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KMID : 0811720060100000337
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Korean Journal of Physiology & Pharmacology
2006 Volume.10 No. 0 p.337 ~ p.0
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MODULATION OF REGULAR MOTILITY IN URETERAL SMOOTH MUSCLE OF MOUSE
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Kim Young-Chul
Lee Moo-Yeol
Kim Wun-Jae
Lee Sang-Jin
Kim Seung-Ryul
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Abstract
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The existence of a pacemaker system in the urinary tract is responsible for movement of urine from the ureteral pelvis to distal urinary tract. This coordination might require a network of cells with pacemaker activity. Recently, the existence of Interstitial cells of Cajal (ICC) which is known as a pacemaker cell of the gut was also reported in urinary tract. Electrical excitation from upper urinary tract propagates to lower area. Therefore, this study was designed to elucidate regulation of pacemaking contraction of murine ureter. Mechanical contractions from circular and longitudinal smooth muscle of murine ureter were measured using Mulvany myograph and vertical contraction measuring system. Most tested tissues showed no significant spontaneous contraction. In the case of High K+ (50 mM), it produced weak contraction less than 0.1 mN. However, 25 mM of K+ produced phasic contraction (0.4 mN). Ba2+ (2～5 mM) also produced regular and phasic contraction (0.76±0.1 mN, 1 cyc/min) but not by tetraetylammonium chloride (TEA, 1～20 mM). Cyclopiazonic acid (CPA, 10μM) did not produce any significant contraction. However, CPA enhanced frequency and amplitude of Ba2+-induced phasic contraction significantly (4±0.2 cyc/min, 1.4±0.1 mN). Enhancing effect of CPA on Ba2+-induced phasic contraction was totally inhibited by isoprenaline (2μM; 0.16± 0.01 cyc/min, 0.3±0.2 mN) and recovered by propranonol (5μM; 3.5±0.1 cyc/min, 1.3±0.04 mN). Ba2+ produced regular phasic contraction in murine ureter. Stimulation of β-adrenergic receptor might play an inhibitory regulation of contraction in murine ureter.
Source: Korean J Physiol Pharmacol.2006 Oct;10(Suppl II):244
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KEYWORD
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Ureter, smooth muscle, Ba2+, adrenergic receptor
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