ABSTRACT
The joint vascular [alpha]-Adrenoceptors change due to acute inflammation from a majority of [alpha]-2 to an equality of [alpha]-1 and [alpha]-2 receptors. This study was done to investigate the role of sympathetic nerves in nerve induced vasoconstriction and changes in joint vascular adrenoceptors due to chronic inflammation. In 21 NZW rabbits, knee joint chronic inflammation was induced by antigen induced arthritis [AIA] method. In experiment day, animals were anesthetized and the carotid artery was cannulated to record blood pressure and jugular vein for injection the anesthetic drugs. The medial belly of gastrocnemius muscle was removed to get access to posterior knee joint capsule and the blood flow was measured by laser flowmetry. Electrical stimulation of PAN resulted in 25.6 +/- 5.6 percent reduction of blood flow measured by laser Doppler flowmetry technique. The half of this response was blocked by prazosine [[alpha]1-agonists] and the other half by youhimbin [[alpha]2-agonist] to 11.8 +/- 4.1 and 10.9 +/- 12.4 percent reduction, respectively but phentolamine completely blocked the constrictor response and reversed it to vasodilation [2.5 +/- 2.1%]. Close intra-arterial injection of different doses of [alpha]-agonists reduced the joint blood flow by the potency rank order of adrenaline>clonidine=phenylepherine, suggesting a balance between [alpha]1 and [alpha]2 adrenoceptors. In previous studies, in normal and acutely inflamed knee joint, stimulation of PAN resulted in 36.5 +/- 4 and 9.9 +/- 2.25 percent reduction of blood flow, respectively that indicated acute inflammation reduces the role of sympathetic nerves in the regulation of knee joint blood flow. Overall this study showed a balance between ?-adrenoceptor subtypes in the chronically inflamed knee joint blood vessels and compared to results of our pervious investigation on acutely inflamed of rabbit knee joint. The sympathetic vasoconstrictor response was mostly recovered without more alteration in [alpha]-adrenoceptor subtypes that happened in acute inflammation