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Isometric contraction of circular smooth muscle of corpus lesser curvature (LC) of human stomach. Contractile properties of circular and longitudinal smooth muscles of corpus LC was studied. Circular muscle of human gastric corpus LC showed spontaneous contraction (A). In panel (B), high-K ＋ produced initial and tonic contraction. Data was summarized in (C). Meanwhile, longitudinal muscles of corpus LC also showed spontaneous contraction (D). However, high K ＋ produced initial contraction followed by weak contraction in longitudinal muscle of corpus LC (E). Data was summarized in (F). We also studied effect of L-NNA on high K ＋-induced contraction in longitudinal muscle of corpus LC (G). L-NNA (100μM) produced tonic (0.5 g) and phasic contractions (0.4 g) and high K ＋ in the presence of L-NNA produced initial (4.5 g) and sustained contraction (6.3 g), respectively. Data was summarized in (H). In (I) and (J), ACh-induced contraction is shown. ACh (10μM) produced initial transient contraction followed by later sustained tonic contraction with superimposed phasic contractions.
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This study was designed to elucidate high-K(+)induced response of circular and longitudinal smooth muscle from human gastric corpus using isometric contraction. Contraction from circular and longitudinal muscle stripes of gastric corpus greater curvature and lesser curvature were compared. Circular smooth muscle from corpus greater curvature showed...
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... shown in Fig. 4A and C, circular smooth muscle of human gastric corpus from LC showed spontaneous con- traction of 0.2±0.04 g with a frequency of 4.0± 0.36 cy- cles/min (n=7; Table 1). High K ＋ produced initial and sus- tained contraction of 4.1±2.1 g and 9.1±1.78 g, respectively (n=10 and 12, respectively; Fig. 4B and C; Table 1). Meanwhile, ACh (10μM) produced initial transient con- traction of 8.0±1.33 g followed by later sustained tonic con- traction of 2.8±0.59 g with superimposed phasic con- tractions of 2.7±2.15 g (n=7, 7 and 4, respectively; Table 1). The frequency of ACh-induced phasic contraction was 2.3±0.83 cycles/min (n=4; Table 1). In control, its phasic contraction and frequency were 0.1±0.02 g and 4.4±0.37 cy- cles/min, respectively ...
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... shown in Fig. 4A and C, circular smooth muscle of human gastric corpus from LC showed spontaneous con- traction of 0.2±0.04 g with a frequency of 4.0± 0.36 cy- cles/min (n=7; Table 1). High K ＋ produced initial and sus- tained contraction of 4.1±2.1 g and 9.1±1.78 g, respectively (n=10 and 12, respectively; Fig. 4B and C; Table 1). Meanwhile, ACh (10μM) produced initial transient con- traction of 8.0±1.33 g followed by later sustained tonic con- traction of 2.8±0.59 g with superimposed phasic con- tractions of 2.7±2.15 g (n=7, 7 and 4, respectively; Table 1). The frequency of ACh-induced phasic contraction was 2.3±0.83 cycles/min (n=4; Table 1). In control, its phasic contraction and frequency were 0.1±0.02 g and 4.4±0.37 cy- cles/min, respectively ...
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... shown in Fig. 4D and F, longitudinal smooth muscle from human gastric corpus from LC showed spontaneous contraction of 0.7±0.14 g with a frequency of 3.36±0.42 cy- cles/min, respectively (n=9, respectively; Table 1). High K ＋ produced initial and sustained contraction of 3.5±1.08 g and 2.6±1.05 g, respectively (n=10 and 12, respectively; Fig. 4E and F). We also studied effect of L-NNA on high K ＋ -induc- ed contraction. In control, longitudinal smooth muscle from LC produced phasic contraction of 0.4±0.1 g with a fre- quency of 4.2±0.13 cycles/min (n=4; Fig. 4H). When L-NNA (100μM) was applied, it produced tonic and phasic con- tractions of 0.5± 0.16 g and 0.4±0.11 g, respectively with a frequency of 3.9± 0.15 cycles/min (n=6, 4 and 4, re- spectively; Fig. 4G and H). In the presence of L-NNA, high K ＋ produced initial and sustained contraction of 4.5±1.4 g and 6.3±2.0 g, respectively (n=4 and 6, respectively; Fig. 4G and H). Meanwhile, ACh (10μM) also produced initial transient contraction of 6.5±1.72 g followed by later sus- tained tonic contraction of 1.7±0.48 g with superimposed phasic contractions of 1.6± 0.93 g (n=6; Fig. 4I and J; Table 1). The frequency of ACh-induced phasic contraction was 2.4±0.62 cycles/min (n=6). In control, phasic contraction and its frequency were 0.6±0.20 g and 3.6±1.22 cycles/min, re- spectively (n=4; Fig. ...
