5‐Carboxamidotryptamine is a selective agonist at 5‐hydroxytryptamine receptors mediating vasodilatation and tachycardia in anaesthetized cats

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Abstract
We have attempted to characterize the 5‐hydroxytryptamine (5‐HT) receptors mediating bronchoconstriction, vasodilatation, vasodepression and tachycardia in anaesthetized cats following bilateral vagosympathectomy and β‐adrenoceptor blockade with propranolol. 5‐HT (1–100 μg kg−1 i.v.) caused dose‐related bronchoconstriction and tachycardia but variable and complex effects on diastolic blood pressure and carotid arterial vascular resistance. In contrast, 5‐carboxamidotryptamine (5‐CT; 0.01–1 μg kg−1 i.v.) caused consistent, dose‐related decreases in diastolic blood pressure and carotid arterial vascular resistance and increases in heart rate. 5‐CT did not cause bronchoconstriction. The 5‐HT‐induced bronchoconstriction was dose‐dependently antagonized by methiothepin, methysergide and ketanserin (10–100 μg kg−1 i.v.). The highest doses used of these antagonists did not antagonize bronchoconstriction induced by prostaglandin F2α. The high potency of all three antagonists indicate a 5‐HT2‐receptor mediated effect. The 5‐HT‐ and 5‐CT‐induced tachycardia as well as the 5‐CT‐induced vasodepressor and carotid arterial vasodilator responses were dose‐dependently antagonized by low doses of methiothepin (10–100 μg kg−1 i.v.) and by high doses of methysergide (100–1000 μg kg−1 i.v.) but were little affected by ketanserin in doses up to 1000 μg kg−1 i.v. These selective effects of 5‐CT appear to be mediated by ‘5‐HT1‐like’ receptors.