Innervation and gap junctions of intestinal striated and smooth muscle cells in the loach

1989 ◽  
Vol 257 (1) ◽  
Author(s):  
Masahiro Hara ◽  
Hiroshi Washioka ◽  
Akira Tonosaki
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Gap Junctions ◽  
Muscle Cells

scholarly journals Involvement of gap junctions between smooth muscle cells in sustained hypoxic pulmonary vasoconstriction development: a potential role for 15-HETE and 20-HETE

2016 ◽  
Vol 310 (8) ◽  
pp. L772-L783 ◽  
Author(s):  
Igor V. Kizub ◽  
Anand Lakhkar ◽  
Vidhi Dhagia ◽  
Sachindra R. Joshi ◽  
Houli Jiang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Gap Junctions ◽  
Force Measurement ◽  
Isometric Force ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Muscle Cells ◽  
Cytochrome P450 Monooxygenases ◽  
Prostaglandin E ◽  
Pulmonary Vasoconstriction

In response to hypoxia, the pulmonary artery normally constricts to maintain optimal ventilation-perfusion matching in the lung, but chronic hypoxia leads to the development of pulmonary hypertension. The mechanisms of sustained hypoxic pulmonary vasoconstriction (HPV) remain unclear. The aim of this study was to determine the role of gap junctions (GJs) between smooth muscle cells (SMCs) in the sustained HPV development and involvement of arachidonic acid (AA) metabolites in GJ-mediated signaling. Vascular tone was measured in bovine intrapulmonary arteries (BIPAs) using isometric force measurement technique. Expression of contractile proteins was determined by Western blot. AA metabolites in the bath fluid were analyzed by mass spectrometry. Prolonged hypoxia elicited endothelium-independent sustained HPV in BIPAs. Inhibition of GJs by 18β-glycyrrhetinic acid (18β-GA) and heptanol, nonspecific blockers, and Gap-27, a specific blocker, decreased HPV in deendothelized BIPAs. The sustained HPV was not dependent on Ca2+entry but decreased by removal of Ca2+and by Rho-kinase inhibition with Y-27632. Furthermore, inhibition of GJs decreased smooth muscle myosin heavy chain (SM-MHC) expression and myosin light chain phosphorylation in BIPAs. Interestingly, inhibition of 15- and 20-hydroxyeicosatetraenoic acid (HETE) synthesis decreased HPV in deendothelized BIPAs. 15-HETE- and 20-HETE-stimulated constriction of BIPAs was inhibited by 18β-GA and Gap-27. Application of 15-HETE and 20-HETE to BIPAs increased SM-MHC expression, which was also suppressed by 18β-GA and by inhibitors of lipoxygenase and cytochrome P450 monooxygenases. More interestingly, 15,20-dihydroxyeicosatetraenoic acid and 20-OH-prostaglandin E2, novel derivatives of 20-HETE, were detected in tissue bath fluid and synthesis of these derivatives was almost completely abolished by 18β-GA. Taken together, our novel findings show that GJs between SMCs are involved in the sustained HPV in BIPAs, and 15-HETE and 20-HETE, through GJs, appear to mediate SM-MHC expression and contribute to the sustained HPV development.

Effects of the gap junction blocker glycyrrhetinic acid on gastrointestinal smooth muscle cells

2005 ◽  
Vol 288 (4) ◽  
pp. G832-G841 ◽  
Author(s):  
Yukari Takeda ◽  
Sean M. Ward ◽  
Kenton M. Sanders ◽  
Sang Don Koh
Keyword(s):  
Smooth Muscle ◽  
Patch Clamp ◽  
Smooth Muscle Cells ◽  
Gap Junctions ◽  
Lucifer Yellow ◽  
Muscle Cells ◽  
Glycyrrhetinic Acid ◽  
Delayed Rectifier ◽  
Dependent Manner ◽  
Patch Clamp Technique