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... shown in Fig. 4D and F, longitudinal smooth muscle from human gastric corpus from LC showed spontaneous contraction of 0.7±0.14 g with a frequency of 3.36±0.42 cy- cles/min, respectively (n=9, respectively; Table 1). High K ＋ produced initial and sustained contraction of 3.5±1.08 g and 2.6±1.05 g, respectively (n=10 and 12, respectively; Fig. 4E and F). We also studied effect of L-NNA on high K ＋ -induc- ed contraction. In control, longitudinal smooth muscle from LC produced phasic contraction of 0.4±0.1 g with a fre- quency of 4.2±0.13 cycles/min (n=4; Fig. 4H). When L-NNA (100μM) was applied, it produced tonic and phasic con- tractions of 0.5± 0.16 g and 0.4±0.11 g, respectively with a frequency of 3.9± 0.15 cycles/min (n=6, 4 and 4, re- spectively; Fig. 4G and H). In the presence of L-NNA, high K ＋ produced initial and sustained contraction of 4.5±1.4 g and 6.3±2.0 g, respectively (n=4 and 6, respectively; Fig. 4G and H). Meanwhile, ACh (10μM) also produced initial transient contraction of 6.5±1.72 g followed by later sus- tained tonic contraction of 1.7±0.48 g with superimposed phasic contractions of 1.6± 0.93 g (n=6; Fig. 4I and J; Table 1). The frequency of ACh-induced phasic contraction was 2.4±0.62 cycles/min (n=6). In control, phasic contraction and its frequency were 0.6±0.20 g and 3.6±1.22 cycles/min, re- spectively (n=4; Fig. ...
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... shown in Fig. 4D and F, longitudinal smooth muscle from human gastric corpus from LC showed spontaneous contraction of 0.7±0.14 g with a frequency of 3.36±0.42 cy- cles/min, respectively (n=9, respectively; Table 1). High K ＋ produced initial and sustained contraction of 3.5±1.08 g and 2.6±1.05 g, respectively (n=10 and 12, respectively; Fig. 4E and F). We also studied effect of L-NNA on high K ＋ -induc- ed contraction. In control, longitudinal smooth muscle from LC produced phasic contraction of 0.4±0.1 g with a fre- quency of 4.2±0.13 cycles/min (n=4; Fig. 4H). When L-NNA (100μM) was applied, it produced tonic and phasic con- tractions of 0.5± 0.16 g and 0.4±0.11 g, respectively with a frequency of 3.9± 0.15 cycles/min (n=6, 4 and 4, re- spectively; Fig. 4G and H). In the presence of L-NNA, high K ＋ produced initial and sustained contraction of 4.5±1.4 g and 6.3±2.0 g, respectively (n=4 and 6, respectively; Fig. 4G and H). Meanwhile, ACh (10μM) also produced initial transient contraction of 6.5±1.72 g followed by later sus- tained tonic contraction of 1.7±0.48 g with superimposed phasic contractions of 1.6± 0.93 g (n=6; Fig. 4I and J; Table 1). The frequency of ACh-induced phasic contraction was 2.4±0.62 cycles/min (n=6). In control, phasic contraction and its frequency were 0.6±0.20 g and 3.6±1.22 cycles/min, re- spectively (n=4; Fig. ...
