Paper Information

Title: 

INVESTIGATION OF ANGII RECEPTOR SUBTYPES AND THE EFFECT OF ANGII AND NO IN JOINT BLOOD FLOW REGULATION IN ACUTE AND CHRONICALLY INFLAMED JOINTS

Type: PAPER
Author(s): NAJAFIPOUR H.*,SADEGHI N.,NIKBAKHT F.
 
 *DEPARTMENT OF PHYSIOLOGY AND PHYSIOLOGY RESEARCH CENTER, KERMAN UNIVERSITY OF MEDICAL SCIENCES
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2007Volume 18
 
 
Abstract: 

Inflammatory joint diseases are common in elderly and regulation of joint blood flow (JBF) is very important in these conditions. The aim of this study was to investigate the response of inflamed joint blood vessels to angiotensin II (AngII) which has been shown to be produced in inflamed joints locally. Also assessment of AngII receptor subtypes in joint blood vessels was the second goal of this study. It has been proved that NO is produced in many tissues in the process of inflammation. Therefore the assessment of role of NO in these conditions was the third aim of this study. The study was performed on 36 New Zealand white rabbits divided into two main groups (acute and chronic inflammation) each divided to 3 subgroups. Acute knee joint inflammation was produced by intraarticular injection of 0.5 ml of a 2% of carrageenan and Chronic inflammation by antigen-induced arthritis method. In experiment day (24 hours after acute and 28 days after chronic inflammation) animals were anaesthetized by thiopental sodium (50mg/kg ip). In the first group of animals, the effect of the intrasaphenous artery administration of 0.1ml of different concentrations of AngII on JBF (recorded by laser Doppler flowmeter) and JVR were investigated. In the second group, the specific AT1 receptor antagonist (losartan) was used before angII administration. In the third group of animals L-NAME (3mg/kg) was injected through the jugular vein before angII. The results suggested that the constrictor response to angII was started from 10-12 M and reached to maximum at 10-5 M. losartan completely inhibited this response with no vasodilation left behind. Therefore the receptor subtypes are AT1 with no AT2 subtype present. AngII receptor subtypes did not change by the process of inflammation. L-NAME potentiated the joint vessel response to angII. NO plays a significant role in the regulation of joint vascular tone and modulates the vasoconstrictor effects of AngII on these vessels.

 
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