Autonomic Nervous System and Vegetative ControlBlockade of nitric oxideevoked smooth muscle contractions by an inhibitor of guanylyl cyclaseOlgart, Caroline1,3; Wiklund, N Peter1,2; Gustafsson, Lars E.1Author Information 1Department of Physiology and Pharmacology, Karolinska Institute, 17176 Stockholm, Sweden 2Department of Urology, Karolinska Hospital, 17176 Stockholm, Sweden 3Corresponding Author: Caroline Olgart ACKNOWLEDGEMENTS: Supported by the Swedish MRC (7919, 11199), Stiftelsen Vârdal, the Swedish Dental Society, the Swedish-Heart-Lung Foundation, the Swedish National Environmental Protection Board, Emma och Erik Granes minnesfond, Lars Hiertas minnesfond and the Karolinska Institute. Website publication 3 October 1997 Received 24 July 1997; accepted 5 August 1997 NeuroReport: October 20th, 1997 - Volume 8 - Issue 15 - p 3355-3357 Buy Abstract NITRIC oxide-induced contractile responses of smooth muscle were studied in vitro in guinea-pig small intestine. Application of nitric oxide (NO; 0.3–30 μM) evoked a small initial relaxation followed by a marked contractile response in plexus-containing longitudinal smooth muscle preparations from small intestine. The extent of the NO-evoked contractile response was dose-dependent and the response was blocked by tetrodotoxin. Atropine significantly reduced the NO-evoked contraction and the remaining part was abolished by the NK1-receptor antagonist CP 96,345. An inhibitor of soluble guanylyl cyclase, ODQ (1H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one), abolished the NO-evoked contractile response. The results suggest that NO, in addition to the classical direct smooth muscle relaxing effect, causes activation of excitatory neurones, via a pathway utilizing soluble guanylyl cyclase, which leads to a smooth muscle contraction. © Lippincott-Raven Publishers.