Purification of Neuropeptide with the Contractile Activity on the Smooth Muscle from the Skin of Conger Eel Conger myriaster

Vascular smooth muscle cells (VSMCs) can regulate arterial mechanics via contractile activity in response to changing mechanical and chemical signals. Contractility is traditionally evaluated via uniaxial isometric testing of isolated rings despite the in vivo environment being very different. Most blood vessels maintain a locally preferred value of in vivo axial stretch while subjected to changes in distending pressure, but both of these phenomena are obscured in uniaxial isometric testing. Few studies have rigorously analyzed the role of in vivo loading conditions in smooth muscle function. Thus, we evaluated effects of uniaxial versus biaxial deformations on smooth muscle contractility by stimulating two regions of the mouse aorta with different vasoconstrictors using one of three testing protocols: (i) uniaxial isometric testing, (ii) biaxial isometric testing, and (iii) axially isometric plus isobaric testing. Comparison of methods (i) and (ii) revealed increased sensitivity and contractile capacity to potassium chloride and phenylephrine (PE) with biaxial isometric testing, and comparison of methods (ii) and (iii) revealed a further increase in contractile capacity with isometric plus isobaric testing. Importantly, regional differences in estimated in vivo axial stretch suggest locally distinct optimal biaxial configurations for achieving maximal smooth muscle contraction, which can only be revealed with biaxial testing. Such differences highlight the importance of considering in vivo loading and geometric configurations when evaluating smooth muscle function. Given the physiologic relevance of axial extension and luminal pressurization, we submit that, when possible, axially isometric plus isobaric testing should be employed to evaluate vascular smooth muscle contractile function.

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Smooth muscle mechanical responses in vitro to bethanechol after progesterone in male rat.

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1978.235.4.e422 ◽

1978 ◽

Vol 235 (4) ◽

pp. E422 ◽

Cited By ~ 2

Author(s):

L A Bruce ◽

F M Behsudi ◽

I E Danhof

Keyword(s):

Smooth Muscle ◽

Contractile Activity ◽

Circular Muscle ◽

Male Rat ◽

Equal Weight ◽

Muscarinic Agonist ◽

Sprague Dawley ◽

Response Curves ◽

Dose Levels

Male Sprague-Dawley rats were pretreated subcutaneously with either progesterone (3 mg/kg per day) in a vehicle or a vehicle only for 3 days. Antral and gastroduodenal junctional tissues (GJT) were excised from both groups of animals and prepared for in vitro mechanical measurements. Responses from the circular muscle axis of these tissues were recorded with strain gauge transducers over a 30-min period. Chemical stimulation of the tissue was achieved with a muscarinic agonist, bethanechol chloride. Log-dose response curves suggested that untreated antral tissue generated stronger contractile activity than untreated GJT on an equal weight basis at bethanechol dose levels of 6.4 X 10(-6) M to 1 X 10(-4) M (P less than 0.005). Antral tissue and GJT contractile activity from the progesterone pretreated animals was significantly reduced (P less than 0.01) compared to the corresponding tissues from untreated animals at bethanechol dose levels of 6.4 X 10(-6) M and 1.28 X 10(-5) M. Progesterone pretreatment appeared to have little effect on the contractile frequency of either tissue. These results suggest possible progesteronic influences on contractile force in gastrointestinal smooth muscle.

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T-type Ca2+channel modulation by otilonium bromide

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00437.2009 ◽

2010 ◽

Vol 298 (5) ◽

pp. G706-G713 ◽

Cited By ~ 12

Author(s):

Peter R. Strege ◽

Lei Sha ◽

Arthur Beyder ◽

Cheryl E. Bernard ◽

Edward Perez-Reyes ◽

...

Keyword(s):

Smooth Muscle ◽

Contractile Activity ◽

Clinical Effectiveness ◽

Smooth Muscle Contraction ◽

Hek293 Cells ◽

Channel Blockers ◽

Patch Clamp Technique ◽

Extracellular Solution ◽

Channel Modulation ◽

Main Pathway

Antispasmodics are used clinically to treat a variety of gastrointestinal disorders by inhibition of smooth muscle contraction. The main pathway for smooth muscle Ca2+entry is through L-type channels; however, there is increasing evidence that T-type Ca2+channels also play a role in regulating contractility. Otilonium bromide, an antispasmodic, has previously been shown to inhibit L-type Ca2+channels and colonic contractile activity. The objective of this study was to determine whether otilonium bromide also inhibits T-type Ca2+channels. Whole cell currents were recorded by patch-clamp technique from HEK293 cells transfected with cDNAs encoding the T-type Ca2+channels, CaV3.1 (α1G), CaV3.2 (α1H), or CaV3.3 (α1I) alpha subunits. Extracellular solution was exchanged with otilonium bromide (10−8to 10−5M). Otilonium bromide reversibly blocked all T-type Ca2+channels with a significantly greater affinity for CaV3.3 than CaV3.1 or CaV3.2. Additionally, the drug slowed inactivation in CaV3.1 and CaV3.3. Inhibition of T-type Ca2+channels may contribute to inhibition of contractility by otilonium bromide. This may represent a new mechanism of action for antispasmodics and may contribute to the observed increased clinical effectiveness of antispasmodics compared with selective L-type Ca2+channel blockers.