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... shown in Fig. 4D and F, longitudinal smooth muscle from human gastric corpus from LC showed spontaneous contraction of 0.7±0.14 g with a frequency of 3.36±0.42 cy- cles/min, respectively (n=9, respectively; Table 1). High K ＋ produced initial and sustained contraction of 3.5±1.08 g and 2.6±1.05 g, respectively (n=10 and 12, respectively; Fig. 4E and F). We also studied effect of L-NNA on high K ＋ -induc- ed contraction. In control, longitudinal smooth muscle from LC produced phasic contraction of 0.4±0.1 g with a fre- quency of 4.2±0.13 cycles/min (n=4; Fig. 4H). When L-NNA (100μM) was applied, it produced tonic and phasic con- tractions of 0.5± 0.16 g and 0.4±0.11 g, respectively with a frequency of 3.9± 0.15 cycles/min (n=6, 4 and 4, re- spectively; Fig. 4G and H). In the presence of L-NNA, high K ＋ produced initial and sustained contraction of 4.5±1.4 g and 6.3±2.0 g, respectively (n=4 and 6, respectively; Fig. 4G and H). Meanwhile, ACh (10μM) also produced initial transient contraction of 6.5±1.72 g followed by later sus- tained tonic contraction of 1.7±0.48 g with superimposed phasic contractions of 1.6± 0.93 g (n=6; Fig. 4I and J; Table 1). The frequency of ACh-induced phasic contraction was 2.4±0.62 cycles/min (n=6). In control, phasic contraction and its frequency were 0.6±0.20 g and 3.6±1.22 cycles/min, re- spectively (n=4; Fig. ...
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... shown in Fig. 4D and F, longitudinal smooth muscle from human gastric corpus from LC showed spontaneous contraction of 0.7±0.14 g with a frequency of 3.36±0.42 cy- cles/min, respectively (n=9, respectively; Table 1). High K ＋ produced initial and sustained contraction of 3.5±1.08 g and 2.6±1.05 g, respectively (n=10 and 12, respectively; Fig. 4E and F). We also studied effect of L-NNA on high K ＋ -induc- ed contraction. In control, longitudinal smooth muscle from LC produced phasic contraction of 0.4±0.1 g with a fre- quency of 4.2±0.13 cycles/min (n=4; Fig. 4H). When L-NNA (100μM) was applied, it produced tonic and phasic con- tractions of 0.5± 0.16 g and 0.4±0.11 g, respectively with a frequency of 3.9± 0.15 cycles/min (n=6, 4 and 4, re- spectively; Fig. 4G and H). In the presence of L-NNA, high K ＋ produced initial and sustained contraction of 4.5±1.4 g and 6.3±2.0 g, respectively (n=4 and 6, respectively; Fig. 4G and H). Meanwhile, ACh (10μM) also produced initial transient contraction of 6.5±1.72 g followed by later sus- tained tonic contraction of 1.7±0.48 g with superimposed phasic contractions of 1.6± 0.93 g (n=6; Fig. 4I and J; Table 1). The frequency of ACh-induced phasic contraction was 2.4±0.62 cycles/min (n=6). In control, phasic contraction and its frequency were 0.6±0.20 g and 3.6±1.22 cycles/min, re- spectively (n=4; Fig. ...
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... shown in Fig. 4D and F, longitudinal smooth muscle from human gastric corpus from LC showed spontaneous contraction of 0.7±0.14 g with a frequency of 3.36±0.42 cy- cles/min, respectively (n=9, respectively; Table 1). High K ＋ produced initial and sustained contraction of 3.5±1.08 g and 2.6±1.05 g, respectively (n=10 and 12, respectively; Fig. 4E and F). We also studied effect of L-NNA on high K ＋ -induc- ed contraction. In control, longitudinal smooth muscle from LC produced phasic contraction of 0.4±0.1 g with a fre- quency of 4.2±0.13 cycles/min (n=4; Fig. 4H). When L-NNA (100μM) was applied, it produced tonic and phasic con- tractions of 0.5± 0.16 g and 0.4±0.11 g, respectively with a frequency of 3.9± 0.15 cycles/min (n=6, 4 and 4, re- spectively; Fig. 4G and H). In the presence of L-NNA, high K ＋ produced initial and sustained contraction of 4.5±1.4 g and 6.3±2.0 g, respectively (n=4 and 6, respectively; Fig. 4G and H). Meanwhile, ACh (10μM) also produced initial transient contraction of 6.5±1.72 g followed by later sus- tained tonic contraction of 1.7±0.48 g with superimposed phasic contractions of 1.6± 0.93 g (n=6; Fig. 4I and J; Table 1). The frequency of ACh-induced phasic contraction was 2.4±0.62 cycles/min (n=6). In control, phasic contraction and its frequency were 0.6±0.20 g and 3.6±1.22 cycles/min, re- spectively (n=4; Fig. ...
