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The effects of frovatriptan and sumatriptan on internal carotid and coronary vascular haemodynamics were investigated and compared in conscious dogs.Frovatriptan and sumatriptan (0.1–100 μg kg−1) induced a transient increase in external coronary artery diameter (eCOD) of up to 2.9±1.2 and 1.8±0.6%, respectively (both P<0.05). This was followed by a prolonged and dose‐dependent decrease in eCOD of up to −5.2±1.2 and −5.3±0.9% (both P<0.05), with ED50values of 86±21 and 489±113 μmol kg−1, respectively. In contrast, only a decrease in the external diameter of the internal carotid artery was observed (−6.0±0.6 and −6.2±1.4%, both P<0.05, and ED50values of 86±41 and 493±162 μmol kg−1, respectively). Frovatriptan was thus 5.7 fold more potent than sumatriptan at the level of both large coronary and internal carotid arteries.After endothelium removal by balloon angioplasty in coronary arteries, the initial dilatation induced by the triptans was abolished and delayed constriction enhanced.The selective antagonist for the 5‐HT1Breceptors SB224289 dose‐dependently blocked the effects of sumatriptan on large coronary and internal carotid arteries whereas the selective antagonist for the 5‐HT1Dreceptors BRL15572 did not affect any of these effects.In conclusion, frovatriptan and sumatriptan initially dilate and subsequently constrict large coronary arteries in the conscious dog, whereas they directly constrict the internal carotid artery. The vascular endothelium modulates the effects of these triptans on large coronary arteries. Finally, 5‐HT1Bbut not 5‐HT1Dreceptors are primarily involved in canine coronary and internal carotid vasomotor responses to sumatriptan.

1 The effects of frovatriptan and sumatriptan on internal carotid and coronary vascular haemodynamics were investigated and compared in conscious dogs. 2 Frovatriptan and sumatriptan (0.1 – 100 μg kg−1) induced a transient increase in external coronary artery diameter (eCOD) of up to 2.9±1.2 and 1.8±0.6%, respectively (both P0.05). This was followed by a prolonged and dose-dependent decrease in eCOD of up to −5.2±1.2 and −5.3±0.9% (both P0.05), with ED50 values of 86±21 and 489±113 μmol kg−1, respectively. In contrast, only a decrease in the external diameter of the internal carotid artery was observed (−6.0±0.6 and −6.2±1.4%, both P0.05, and ED50 values of 86±41 and 493±162 μmol kg−1, respectively). Frovatriptan was thus 5.7 fold more potent than sumatriptan at the level of both large coronary and internal carotid arteries. 3 After endothelium removal by balloon angioplasty in coronary arteries, the initial dilatation induced by the triptans was abolished and delayed constriction enhanced. 4 The selective antagonist for the 5-HT1B receptors SB224289 dose-dependently blocked the effects of sumatriptan on large coronary and internal carotid arteries whereas the selective antagonist for the 5-HT1D receptors BRL15572 did not affect any of these effects. 5 In conclusion, frovatriptan and sumatriptan initially dilate and subsequently constrict large coronary arteries in the conscious dog, whereas they directly constrict the internal carotid artery. The vascular endothelium modulates the effects of these triptans on large coronary arteries. Finally, 5-HT1B but not 5-HT1D receptors are primarily involved in canine coronary and internal carotid vasomotor responses to sumatriptan. British Journal of Pharmacology (2001) 132, 1071 – 1083