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Membrane stretch evoked by cell swelling increases contractile activity in vascular smooth muscle through dihydropyridine-sensitive pathways

Acta Physiologica Scandinavica ◽

10.1111/j.1748-1716.1994.tb09824.x ◽

1994 ◽

Vol 152 (4) ◽

pp. 419-427 ◽

Cited By ~ 12

Author(s):

A. BÜLOW ◽

B. JOHANSSON

Keyword(s):

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Contractile Activity ◽

Cell Swelling ◽

Membrane Stretch

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Study on the by-catch prevention device of spring frame net trap for conger eel, Conger myriaster

Journal of the Korean society of Fisheries Technology ◽

10.3796/ksft.2006.42.1.001 ◽

2006 ◽

Vol 42 (1) ◽

pp. 1-10 ◽

Cited By ~ 3

Author(s):

Wook-Sung Kim ◽

Ju-Hee Lee ◽

Byeong-Guk Kwon ◽

Jae-Bum Yoo ◽

Bu-Yeung Kim ◽

...

Keyword(s):

Conger Myriaster ◽

By Catch ◽

Conger Eel

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Electrophysiology of Syncytial Smooth Muscle

Journal of Experimental Neuroscience ◽

10.1177/1179069518821917 ◽

2019 ◽

Vol 13 ◽

pp. 117906951882191 ◽

Cited By ~ 4

Author(s):

Rohit Manchanda ◽

Shailesh Appukuttan ◽

Mithun Padmakumar

Keyword(s):

Smooth Muscle ◽

Action Potentials ◽

Signal Analysis ◽

Computational Models ◽

Vas Deferens ◽

Contractile Activity ◽

Smooth Muscles ◽

Biophysical Analysis ◽

Recent Developments ◽

The Many

As in other excitable tissues, two classes of electrical signals are of fundamental importance to the functioning of smooth muscles: junction potentials, which arise from neurotransmission and represent the initiation of excitation (or in some instances inhibition) of the tissue, and spikes or action potentials, which represent the accomplishment of excitation and lead on to contractile activity. Unlike the case in skeletal muscle and in neurons, junction potentials and spikes in smooth muscle have been poorly understood in relation to the electrical properties of the tissue and in terms of their spatiotemporal spread within it. This owes principally to the experimental difficulties involved in making precise electrical recordings from smooth muscles and also to two inherent features of this class of muscle, ie, the syncytial organization of its cells and the distributed innervation they receive, which renders their biophysical analysis problematic. In this review, we outline the development of hypotheses and knowledge on junction potentials and spikes in syncytial smooth muscle, showing how our concepts have frequently undergone radical changes and how recent developments hold promise in unraveling some of the many puzzles that remain. We focus especially on computational models and signal analysis approaches. We take as illustrative examples the smooth muscles of two organs with distinct functional characteristics, the vas deferens and urinary bladder, while also touching on features of electrical functioning in the smooth muscles of other organs.

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Negative-feedback regulation of excitation-contraction coupling in gastric smooth muscle

AJP Cell Physiology ◽

10.1152/ajpcell.1992.263.6.c1160 ◽

1992 ◽

Vol 263 (6) ◽

pp. C1160-C1171 ◽

Cited By ~ 14

Author(s):

H. Ozaki ◽

L. Zhang ◽

I. L. Buxton ◽

K. M. Sanders ◽

N. G. Publicover

Keyword(s):

Smooth Muscle ◽

Negative Feedback ◽

Contractile Activity ◽

Slow Waves ◽

Plateau Phase ◽

Negative Feedback Regulation ◽

Excitation Contraction Coupling ◽

Contraction Coupling ◽

Pi Turnover ◽

Resting Tension

The role of phosphatidylinositol (PI) turnover in excitation-contraction coupling was investigated in canine antral smooth muscle. Acetylcholine (ACh; 0.1-1 microM) transiently increased tissue levels of inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] and increased the amplitudes of the plateau phase of slow waves and associated Ca2+ transients and phasic contractions. ACh also increased basal concentrations of cytosolic Ca2+ ([Ca2+]c), but these changes were not associated with an increase in resting tension. ATP (0.3 mM) had similar effects on Ins(1,4,5)P3 levels, basal [Ca2+]c, and resting tension. However, in contrast to the effects of ACh, ATP transiently reduced the amplitude of the plateau phase of slow waves and reduced the amplitudes of associated Ca2+ transients and phasic contractions. We investigated the possibility that two products of PI turnover, diacylglycerol (DAG) and Ins(1,4,5)P3, might provide negative feedback to regulate Ca2+ entry during slow waves. 1) DAG is known to activate protein kinase C (PKC). Activation of PKC by phorbol 12,13-dibutyrate (PDBu, 0.5 microM) reduced the amplitude of the plateau phase of slow waves and corresponding Ca2+ transients and phasic contractions. Assay of PKC showed that ACh, ATP, and PDBu stimulated enzyme activity. 2) Ins(1,4,5)P3 is known to increase [Ca2+]c by release of Ca2+ from internal stores. Basal [Ca2+]c was also increased by elevated external K+, ionomycin, thapsigargin, or caffeine. Each of these compounds reduced the amplitude and duration of slow waves. Results suggest that products of PI turnover may provide negative-feedback control of Ca2+ influx during slow waves, tending to reduce the amplitude of phasic contractile activity in gastric muscles. Differences in responses to ACh and ATP can be explained by a G protein-dependent mechanism in which ACh suppresses the voltage dependence of Ca(2+)-activated K+ channels.

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