Study on vasodilator nerve in rat hind limb / 中国药理学通报

ABSTRACT

AIM To investigate whether there is vasodilator nerve innervation in rat hind limb and what the nature of vasodilator nerve is. METHODS Wistar rats were treated with reserpine 1 mg?kg -1 ip at 24 h before experiment. The rats were pithed and the hind limb vascular bed was perfused with Krebs-Henseleite solution containing 1 mmol?L -1 phenylephrine at 2 ml?min -1 speed. The hind limb perfused pressure (HPP) as a main index was continuously recorded. Spinal cord electrical stimulation (SES) was repeatedly applied via an electrode at L 1～2 level of lumber vertebra. The various tool drugs were administered by iv or infusion by added to persusion solution. The data is expressed as decrease percentages of HPP increased by continuous infusion of phenylephrine. RESULTS HPP was increased from (5 7?1 5) to (21 6?3 7) kPa ( n =37) after phenylephrine perfusion. SES caused a fall of HPP in frequency dependent and voltage dependent manner. An optimum parameters of SES (10 Hz, 50 V and 1 msec) was selected to observe effects of various tool drugs on depressor response of HPP to SES. Tetrotodoxin (0 3 ?mol?L -1 ) abolished the effect completely. L NAME (10 ?mol?L -1 ), a NO synthase inhibitor, had no effect. Ganglion blocker arfonad (110 mg?kg -1 , iv, M R blocker atropine (10 ?mol?L -1 ), ? receptor blocker propranolol (1 ?mol?L -1 ) and P 1 receptor blocker aminophylline (10 ?mol?L -1 ) had also no effect. Glibenclamide (0 1 mmol?L -1 ), an ATP sensitive K + channel blocker, markedly abolished and slightly reversed the effect. CONCLUTION The nonadrenergic noncholinergic vasodilator nerve exists in rat hind limb and is not nitroxidergic or purinergic nerve. This nerve may be peptidergic nerve which releases some peptide such as CGRP and the major mechanism of vasodilatation probably activates the ATP sensitive K + channel.