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. 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. Exogenous NE also induced a significantly higher contractile response in the ECB. 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 alpha 1-adrenoceptors. 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. Ketanserine (10(-8) M) antagonised both responses, indicating the involvement of 5-HT2 receptors. 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. 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. Furthermore, the response to 5-HT in the ECB was modulated by a subthreshold sympathetic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
