Editor’s Note: RhoA activation and interaction with Caveolin-1 are critical for pressure-induced myogenic tone in rat mesenteric resistance arteries [Cardiovasc Res 2007;73:190-197]

2020 ◽  
Keyword(s):  
Myogenic Tone ◽  
Resistance Arteries ◽  
Caveolin 1 ◽  
Rhoa Activation

scholarly journals RhoA activation and interaction with Caveolin-1 are critical for pressure-induced myogenic tone in rat mesenteric resistance arteries

2007 ◽  
Vol 73 (1) ◽  
pp. 190-197 ◽  
Author(s):  
C DUBROCA ◽  
X LOYER ◽  
K RETAILLEAU ◽  
G LOIRAND ◽  
P PACAUD ◽  
...  
Keyword(s):  
Myogenic Tone ◽  
Resistance Arteries ◽  
Caveolin 1 ◽  
Rhoa Activation

Enhanced resistance artery sensitivity to agonists under isobaric compared with isometric conditions

1994 ◽  
Vol 266 (1) ◽  
pp. H147-H155 ◽  
Author(s):  
W. R. Dunn ◽  
G. C. Wellman ◽  
J. A. Bevan
Keyword(s):  
Membrane Potential ◽  
Angiotensin Ii ◽  
Myogenic Tone ◽  
Isometric Contractions ◽  
Fundamental Interaction ◽  
Resistance Artery ◽  
Resistance Arteries ◽  
Enhanced Resistance ◽  
Increased Sensitivity

We have compared the responsiveness of rabbit mesenteric resistance arteries with agonists under isometric and isobaric conditions. When pressurized (60 mmHg), arteries spontaneously reduced their diameter by 18.1%. An equivalent isometric stress did not generate force in a “wire” myograph. Subsequently, much higher concentrations of norepinephrine (NE) and histamine were required to cause isometric contractions than were needed to reduce vascular diameter of pressurized vessels, whereas angiotensin II produced a maintained response only in pressurized arteries. Reducing transmural pressure to 20 mmHg abolished pressure-induced myogenic tone and decreased arterial sensitivity to NE. Under isometric conditions, partial depolarization with KCl increased sensitivity to NE and histamine to within the concentration range effective in pressurized vessels and also "revealed" responses to angiotensin II. The membrane potential of the vascular smooth muscle cells under partially depolarized conditions was similar to that found in vivo and in vessels studied isobarically. These observations demonstrate a fundamental interaction between pressure-induced myogenic tone and the sensitivity of resistance arteries to vasoactive stimuli. This influence was mimicked in isometrically mounted vessels by partial depolarization, indicating a possible pivotal role for membrane potential in determining the reactivity of the resistance vasculature.

Abstract 485: Novel Mechanisms at Immune-vascular Interfaces Regulates Myogenic Tone of Resistance Arteries and Induce Hypertension in Mice

2018 ◽  
Vol 38 (Suppl_1) ◽  
Author(s):  
Daniela Carnevale ◽  
Iolanda Vinciguerra ◽  
Manuel Casaburo ◽  
Marialuisa Perrotta ◽  
Roberta Iacobucci ◽  
...  
Keyword(s):  
Myogenic Tone ◽  
Resistance Arteries

scholarly journals Caveolin-1 and caveolin-3 regulate Ca2+ homeostasis of single smooth muscle cells from rat cerebral resistance arteries

2007 ◽  
Vol 293 (1) ◽  
pp. H204-H214 ◽  
Author(s):  
T. Kamishima ◽  
T. Burdyga ◽  
J. A. Gallagher ◽  
J. M. Quayle
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Removal Rate ◽  
Muscle Cells ◽  
Amino Acid Residues ◽  
Resistance Arteries ◽  
Inhibitory Peptide ◽  
Caveolin 1 ◽  
Domain Peptide ◽  
Cerebral Resistance

The role of caveolins, signature proteins of caveolae, in arterial Ca2+ regulation is unknown. We investigated modulation of Ca2+ homeostasis by caveolin-1 and caveolin-3 using smooth muscle cells from rat cerebral resistance arteries. Membrane current and Ca2+ transients were simultaneously measured with voltage-clamped single cells. Membrane depolarization triggered Ca2+ current and increased intracellular Ca2+ concentration ([Ca2+]i). After repolarization, elevated [Ca2+]i returned to the resting level. Ca2+ removal rate was determined from the declining phase of the Ca2+ transient. Application of caveolin-1 antibody or caveolin-1 scaffolding domain peptide, corresponding to amino acid residues 82–101 of caveolin-1, significantly slowed Ca2+ removal rate at a measured [Ca2+]i of 250 nM, with little effect at a measured [Ca2+]i of 600 nM. Application of caveolin-3 antibody or caveolin-3 scaffolding domain peptide, corresponding to amino acid residues 55–74 of caveolin-3, also significantly slowed Ca2+ removal rate at a measured [Ca2+]i of 250 nM, with little effect at a measured [Ca2+]i of 600 nM. Likewise, application of calmodulin inhibitory peptide, autocamtide-2-related inhibitory peptide, and cyclosporine A, inhibitors for calmodulin, Ca2+/calmodulin-dependent protein kinase II, and calcineurin, also significantly inhibited Ca2+ removal rate at a measured [Ca2+]i of 250 nM but not at 600 nM. Application of cyclopiazonic acid, a sarcoplasmic reticulum Ca2+ ATPase inhibitor, also significantly inhibited Ca2+ removal rate at a measured [Ca2+]i of 250 nM but not at 600 nM. Our results suggest that caveolin-1 and caveolin-3 are important in Ca2+ removal of resistance artery smooth muscle cells.

