Rhythmic contraction generates adjustable passive stiffness in rabbit detrusor

The length-tension ( L-T) relationships in airway and vascular smooth muscles have been shown to adapt with length changes over time. Our prior studies have shown that the active and passive L-T relationships in rabbit detrusor smooth muscle (DSM) can adapt and that DSM exhibits adjustable passive stiffness (APS) characterized by a passive L-T curve that is a function of strain and activation history. The present study demonstrates that passive tension due to APS can represent a substantial fraction of total tension over a broad length range. Our previous studies have shown that maximal KCl-induced contractions at short muscle lengths generate APS that is revealed by increased pseudo-steady-state passive tension at longer lengths compared with previous measurements at those lengths. The objective of the present study was to determine the mechanisms involved in APS generation. Increasing the number of KCl-induced contractions or the duration of a contraction increased the amount of APS generated. Furthermore, a fraction of APS was restored in calcium-free solution and was sensitive to the general serine and threonine protein kinase inhibitor staurosporine. Most importantly, rhythmic contraction (RC) generated APS, and because RC occurs spontaneously in human bladder, a physiological role for RC was potentially identified.

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Adaptation of the length-active tension relationship in rabbit detrusor

AJP Renal Physiology ◽

10.1152/ajprenal.00298.2009 ◽

2009 ◽

Vol 297 (4) ◽

pp. F1119-F1128 ◽

Cited By ~ 25

Author(s):

John E. Speich ◽

Atheer M. Almasri ◽

Hersch Bhatia ◽

Adam P. Klausner ◽

Paul H. Ratz

Keyword(s):

Smooth Muscles ◽

Muscle Length ◽

Strain History ◽

Detrusor Smooth Muscle ◽

Active Tension ◽

Passive Stiffness ◽

Vascular Smooth Muscles ◽

Length Changes ◽

Adjustable Passive Stiffness ◽

First Time

Studies have shown that the length-tension ( L-T) relationships in airway and vascular smooth muscles are dynamic and can adapt to length changes over a period of time. Our prior studies have shown that the passive L-T relationship in rabbit detrusor smooth muscle (DSM) is also dynamic and that DSM exhibits adjustable passive stiffness (APS) characterized by a passive L-T curve that can shift along the length axis as a function of strain history and activation history. The present study demonstrates that the active L-T curve for DSM is also dynamic and that the peak active tension produced at a particular muscle length is a function of both strain and activation history. More specifically, this study reveals that the active L-T relationship, or curve, does not have a unique peak tension value with a single ascending and descending limb, but instead reveals that multiple ascending and descending limbs can be exhibited in the same DSM strip. This study also demonstrates that for DSM strips not stretched far enough to reveal a descending limb, the peak active tension produced by a maximal KCl-induced contraction at a short, passively slack muscle length of 3 mm was reduced by 58.6 ± 4.1% ( n = 1 5) following stretches to and contractions at threefold the original muscle length, 9 mm. Moreover, five subsequent contractions at the short muscle length displayed increasingly greater tension; active tension produced by the sixth contraction was 91.5 ± 9.1% of that produced by the prestretch contraction at that length. Together, these findings indicate for the first time that DSM exhibits length adaptation, similar to vascular and airway smooth muscles. In addition, our findings demonstrate that preconditioning, APS and adaptation of the active L-T curve can each impact the maximum total tension observed at a particular DSM length.

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Adjustable passive stiffness in mouse bladder: regulated by Rho kinase and elevated following partial bladder outlet obstruction

AJP Renal Physiology ◽

10.1152/ajprenal.00177.2011 ◽

2012 ◽

Vol 302 (8) ◽

pp. F967-F976 ◽

Cited By ~ 11

Author(s):

John E. Speich ◽

Jordan B. Southern ◽

Sheree Henderson ◽

Cameron W. Wilson ◽

Adam P. Klausner ◽

...

Keyword(s):

Bladder Outlet Obstruction ◽

Bladder Wall ◽

Rho Kinase ◽

Outlet Obstruction ◽

Prostaglandin E ◽

Passive Stiffness ◽

Regulatory Pathways ◽

Partial Bladder Outlet Obstruction ◽

Length Changes ◽

Adjustable Passive Stiffness

Detrusor smooth muscle (DSM) contributes to bladder wall tension during filling, and bladder wall deformation affects the signaling system that leads to urgency. The length-passive tension ( L-Tp) relationship in rabbit DSM can adapt with length changes over time and exhibits adjustable passive stiffness (APS) characterized by a L-Tpcurve that is a function of both activation and strain history. Muscle activation with KCl, carbachol (CCh), or prostaglandin E2at short muscle lengths can increase APS that is revealed by elevated pseudo-steady-state Tpat longer lengths compared with prior Tpmeasurements at those lengths, and APS generation is inhibited by the Rho Kinase (ROCK) inhibitor H-1152. In the current study, mouse bladder strips exhibited both KCl- and CCh-induced APS. Whole mouse bladders demonstrated APS which was measured as an increase in pressure during passive filling in calcium-free solution following CCh precontraction compared with pressure during filling without precontraction. In addition, CCh-induced APS in whole mouse bladder was inhibited by H-1152, indicating that ROCK activity may regulate bladder compliance during filling. Furthermore, APS in whole mouse bladder was elevated 2 wk after partial bladder outlet obstruction, suggesting that APS may be relevant in diseases affecting bladder mechanics. The presence of APS in mouse bladder will permit future studies of APS regulatory pathways and potential alterations of APS in disease models using knockout transgenetic mice.

