Prazosin, and α1-adrenergic receptor antagonist, suppresses experimental autoimmune encephalomyelitis in the Lewis rat

Abstract

Prazosin, an antagonist of α1-adrenergic receptors, has been found to suppress the clinical and histological expression of experimental autoimmune encephalomyelitis (EAE) in the Lewis rat. Suppression was more significant in females than in males and was a dose-dependent phenomenon. Analysis of the effect of other adrenergic receptor antagonists supports the conclusion that the suppressive effect of prazosin is a consequence of blockade of the α1-receptor since treatment with either the α2-antagonist yohimbine or the β-antagonist propranolol exacerbated the disease, whereas treatment with the long-acting mixed α1/α2-antagonist phenoxybenzamine had some suppressive activity. Treatment with prazosin was also able to suppress clinical and histological signs of EAE in animals sensitized by adoptive transfer with activated spleen or lymph node cells. Whether prazosin acts through altering vascular permeability of the immune response, or both, remains to be determined.