Invited Symposium: Hypertension I: Structure of Small Arteries in Hypertension
McGrath, JC (Autonomic Physiology Unit, University of Glasgow, Scotland, UK)
Dominiczak, AF (Dept. of Medicine & Therapeutics, University of Glasgow, Scotland, UK)
Gonzalez, MC (Dept. Fisiologia, Fac. Medicina, Universidad Autonoma de Madrid, Spain)
Chronic inhibition of NOS induces hypertension and structural alterations in rat basilar arteries: reduced lumen, decreased smooth muscle (SMC) and endothelial cell number, increased adventitial cell number and thickness (1). Objective: to determine the functional alterations related to these changes. Methods: WKY rats treated for 3 weeks with 10 mg/kg/day L-NAME, n=10; or untreated, n=10 were used. Function was studied with wire myography at 0.9l100. Results: L-NAME treatment reduced bradykinin relaxations (untreated max.= 75.5±7.5 %; L-NAME max.= 21.6±6.8 %, p<0.01) and increased serotonin (untreated max.=1.5±0.2 mN/mm; L-NAME max.= 2.8±0.3 mN/mm, p<0.01), but not KCl contractions. Pre-incubation with L-arginine had no effect on bradykinin responses, but significantly reduced serotonin contractions. Conclusions: In rat basilar arteries chronic NOS inhibition reduces endothelium-derived NO production and might induce iNOS. The reduction of smooth muscle cell number induced by treatment is not related to an alteration of contractile capacity and could be explained by the iNOS induction in the vessel wall. Supported by MRC, Wellcome Trust and CAM.
Back to the top.
| Discussion Board | Next Page | Your Symposium |
|Arribas, SM; McGrath, JC; Dominiczak, AF; Gonzalez, MC; (1998). Functional Alterations in Rat Basilar Artery Induced by Chronic Inhibition of Nitric Oxide Synthase (NOS). Are They Related to Vascular Remodeling?. Presented at INABIS '98 - 5th Internet World Congress on Biomedical Sciences at McMaster University, Canada, Dec 7-16th. Invited Symposium. Available at URL http://www.mcmaster.ca/inabis98/mulvany/arribas0145/index.html|
|© 1998 Author(s) Hold Copyright|