Relaxant effect of 4-aminopyridine on the mesenteric artery of rat.
- Author:
Se Hoon KIM
1
;
Tae Im LEE
Author Information
1. Department of Physiology, College of Medicine, Konyang University, 26 Nae-dong, Nonsan, Chungnam, South Korea. sehkim@kytis.konyang.ac.kr
- Publication Type:Original Article
- Keywords:
Mesenteric artery;
4-aminopyridine;
Vasorelaxation
- MeSH:
4-Aminopyridine*;
Animals;
Aorta;
Arteries;
Calcimycin;
Glyburide;
Guanylate Cyclase;
Membranes;
Mesenteric Arteries*;
Methylene Blue;
Muscle, Smooth;
Muscle, Smooth, Vascular;
Nitric Oxide Synthase;
Nitroarginine;
Norepinephrine;
Rats*;
Relaxation;
Vasodilation
- From:The Korean Journal of Physiology and Pharmacology
2000;4(6):463-469
- CountryRepublic of Korea
- Language:English
-
Abstract:
It has been well known that 4-aminopyridine (4-AP) has an excitatory effect on vascular smooth muscle due to causing membrane depolarization by blocking K+-channel. However, we observed that 4-AP had an inhibitory effect on the mesenteric artery of rat. Therefore, we investigated the mechanism of 4-AP-induced vasorelaxation. The mesenteric arcuate artery and its branches were isolated and cut into ring. The ring segment was immersed in HEPES-buffered solution and its isometric tension was measured. 4-AP (0.1 ~ 10 mM) induced a concentration-dependent relaxation, which was unaffected by NO synthase inhibitor, NG-nitro-L-arginine methylester (100 micrometer) or soluble guanylate cyclase inhibitor, methylene blue (10 micrometer). Glibenclamide (10 micrometer), ATP-sensitive K+ channel blocker, did not exert any effect on the 4-AP-induced vasorelaxation. 4-AP relaxed the sustained contraction induced by 100 mM K+ or Ca2+ ionophore, A23187 (10 micrometer) in a dose-dependent manner. In addition, 4-AP significantly decreased the phasic contractile response to norepinephrine in the absence of extracellular Ca2+. However, 4-AP did not block the 45Ca influx of rat aorta. From the above results, we suggest that 4-AP may not block the Ca2+ influx through Ca2+-channel, but act as a nonspecific vasorelaxant in arterial smooth muscle.