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... shown in Fig. 4D and F, longitudinal smooth muscle from human gastric corpus from LC showed spontaneous contraction of 0.7±0.14 g with a frequency of 3.36±0.42 cy- cles/min, respectively (n=9, respectively; Table 1). High K ＋ produced initial and sustained contraction of 3.5±1.08 g and 2.6±1.05 g, respectively (n=10 and 12, respectively; Fig. 4E and F). We also studied effect of L-NNA on high K ＋ -induc- ed contraction. In control, longitudinal smooth muscle from LC produced phasic contraction of 0.4±0.1 g with a fre- quency of 4.2±0.13 cycles/min (n=4; Fig. 4H). When L-NNA (100μM) was applied, it produced tonic and phasic con- tractions of 0.5± 0.16 g and 0.4±0.11 g, respectively with a frequency of 3.9± 0.15 cycles/min (n=6, 4 and 4, re- spectively; Fig. 4G and H). In the presence of L-NNA, high K ＋ produced initial and sustained contraction of 4.5±1.4 g and 6.3±2.0 g, respectively (n=4 and 6, respectively; Fig. 4G and H). Meanwhile, ACh (10μM) also produced initial transient contraction of 6.5±1.72 g followed by later sus- tained tonic contraction of 1.7±0.48 g with superimposed phasic contractions of 1.6± 0.93 g (n=6; Fig. 4I and J; Table 1). The frequency of ACh-induced phasic contraction was 2.4±0.62 cycles/min (n=6). In control, phasic contraction and its frequency were 0.6±0.20 g and 3.6±1.22 cycles/min, re- spectively (n=4; Fig. ...
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... shown in Fig. 4A and C, circular smooth muscle of human gastric corpus from LC showed spontaneous contraction of 0.2±0.04 g with a frequency of 4.0± 0.36 cycles/min (n=7; Table 1). High K ＋ produced initial and sustained contraction of 4.1±2.1 g and 9.1±1.78 g, respectively (n=10 and 12, respectively; Fig. 4B and C; Table 1). Meanwhile, ACh (10μM) ...
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... shown in Fig. 4A and C, circular smooth muscle of human gastric corpus from LC showed spontaneous contraction of 0.2±0.04 g with a frequency of 4.0± 0.36 cycles/min (n=7; Table 1). High K ＋ produced initial and sustained contraction of 4.1±2.1 g and 9.1±1.78 g, respectively (n=10 and 12, respectively; Fig. 4B and C; Table 1). Meanwhile, ACh (10μM) produced initial transient contraction of 8.0±1.33 g followed by later sustained tonic contraction of 2.8±0.59 g with superimposed phasic contractions of 2.7±2.15 g (n=7, 7 and 4, respectively; Table 1). The frequency of ACh-induced phasic contraction was 2.3±0.83 cycles/min (n=4; Table 1). In ...
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... shown in Fig. 4D and F, longitudinal smooth muscle from human gastric corpus from LC showed spontaneous contraction of 0.7±0.14 g with a frequency of 3.36±0.42 cycles/min, respectively (n=9, respectively; Table 1). High K ＋ produced initial and sustained contraction of 3.5±1.08 g and 2.6±1.05 g, respectively (n=10 and 12, respectively; Fig. 4E and F). ...
