Regulation of pulpal microcirculation by calcitonin gene-related peptide.
10.5395/JKACD.2005.30.6.470
- Author:
Sung Kyo KIM
1
;
Young Kyung KIM
;
Myoung Uk JIN
Author Information
1. Department of Conservative Dentistry and Laboratory of Pulp Biology, School of Dentistry, Kyungpook National University, Korea. skykim@knu.ac.kr
- Publication Type:Original Article
- Keywords:
Dental pulp;
Blood flow;
Calcitonin gene related peptide (CGRP);
Sympathetic nerve stimulation;
Neurogenic inflammation;
Laser Doppler flowmeter
- MeSH:
Anesthesia, General;
Animals;
Blood Pressure;
Calcitonin Gene-Related Peptide*;
Calcitonin*;
Carotid Artery, External;
Cats;
Cuspid;
Dental Pulp;
Electric Stimulation;
Femoral Vein;
Flowmeters;
Microcirculation*;
Neurogenic Inflammation;
Vasoconstriction
- From:Journal of Korean Academy of Conservative Dentistry
2005;30(6):470-476
- CountryRepublic of Korea
- Language:English
-
Abstract:
The purpose of this study was to investigate the function of calcitonin gene-related peptide (CGRP) in regulatory mechanism of pulpal microcirculation with the aim of elucidating neurogenic inflammation. Experiments were performed on twelve cats under general anesthesia. CGRP was administered through the femoral vein to see the systemic influence and through the external carotid artery to see the local effect. Sympathetic nerve to the dental pulp was stimulated electrically and pulpal blood flow (PBF) was measured with a laser Doppler flowmeter on the canine teeth to the drug administration. The paired variables of control and experimental data were compared by paired t-test and differences with p < 0.05 were considered statistically significant. Systemic administration of CGRP (0.3 microg/kg) exerted decreases in systemic blood pressure and caused changes in PBF with an initial increase followed by decrease and a more marked second increase and decrease. Close intra-arterial (i.a.) injection of CGRP (0.03 microg/kg) resulted in slight PBF increase. The effect of CGRP resulted in no significant increase in PBF in the presence of CGRP8-37. The electrical stimulation of the sympathetic nerve alone resulted in PBF decreases. The i.a. administration of CGRP following the electrical stimulation of the sympathetic nerve compensated the decreased PBF. Therefore, CGRP effectively blocked the sympathetic nerve stimulation-induced PBF decrease. Results of the present study have provided evidences that even though the local vasodilatory function of CGRP are weak, CGRP is effectively involved in blocking the vasoconstriction caused by sympathetic nerve stimulation in the feline dental pulp.
