Sympathetically induced paradoxical increases of the cutaneous blood flow in chronically inflamed rats

Abstract In adjuvant arthritic (AA) rats, an abnormal responsiveness of nociceptors (C-fibre polymodal receptors) to sympathetic activities, i.e., α 2 -adrenoceptor mediated activation of C-fibre polymodal receptors (CPRs), has been observed. The present investigations were undertaken to determine if a similar plastic change would occur in the cutaneous vascular system in the rat chronic inflammation model. The vascular responses were measured by a laser-Doppler flowmeter in the hindpaw skin of the AA rats after electrical stimulation of lumbar sympathetic trunk (sympathetic stimulation). In control non-arthritic rats, the sympathetic stimulation caused decrease in blood flow of the skin (SkBF) in all animals tested ( n = 7). On the other hand, the sympathetic stimulation in the AA rats caused both increase ( n = 15) as well as decrease ( n = 11) in SkBF. In contrast to the abnormal responsiveness of CPRs, the intra-arterial injection of noradrenaline caused the expected decrease in SkBF in all animals tested, and in no instances increases in SkBF were observed. To determine whether activation of nitric oxide (NO), which is known to be a potent endogenous vasodilatation substance, was involved in the vasodilating effect to sympathetic stimulation, an inhibitor of NO synthase, N G -monomethyl-L-arginine (L-NMMA), was applied systemically. L-NMMA significantly increased baseline blood pressure in the control and the AA rats, but it did not significantly alter the SkBF in the control or the AA rats after the sympathetic stimulation, suggesting the NO is not a mediator in the vasoactive responses. The results of the current studies showed for the first time that electrical stimulation of the lumbar sympathetic trunk causes vasodilatation in the skin of the AA rats. This abnormal responsiveness of regional SkBF after sympathetic stimulation was not mediated by adrenergic or NO system.