Regional hemodynamic responses to central administration of corticotropin-releasing factor (CRF)

Central administration of corticotropin-releasing factor (CRF) produces a marked increase in both mean arterial pressure and heart rate. These increases appear to be mediated almost exclusively by an activation of the sympathetic nervous system. We studied the hemodynamic mechanisms of the response by determining the contribution of the major vascular beds to the increase in arterial pressure. Experiments were done in conscious, freely moving, male Sprague-Dawley rats. Animals were prepared for measurement of regional blood flow using miniaturized pulsed Doppler flow probes placed on the renal, mesenteric and abdominal aortic arteries. Intracerebroventricular injection of CRF (28.5-570 pmol) produced a dose-dependent increase in both mean arterial pressure and heart rate. A significant increase in vascular resistance was observed in the mesenteric and renal but not in the hindquarter vascular bed at the highest dose of CRF. These data indicate that vasoconstriction in the renal and mesenteric circulations contributes to the centrally mediated pressor effect of CRF.