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... shown in Fig. 4D and F, longitudinal smooth muscle from human gastric corpus from LC showed spontaneous contraction of 0.7±0.14 g with a frequency of 3.36±0.42 cycles/min, respectively (n=9, respectively; Table 1). High K ＋ produced initial and sustained contraction of 3.5±1.08 g and 2.6±1.05 g, respectively (n=10 and 12, respectively; Fig. 4E and F). We also studied effect of L-NNA on high K ＋ -induced contraction. In control, longitudinal smooth muscle from LC produced phasic contraction of 0.4±0.1 g with a frequency of 4.2±0.13 cycles/min (n=4; Fig. 4H). When L-NNA (100μM) was applied, it produced tonic and phasic contractions of 0.5± 0.16 g and 0.4±0.11 g, respectively ...
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... Table 1). High K ＋ produced initial and sustained contraction of 3.5±1.08 g and 2.6±1.05 g, respectively (n=10 and 12, respectively; Fig. 4E and F). We also studied effect of L-NNA on high K ＋ -induced contraction. In control, longitudinal smooth muscle from LC produced phasic contraction of 0.4±0.1 g with a frequency of 4.2±0.13 cycles/min (n=4; Fig. 4H). When L-NNA (100μM) was applied, it produced tonic and phasic contractions of 0.5± 0.16 g and 0.4±0.11 g, respectively with a frequency of 3.9± 0.15 cycles/min (n=6, 4 and 4, respectively; Fig. 4G and H). In the presence of L-NNA, high K ＋ produced initial and sustained contraction of 4.5±1.4 g and 6.3±2.0 g, respectively (n=4 and 6, ...
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... contraction. In control, longitudinal smooth muscle from LC produced phasic contraction of 0.4±0.1 g with a frequency of 4.2±0.13 cycles/min (n=4; Fig. 4H). When L-NNA (100μM) was applied, it produced tonic and phasic contractions of 0.5± 0.16 g and 0.4±0.11 g, respectively with a frequency of 3.9± 0.15 cycles/min (n=6, 4 and 4, respectively; Fig. 4G and H). In the presence of L-NNA, high K ＋ produced initial and sustained contraction of 4.5±1.4 g and 6.3±2.0 g, respectively (n=4 and 6, respectively; Fig. 4G and H). Meanwhile, ACh (10μM) also produced initial transient contraction of 6.5±1.72 g followed by later sustained tonic contraction of 1.7±0.48 g with superimposed phasic ...
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... When L-NNA (100μM) was applied, it produced tonic and phasic contractions of 0.5± 0.16 g and 0.4±0.11 g, respectively with a frequency of 3.9± 0.15 cycles/min (n=6, 4 and 4, respectively; Fig. 4G and H). In the presence of L-NNA, high K ＋ produced initial and sustained contraction of 4.5±1.4 g and 6.3±2.0 g, respectively (n=4 and 6, respectively; Fig. 4G and H). Meanwhile, ACh (10μM) also produced initial transient contraction of 6.5±1.72 g followed by later sustained tonic contraction of 1.7±0.48 g with superimposed phasic contractions of 1.6± 0.93 g (n=6; Fig. 4I and J; Table 1). The frequency of ACh-induced phasic contraction was 2.4±0.62 cycles/min (n=6). In control, phasic contraction ...
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... of L-NNA, high K ＋ produced initial and sustained contraction of 4.5±1.4 g and 6.3±2.0 g, respectively (n=4 and 6, respectively; Fig. 4G and H). Meanwhile, ACh (10μM) also produced initial transient contraction of 6.5±1.72 g followed by later sustained tonic contraction of 1.7±0.48 g with superimposed phasic contractions of 1.6± 0.93 g (n=6; Fig. 4I and J; Table 1). The frequency of ACh-induced phasic contraction was 2.4±0.62 cycles/min (n=6). In control, phasic contraction and its frequency were 0.6±0.20 g and 3.6±1.22 cycles/min, respectively (n=4; Fig. ...
