,247 (50 µg/kg), a selective agonist for the non‐rodent 5‐HT1B and 5‐HT1D receptors, on the vagally induced bradycardia.

In conclusion, in the present study, experimental diabetes evoked changes in both the nature and 5‐HT receptor types/subtypes involved in vagally induced bradycardia.

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