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In anaesthetized cats the electrical stimulation of the cervical sympathetic nerve induces a considerable increase (150-250%) in the nociceptive jaw opening reflex elicited by tooth pulp stimulation (JOR). The mechanisms potentially responsible for this effect are discussed and the possibility is suggested, that a portion of the response is due to a modulatory action exerted by the sympathetic on the nociceptive input.

The sympathetic system can influence skeletal muscle function through an action exerted at the peripheral level, namely on muscle spindle afferent information and muscular contraction. Data supporting such a conclusion are briefly reviewed. Also, the results described in the present paper suggest that the sympathetic nervous command affecting muscle function is tonic in nature and that it can be modulated by inputs which are known to influence other sections of the sympathetic system.

This study is the first to report on vascular effect of the chromogranin A derived Vasostatin-I (CgA(1-76)) in vivo. Cardiovascular parameters were recorded in 29 rabbits with sympathetically decentralized right carotid vascular bed. The recombinant human STA CgA(1-78) (VS-1) was infused at 480 mu g/kg over 25 min. Group I was kept awake while groups II-V were anesthetized with Ketamine-xylazine. VS-1 was given alone in groups I-II while in presence of either phentolamine, phentolamine plus propranolol or hexamethonium in groups III-V. Serum VS-1 peaked at 2 mu g/ml (200 nM) before onset of vascular effects and declined rapidly to similar to 200 ng/ml within 30 min. In all groups but III and IV VS-1 induced a brief vasoconstriction, being larger in intact than in sympathetically decentralized beds. The VS-1 induced vasoconstriction was not altered by hexamethonium but was abolished by phentolamine. In presence of the a-adrenergic blocker a long lasting vasodilatation, unaffected by propranolol, was apparent on both innervated and decentralized sides. In conclusion, VS-1 induced an alpha-adrenoceptor-mediated vasoconstriction presumably brought about by noradrenaline release from sympathetic nerves when infused at a dose giving an initial serum concentration of similar to 200 nM. This initial vasoconstriction masked a persistent adrenoceptor-independent vasodilatation, consistent with previous reports from in vitro models. (C) 2011 Elsevier B.V. All rights reserved.