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... of 6.5±1.72 g followed by later sustained tonic contraction of 1.7±0.48 g with superimposed phasic contractions of 1.6± 0.93 g (n=6; Fig. 4I and J; Table 1). The frequency of ACh-induced phasic contraction was 2.4±0.62 cycles/min (n=6). In control, phasic contraction and its frequency were 0.6±0.20 g and 3.6±1.22 cycles/min, respectively (n=4; Fig. ...
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This study was designed to examine the effects of histamine on gastric motility and its specific receptor in the circular smooth muscle of the human gastric corpus. Histamine mainly produced tonic relaxation in a concentration-dependent and reversible manner, although histamine enhanced contractility in a minor portion of tissues tested. Histamine-...
Citations
... From these responses, increased intracellular Ca 2+ produces contractions (12). In the GI tract, smooth muscle contractions can be blocked by agents such as tetraethylammonium (TEA) and 4-aminopyridine (4-AP), which are known to block Ca 2+ -activated K + channels and voltage-dependent K + channels, respectively (18,19). Therefore, each channel associated with excitability and contractility in the GI tract should be examined to elucidate its main physiological action of channel in GI tract. ...
... Written informed consent was obtained from all patients who donated their gastric tissue. Human gastric tissues from the greater curvature (tissue samples from corpus and/or antrum) were obtained from 243 patients who underwent gastrectomies between 2011 and 2020 (10,11,(18)(19)(20)(21). Specimens of macroscopically normal tissue in the neoplastic areas were removed immediately after the surgical resection of the stomach. ...
Gastric motility is controlled by slow waves. In general, the activation of the ATP-sensitive K⁺ (KATP) channels in the smooth muscle opposes the membrane excitability and produces relaxation. Since metabolic inhibition and/or diabetes mellitus are accompanied by dysfunctions of gastric smooth muscle, we examined the possible roles of KATP channels in human gastric motility. We used human gastric corpus and antrum smooth muscle preparations and recorded the mechanical activities with a conventional contractile measuring system. We also identified the subunits of the KATP channels using Western blot. Pinacidil (10 μM), a KATP channel opener, suppressed contractions to 30% (basal tone to −0.2 g) of the control. The inhibitory effect of pinacidil on contraction was reversed to 59% of the control by glibenclamide (20 μM), a KATP channel blocker. The relaxation by pinacidil was not affected by a pretreatment with L-arginine methyl ester, tetraethylammonium, or 4-aminopyridine. Pinacidil also inhibited the acetylcholine (ACh)-induced tonic and phasic contractions in a glibenclamide-sensitive manner (42% and 6% of the control, respectively). Other KATP channel openers such as diazoxide, cromakalim and nicorandil also inhibited the spontaneous and ACh-induced contractions. Calcitonin gene-related peptide (CGRP), a gastric neuropeptide, induced muscle relaxation by the activation of KATP channels in human gastric smooth muscle. Finally, we have found with Western blot studies, that human gastric smooth muscle expressed KATP channels which were composed of Kir 6.2 and SUR2B subunits.
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Aim:
To investigate the effects and underlying mechanisms of resveratrol and genistein on contractile responses of rat gastrointestinal smooth muscle.
Methods:
Isolated strips of gastrointestinal smooth muscle from Spraque-Dawley rats were suspended in organ baths containing Kreb's solution, and the contractility of smooth muscles was measured before and after incubation with resveratrol and genistein, and the related mechanisms were studied by co-incubation with various inhibitors.
Results:
Resveratrol and genistein dose-dependently decreased the resting tension, and also reduced the mean contractile amplitude of gastrointestinal smooth muscle. Estrogen receptor blockades (ICI 182780 and tamoxifen) failed to alter the inhibitory effects induced by resveratrol and genistein. However, their effects were attenuated by inhibitions of α-adrenergic receptor (phentolamine), nitric oxide synthase (levorotatory-NG-nitroarginine), ATP-sensitive potassium channels (glibenclamide), and cyclic adenosine monophosphate (SQ22536). In high K(+)/Ca(2+)-free Kreb's solution containing 0.01 mmol/L egtazic acid, resveratrol and genistein reduced the contractile responses of CaCl2, and shifted its cumulative concentration-response curves rightward.