In the tunica muscularis of the gastrointestinal (GI) tract, gap junctions form low-resistance pathways between pacemaker cells known as interstitial cells of Cajal (ICCs) and between ICC and smooth muscle cells. Coupling via these junctions facilitates electrical slow-wave propagation and responses of smooth muscle to enteric motor nerves. Glycyrrhetinic acid (GA) has been shown to uncouple gap junctions, but previous studies have shown apparent nonspecific effects of GA in a variety of tissues. We tested the effects of GA using isometric force measurements, intracellular microelectrode recordings, the patch-clamp technique, and the spread of Lucifer yellow within cultured ICC networks. In murine small intestinal muscles, β-GA (10 μM) decreased phasic contractions and depolarized resting membrane potential. Preincubation of GA inhibited the spread of Lucifer yellow, increased input resistance, and decreased cell capacitance in ICC networks, suggesting that GA uncoupled ICCs. In patch-clamp experiments of isolated jejunal myocytes, GA significantly decreased L-type Ca2+ current in a dose-dependent manner without affecting the voltage dependence of this current. The IC50 for Ca2+ currents was 1.9 μM, which is lower than the concentrations used to block gap junctions. GA also significantly increased large-conductance Ca2+-activated K+ currents but decreased net delayed rectifier K+ currents, including 4-aminopyridine and tetraethylammonium-resistant currents. In conclusion, the reduction of phasic contractile activity of GI muscles by GA is likely a consequence of its inhibitory effects on gap junctions and voltage-dependent Ca2+ currents. Membrane depolarization may be a consequence of uncoupling effects of GA on gap junctions between ICCs and smooth muscles and inhibition of K+ conductances in smooth muscle cells.

Gap Junctions Formed of Connexin43 Are Found Between Smooth Muscle Cells of Human Corpus Cavernosum

1993 ◽  
Vol 149 (6) ◽  
pp. 1568-1575 ◽  
Author(s):  
A.C. Campos De Carvalho ◽  
C. Roy ◽  
A.P. Moreno ◽  
A. Melman ◽  
E.L. Hertzberg ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Gap Junctions ◽  
Corpus Cavernosum ◽  
Muscle Cells

Gap junctions and direct intercellular communication between rat uterine smooth muscle cells

1985 ◽  
Vol 249 (1) ◽  
pp. C20-C31 ◽  
Author(s):  
W. C. Cole ◽  
R. E. Garfield ◽  
J. S. Kirkaldy
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Gap Junctions ◽  
Intercellular Communication ◽  
Contractile Activity ◽  
Muscle Cells ◽  
Uterine Wall ◽  
Longitudinal Distribution ◽  
Uterine Smooth Muscle ◽  
Apparent Diffusion

We have tested the hypothesis that an increase in direct intercellular communication accompanies the development of gap junctions (GJs) between rat uterine smooth muscle cells at parturition. Intercellular communication in these tissues was studied by exposing one portion of small strips of myometrium to 2-[3H]deoxy-D-glucose (2-DG) and determining the longitudinal distribution of tracer after a 5-h period of diffusion. The distribution of 2-DG was greater in parturient compared with ante- and postpartum tissues. Similarly, the apparent diffusion coefficient of 2-DG was almost 10-fold greater in delivering tissues (1.86 X 10(-6) cm2/s) than before (0.199 X 10(-6) cm2/s) or after (0.296 X 10(-6) cm2/s) parturition. Control experiments indicated that the redistribution of 2-DG was dependent on the presence of GJs and was the result of intracellular and direct cell-to-cell diffusion. The appearance of GJs is the myometrium at term facilitates direct intercellular communication between uterine smooth muscle cells during labor. This improved communication may be responsible for synchronizing and coordinating electrical, metabolic, and contractile activity in the uterine wall and, hence, the effective expulsion of fetuses.

Changes of gap junctions in myometrium of guinea pig at parturition and abortion

1982 ◽  
Vol 60 (3) ◽  
pp. 335-341 ◽  
Author(s):  
R. E. Garfield ◽  
E. E. Daniel ◽  
M. Dukes ◽  
J. D. Fitzgerald
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Smooth Muscle Cells ◽  
Gap Junctions ◽  
Gap Junction ◽  
Electron Micrographs ◽  
Guinea Pigs ◽  
Muscle Cells ◽  
Similar Increase ◽  
Junction Area

Myometrial tissues from guinea pigs were quantitatively examined for gap junctions in electron micrographs. Small numbers of gap junctions were present between smooth muscle cells in myometria of pregnant guinea pigs at days 50 and 65 of gestation. The junctions increased in number and size at parturition on day 69 and decreased again to control levels 24 h after parturition. A similar increase in junctions occurred when abortion was induced by 16,16-dimethylprostaglandin E2 (PGE2) on day 65. There were no consistent or significant differences in numbers of gap junctions from myometrium taken over sites of placental attachment and from other sites. These results together with previous studies suggest that an increase in myometrial gap junction area is associated with and may be essential for parturition in guinea pigs, but the control of their development may differ from that in other mammals.