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Vasopressin for treatment of hemodynamic disorders

Medicina ◽

10.3390/medicina44020021 ◽

2008 ◽

Vol 44 (2) ◽

pp. 167

Author(s):

Dalia Adukauskienë ◽

Edmundas Ðirvinskas ◽

Egidijus Këvelaitis

Keyword(s):

Alternative Therapy ◽

Smooth Muscles ◽

Physiological Role ◽

Vascular Smooth Muscles ◽

Amino Acid Peptide ◽

Oxytocin Receptors ◽

Vasopressin Receptors ◽

Posterior Pituitary Gland

Vasopressin is a 9-amino acid peptide synthesized by magnocellular neurons of the hypothalamus and released from posterior pituitary gland. The primary physiological role of vasopressin is the maintenance of fluid homeostasis. In this review, the classification of vasopressin receptors, namely V1 vascular, V2 renal, V3 pituitary, oxytocin receptors, and purinergic receptors, and the effects of vasopressin on vascular smooth muscles, the heart, and the kidneys are discussed. Mortality rates of vasodilatory (or distributive), for example septic shock, are high. The use of vasopressin is an alternative therapy for vasodilatory shock with better outcome. Vasopressin is effective in resuscitation of adults after ventricular fibrillation or pulseless tachycardia, when epinephrine is not effective.

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Effects of Sodium Vanadate on Various Types of Vascular Smooth Muscles

Journal of Vascular Research ◽

10.1159/000158628 ◽

1986 ◽

Vol 23 (3) ◽

pp. 113-124 ◽

Cited By ~ 4

Author(s):

Tomoko Shimada ◽

Keiichi Shimamura ◽

Satoru Sunano

Keyword(s):

Smooth Muscles ◽

Vascular Smooth Muscles ◽

Sodium Vanadate

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Glabridin Relaxes Vascular Smooth Muscles by Activating BKCa Channels and Inhibiting Phosphodiesterase in Human Saphenous Vein

Current Medical Science ◽

10.1007/s11596-021-2358-6 ◽

2021 ◽

Vol 41 (2) ◽

pp. 381-389

Author(s):

Cengiz Güven ◽

Ali Parlar

Keyword(s):

Saphenous Vein ◽

Smooth Muscles ◽

Vascular Smooth Muscles ◽

Human Saphenous Vein ◽

Bkca Channels

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Modeling of the Bayliss‐Effect in Vascular Smooth Muscles

PAMM ◽

10.1002/pamm.202000273 ◽

2021 ◽

Vol 20 (1) ◽

Author(s):

Klemens Uhlmann ◽

Daniel Balzani

Keyword(s):

Smooth Muscles ◽

Vascular Smooth Muscles ◽

Bayliss Effect

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BM-520, an original TXA2 modulator, inhibits the action of thromboxane A2 and 8-iso-prostaglandin F2α in vitro and in vivo on human and rodent platelets, and aortic vascular smooth muscles from rodents

Prostaglandins & Other Lipid Mediators ◽

10.1016/j.prostaglandins.2007.03.002 ◽

2007 ◽

Vol 84 (1-2) ◽

pp. 14-23 ◽

Cited By ~ 7

Author(s):

S. Rolin ◽

J. Hanson ◽

C. Vastersaegher ◽

C. Cherdon ◽

D. Pratico ◽

...

Keyword(s):

Smooth Muscles ◽

Prostaglandin F2α ◽

Thromboxane A2 ◽

Vascular Smooth Muscles

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Plasticity of KIR channels in human smooth muscle cells from internal thoracic artery

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00559.2002 ◽

2003 ◽

Vol 284 (6) ◽

pp. H2325-H2334 ◽

Cited By ~ 25

Author(s):

Tom Karkanis ◽

Shaohua Li ◽

J. Geoffrey Pickering ◽

Stephen M. Sims

Keyword(s):

Smooth Muscle ◽

Current Density ◽

Internal Thoracic Artery ◽

Smooth Muscles ◽

Vascular Smooth Muscles ◽

Rt Pcr ◽

Regulation Of Proliferation ◽

Negative Membrane Potential ◽

Inwardly Rectifying ◽

Contractile Cells

Inwardly rectifying K+ (KIR) currents are present in some, but not all, vascular smooth muscles. We used patch-clamp methods to examine plasticity of this current by comparing contractile and proliferative phenotypes of a clonal human vascular smooth muscle cell line. Hyperpolarization of cells under voltage clamp elicited a large inward current that was selective for K+ and blocked by Ba2+. Current density was greater in proliferative compared with contractile cells (−4.5 ± 0.9 and −1.4 ± 0.3 pA/pF, respectively; P < 0.001). RT-PCR of mRNA from proliferative cells identified transcripts for Kir2.1 and Kir2.2 but not Kir2.3 potassium channels. Western blot analysis demonstrated greater expression of Kir2.1 protein in proliferative cells, consistent with the higher current density. Proliferative cells displayed a more negative membrane potential than contractile cells (−71 ± 2 and −35 ± 4 mV, respectively; P < 0.001). Ba2+ depolarized all cells, whereas small increases in extracellular K+ concentration elicited hyperpolarization only in contractile cells. Ba2+ inhibited [3H]thymidine incorporation, indicating a possible role for KIR channels in the regulation of proliferation. The phenotype-dependent plasticity of KIR channels may have relevance to vascular remodeling.

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