Conclusion:
Resveratrol and genistein relax gastrointestinal smooth muscle via α-adrenergic receptors, nitric oxide and cyclic adenosine monophosphate pathways, ATP-sensitive potassium channels, and inhibition of L-type Ca(2+) channels.
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... When it is required to rule out nerve mediated response, tetrodotoxin (TTX, 0.4 μM) only and/or nerve blockers cocktail (NBC) was used. NBC contained TTX (0.4 μM), guanethidine (1 μM), and atropine (ATR, 1 μM) [10,11]. All drugs used in this study were purchased from Sigma. ...
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... Connective tissue from the uteri was removed and the muscle layers were isolated from the endometrium. For the measurement of mechanical contractions, strips (0.2×0.7 cm) of circular muscle were mounted in an organ bath (25 ml) of an isometric contractile measuring system [24]. In this system, one end of the tissue was tied tightly to a fixed holder and the other side was linked by a hook type holder to a force transducer (Harvard Apparatus, Holliston, MA, USA). ...
... As shown in Fig. 5, TASK-2 channels inhibitors such as quinidine, and lidocaine produced robust contractions even in the presence of TEA, 4-AP, and/or L-methionine. Even data not shown, these contractile effect of TASK-2 channels inhibitors on uterine contraction was not affected by nerve blockers such as nerve blocker cocktail (0.4 μM tetrodotoxin (TTX), 1 μM guanethidine, and 1 μM atropine (ATR)) [24]. This result strongly suggests that TASK-2 channels might play a central role in the regulation of uterine circular muscle contractility. ...
Plasma pH can be altered during pregnancy and at labor. Membrane excitability of smooth muscle including uterine muscle is suppressed by the activation of K(+) channels. Because contractility of uterine muscle is regulated by extracellular pH and humoral factors, K(+) conductance could be connected to factors regulating uterine contractility during pregnancy. Here, we showed that TASK-2 inhibitors such as quinidine, lidocaine, and extracellular acidosis produced contraction in uterine circular muscle of mouse. Furthermore, contractility was significantly increased in pregnant uterine circular muscle than that of non-pregnant muscle. These patterns were not changed even in the presence of tetraetylammonium (TEA) and 4-aminopyridine (4-AP). Finally, TASK-2 inhibitors induced strong myometrial contraction even in the presence of L-methionine, a known inhibitor of stretchactivated channels in myometrium. When compared to non-pregnant myometrium, pregnant myometrium showed increased immunohistochemical expression of TASK-2. Therefore, TASK-2, seems to play a key role during regulation of myometrial contractility in the pregnancy and provides new insight into preventing preterm delivery.
... Although nitrate has historically been reported to have deleterious effects in humans, such as infant methemoglobinemia [6], recent evidence suggests a beneficial, antimicrobial role for inorganic nitrate in several systems in humans, including the gastrointestinal tract, oral cavity and skin [7][8][9]. In the oral cavity, inorganic nitrate is present in saliva in high concentrations. ...
Objective:
Nitric Oxide (NO) is one of the most powerful antibacterial compounds. The aim of this study was to determine the association between salivary NO, dental caries and cariogenic bacteria.
Materials and methods:
The salivary NO concentration of 257 Korean children was analyzed by the Griess colorimetric reaction method. Salivary mutans streptococci (MS) and Lactobacilli (LB) were counted using the Dentocult MS and Dentocult LB kit, respectively. Dental caries status was examined using the WHO criteria. Confounders were age, gender, salivary flow rate and salivary buffer capacity. Analysis of covariance (ANCOVA) was used to evaluate the association among NO, salivary MS level, salivary LB level and dental caries status after adjusting for the effects of confounders.
Results:
A significant decrease was found in salivary NO levels as the salivary LB count increased after controlling for confounders (p = 0.049). However, the MS level, caries experience and active caries status showed no significant association.