Gap junctions between human corpus cavernosum smooth muscle cells: gating properties and unitary conductance

1993 ◽  
Vol 264 (1) ◽  
pp. C80-C92 ◽  
Author(s):  
A. P. Moreno ◽  
A. C. Campos de Carvalho ◽  
G. Christ ◽  
A. Melman ◽  
D. C. Spray
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Gap Junctions ◽  
Single Channel ◽  
Corpus Cavernosum ◽  
Second Messenger ◽  
Muscle Cells ◽  
Major Protein ◽  
Messenger Molecules ◽  
And Function

We previously showed that corpus cavernosum smooth muscle cells are connected via gap junctions in situ and in culture and that a major protein component of these gap junctions is connexin43. To characterize the physiological properties of the gap junctions between corpus cavernosum smooth muscle cells, we now demonstrate that the cells are dye and electrically coupled and describe some of the gating properties of these gap junctional channels at macroscopic and single-channel levels. Junctional conductance (gj) between corporal smooth muscle cells was moderately voltage sensitive; was reduced rapidly, reversibly, and completely by halothane; and was increased by treatment with a tumor-promoting phorbol ester [12-O-tetradecanoylphorbol-13-acetate (TPA)] and decreased by isoproterenol. Histograms of unitary junctional currents revealed multiple conductance peaks with events of approximately 90 pS being the most abundant. TPA and phenylephrine produced large increases in relative frequencies of the smaller events, whereas isoproterenol and 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP) slightly increased the relative frequencies of the larger events. None of the tested drugs substantially affected the steady-state voltage dependence of gj. These second messenger systems also affected expression of connexin43 by corpus cavernosum smooth muscle cells, as judged by immunoblots. At 6 h of treatment, both TPA- and 8-BrcAMP-treated cultures showed markedly elevated levels of connexin43, whereas at 24 h, the level of connexin43 in TPA-treated cultures had returned to control levels. Together, these data indicate that second messenger molecules involved in penile erection produce changes in gap junction expression and function; it is plausible that these changes could be physiologically relevant in altering and propagating changes in vasomotor tone.

scholarly journals Involvement of connexin 43 phosphorylation and gap junctional communication between smooth muscle cells in vasopressin-induced ROCK-dependent vasoconstriction after hemorrhagic shock

2017 ◽  
Vol 313 (4) ◽  
pp. C362-C370 ◽  
Author(s):  
Guangming Yang ◽  
Xiaoyong Peng ◽  
Yue Wu ◽  
Tao Li ◽  
Liangming Liu
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Gap Junctions ◽  
Hemorrhagic Shock ◽  
Connexin 43 ◽  
Muscle Cells ◽  
Gap Junctional Communication ◽  
Contractile Effect ◽  
Junctional Communication ◽  
Gap Junctional

We examined the roles played by gap junctions (GJs) and the GJ channel protein connexin 43 (Cx43) in arginine vasopressin (AVP)-induced vasoconstriction after hemorrhagic shock and their relationship to Rho kinase (ROCK) and protein kinase C (PKC). The results showed that AVP induced an endothelium-independent contraction in rat superior mesenteric arteries (SMAs). Blocking the GJs significantly decreased the contractile response of SMAs and vascular smooth muscle cells (VSMCs) to AVP after shock and hypoxia. The selective Cx43-mimetic peptide inhibited the vascular contractile effect of AVP after shock and hypoxia. AVP restored hypoxia-induced decrease of Cx43 phosphorylation at Ser262 and gap junctional communication in VSMCs. Activation of RhoA with U-46619 increased the contractile effect of AVP. This effect was antagonized by the ROCK inhibitor Y27632 and the Cx43-mimetic peptide. In contrast, neither an agonist nor an inhibitor of PKC had significant effects on AVP-induced contraction after hemorrhagic shock. In addition, silencing of Cx43 with siRNA blocked the AVP-induced increase of ROCK activity in hypoxic VSMCs. In conclusion, AVP-mediated vascular contractile effects are endothelium and myoendothelial gap junction independent. Gap junctions between VSMCs, gap junctional communication, and Cx43 phosphorylation at Ser262 play important roles in the vascular effects of AVP. RhoA/ROCK, but not PKC, is involved in this process.

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