Vasomotor responses in the isolated perfused external and internal carotid vascular beds of the rat

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1. 1. The external (ECB) or the internal (ICB) carotid vascular beds of the rat were isolated and perfused with Krebs-Henseleit solution at constant flow (1 ml/min). Changes in perfusion pressure (PP) were recorded after cervical sympathetic stimulation and after the administration of norepinephrine (NE) and serotonin (5-HT). 2. 2. Sympathetic stimulation induced an increase in PP (vasoconstriction) in both vascular beds, however, this effect was significantly higher in the ECB than in the ICB. 3. 3. Exogenous NE also induced a significantly higher contractile response in the ECB. 4. 4. Prazosin (10 −8 M) significantly inhibited the response to sympathetic stimulation and to NE both in the ECB and in the ICB, but yohimbine (10 −7 M) had no effect, suggesting that the vasoconstriction was mainly due to the activation of α 1-adrenoceptors. 5. 5. 5-HT induced a contractile response both in the ECB and the ICB. In contrast with the response to NE, the contraction induced by 5-HT in the ICB was significantly higher than in the ECB. 6. 6. Ketanserine (10 −8 M) antagonised both responses, indicating the involvement of 5-HT 2 receptors. 7. 7. The contractile effect of 5-HT in the ECB was significantly enhanced by a subthreshold sympathetic stimulation that did not modify the PP by itself. This effect was not seen in the ICB. 8. 8. The differential perfusions of the ECB or the ICB demonstrated a different reactivity of ECB and ICB, both to sympathetic stimulation and to the administration of exogenous NE or 5-HT. 9. 9. Furthermore, the response to 5-HT in the ECB was modulated by a subthreshold sympathetic stimulation. 10. 10. The results suggest that the different reactivity of the ECB and the ICB may be due to differences in the characteristics and/or density of adrenoceptors and 5-HT receptors in both vascular beds.