Cerebral vasoconstrictor responses to serotonin during chronic hypertension.

The goal of this study was to determine whether responses of cerebral vessels to intravascular administration of serotonin are altered in stroke-prone spontaneously hypertensive rats. We measured pressure in pial arterioles and cerebral blood flow in normotensive and hypertensive rats during intra-atrial infusion of serotonin. In normotensive rats, pial arteriolar pressure was 48 +/- 3 mm Hg (mean +/- SEM) and cerebral blood flow was 48 +/- 5 ml/min/100 g under control conditions. Intra-atrial infusion of serotonin (5 and 50 micrograms/kg/min for 5 minutes) produced only minimal changes in pial arteriolar pressure (-3 +/- 4 and -4 +/- 4 mm Hg, respectively) and did not alter cerebral blood flow. In hypertensive rats, pial arteriolar pressure was 95 +/- 9 mm Hg and cerebral blood flow was 57 +/- 4 ml/min/100 g under control conditions. In contrast to normotensive rats, intra-atrial infusion of serotonin (5 and 50 micrograms/kg/min for 5 minutes) in hypertensive rats profoundly decreased pial arteriolar pressure (-29 +/- 7 and -44 +/- 4 mm Hg, respectively) without altering cerebral blood flow. To determine whether altered responses of cerebral arterioles to serotonin in hypertensive rats were related to nonspecific increases in vascular reactivity, we examined the effects of angiotensin in normotensive and hypertensive rats. Responses to angiotensin (1 and 3 micrograms/kg/min i.v. for 5 minutes) were not potentiated in hypertensive rats. Thus, constrictor responses of cerebral vessels to intravascular serotonin are potentiated in hypertensive rats. We speculate that when serotonin is released by platelets, augmented vasoconstrictor responses to serotonin may have important implications for the pathogenesis of cerebral ischemia, and perhaps stroke, during chronic hypertension.