Conclusion:
This result indicates that NO production might be a host defense mechanism against the growth of cariogenic bacteria.
... Among various conditions, high K ＋ stimulation produces contraction through membrane depolarization , which activates VDCCL in gastric smooth muscle [12]. This mechanism is true except for the longitudinal muscles of the fundus, where high K ＋ produces relaxation [13] . We recently found high K ＋ -induced relaxation of human corporal longitudinal smooth muscle is NO mediated. ...
... In particular, NO is a principal candidate for fundus relaxation [16] . We recently discovered NO-dependent relaxation in the corpus [13] . We also found that L-NNA inhibited high K ＋ -induced relaxation in longitudinal smooth muscle of the fundus GC, as shown in Figs. ...
... These findings suggest that the NO/sGC pathway is selectively involved (Fig. 3D and 3E ). In fact, K ＋ channels such as the KV channel [17,30] and KCa channel [31] are directly regulated by the NO/sGC pathway in smooth muscle [13]. In addition, nNOS neurons are found in the myenteric region of the human stomach [32]. ...
This study was designed to elucidate high K(+)-induced relaxation in the human gastric fundus. Circular smooth muscle from the human gastric fundus greater curvature showed stretch-dependent high K(+) (50 mM)-induced contractions. However, longitudinal smooth muscle produced stretch-dependent high K(+)-induced relaxation. We investigated several relaxation mechanisms to understand the reason for the discrepancy. Protein kinase inhibitors such as KT 5823 (1 µM) and KT 5720 (1 µM) which block protein kinases (PKG and PKA) had no effect on high K(+)-induced relaxation. K(+) channel blockers except 4-aminopyridine (4-AP), a voltage-dependent K(+) channel (K(V)) blocker, did not affect high K(+)-induced relaxation. However, N(G)-nitro-L-arginine and 1H-(1,2,4)oxadiazolo (4,3-A)quinoxalin-1-one, an inhibitors of soluble guanylate cyclase (sGC) and 4-AP inhibited relaxation and reversed relaxation to contraction. High K(+)-induced relaxation of the human gastric fundus was observed only in the longitudinal muscles from the greater curvature. These data suggest that the longitudinal muscle of the human gastric fundus greater curvature produced high K(+)-induced relaxation that was activated by the nitric oxide/sGC pathway through a K(V) channel-dependent mechanism.
Background
Delayed gastric emptying (DGE) is the main complication after pancreaticoduodenectomy (PD), but the mechanism is still unclear. The aim of this study was to elucidate the role of complete resection of the gastric antrum in decreasing incidence and severity of DGE after PD.
Methods
Sprague-Dawley rats were divided into three groups: expanded resection (ER group), complete resection (CR group), and incomplete resection (IR group) of the gastric antrum. The tension (g) of remnant stomach contraction was observed. We analyzed the histological morphology of the gastric wall by different excisional methods after distal gastrectomy. Moreover, patients underwent PD at our department between January 2012 and May 2016 were included in the study. These cases were divided into IR group and CR group of the gastric antrum, and the clinical data were retrospectively analyzed.
Results
The ex vivo remnant stomachs of CR group exhibited much greater contraction tension than others (P < 0.05). The contraction tension of the remnant stomach increased with increasing acetylcholine concentration, while remained stable at the concentration of 10 × 10⁻⁵ mol/L Furthermore, 174 consecutive patients were included and retrospectively analyzed in the study. The incidence of DGE in patients was significantly lower (3.5% vs. 21.3%, P < 0.01) and postoperative hospital stay was significantly shorter (16 vs. 22 days, P < 0.05) in CR group than those in IR group. In addition, hematoxylin-eosin staining analyses of the gastric wall confirmed that the number of transected circular smooth muscle bundles were higher in IR group than those in CR group (8.24 ± 0.65 vs. 3.76 ± 0.70, P < 0.05).
Conclusions
The complete resection of the gastric antrum is associated with decreased incidence and severity of DGE after PD. Gastric electrophysiological and physiopathological disorders caused by damage to gastric smooth muscles might be the mechanism underlying DGE.