Role of T-type calcium channels in myogenic tone of skeletal muscle resistance arteries

2002 ◽  
Vol 283 (6) ◽  
pp. H2239-H2243 ◽  
Author(s):  
Ed VanBavel ◽  
Oana Sorop ◽  
Ditte Andreasen ◽  
Martin Pfaffendorf ◽  
Boye L. Jensen
Keyword(s):  
Calcium Channels ◽  
Southern Blotting ◽  
Myogenic Tone ◽  
Cremaster Muscle ◽  
Resistance Arteries ◽  
Rt Pcr ◽  
Response Curves ◽  
Potent Effect ◽  
Channel Expression

T-type calcium channels may be involved in the maintenance of myogenic tone. We tested their role in isolated rat cremaster arterioles obtained after CO2anesthesia and decapitation. Total RNA was analyzed by RT-PCR and Southern blotting for calcium channel expression. We observed expression of voltage-operated calcium (CaV) channels CaV3.1 (T-type), CaV3.2 (T-type), and CaV1.2 (L-type) in cremaster arterioles ( n= 3 rats). Amplification products were observed only in the presence of reverse transcriptase and cDNA. Concentration-response curves of the relatively specific L-type blocker verapamil and the relatively specific T-type blockers mibefradil and nickel were made on cannulated vessels with either myogenic tone (75 mmHg) or a similar level of constriction induced by 30 mM K+ at 35 mmHg. Mibefradil and nickel were, respectively, 162-fold and 300-fold more potent in inhibiting myogenic tone compared with K+-induced constriction [log(IC50, M): mibefradil, basal −7.3 ± 0.2 ( n = 9) and K+ −5.1 ± 0.1 ( n = 5); nickel, basal −4.1 ± 0.2 ( n = 5) and K+ −1.6 ± 0.5 ( n = 5); means ± SE]. Verapamil had a 17-fold more potent effect [log(IC50, M): basal −6.6 ± 0.1 ( n = 5); K+ −5.4 ± 0.3 ( n = 4); all log(IC50) P < 0.05, basal vs. K+]. These data suggest that T-type calcium channels are expressed and involved in maintenance of myogenic tone in rat cremaster muscle arterioles.

Myogenic tone, reactivity, and forced dilatation: a three-phase model of in vitro arterial myogenic behavior

2002 ◽  
Vol 283 (6) ◽  
pp. H2260-H2267 ◽  
Author(s):  
George Osol ◽  
Johan Fredrik Brekke ◽  
Keara McElroy-Yaggy ◽  
Natalia I. Gokina
Keyword(s):  
Cerebral Arteries ◽  
Peripheral Resistance ◽  
Force Production ◽  
Cytosolic Calcium ◽  
Myogenic Tone ◽  
Wall Tension ◽  
Resistance Arteries ◽  
Cellular Mechanisms ◽  
Initial Development

Myogenic behavior, prevalent in resistance arteries and arterioles, involves arterial constriction in response to intravascular pressure. This process is often studied in vitro by using cannulated, pressurized arterial segments from different regional circulations. We propose a comprehensive model for myogenicity that consists of three interrelated but dissociable phases: 1) the initial development of myogenic tone (MT), 2) myogenic reactivity to subsequent changes in pressure (MR), and 3) forced dilatation at high transmural pressures (FD). The three phases span the physiological range of transmural pressures (e.g., MT, 40–60 mmHg; MR, 60–140 mmHg; FD, >140 mmHg in cerebral arteries) and are characterized by distinct changes in cytosolic calcium ([Ca2+]i), which do not parallel arterial diameter or wall tension, and therefore suggest the existence of additional regulatory mechanisms. Specifically, the development of MT is accompanied by a substantial (200%) elevation in [Ca2+]i and a reduction in lumen diameter and wall tension, whereas MR is associated with relatively small [Ca2+]i increments (<20% over the entire pressure range) despite considerable increases in wall tension and force production but little or no change in diameter. FD is characterized by a significant additional elevation in [Ca2+]i (>50%), complete loss of force production, and a rapid increase in wall tension. The utility of this model is that it provides a framework for comparing myogenic behavior of vessels of different size and anatomic origin and for investigating the underlying cellular mechanisms that govern vascular smooth muscle mechanotransduction and contribute to the regulation of peripheral resistance.

Akt and RhoA activation in response to high glucose require caveolin-1 phosphorylation in mesangial cells

2014 ◽  
Vol 306 (11) ◽  
pp. F1308-F1317 ◽  
Author(s):  
Su-Zhen Wu ◽  
Fang-Fang Peng ◽  
Jia-Lin Li ◽  
Feng Ye ◽  
Shao-Qing Lei ◽  
...  
Keyword(s):  
Renal Disease ◽  
High Glucose ◽  
Mesangial Cells ◽  
Src Kinase ◽  
Specific Inhibitor ◽  
Membrane Translocation ◽  
Caveolin 1 ◽  
Rhoa Activation ◽  
Diabetic Renal Disease ◽  
Src Activation

Glomerular matrix accumulation is a hallmark of diabetic renal disease. Serine/threonine kinase PKC-β1 mediates glucose-induced Akt S473 phosphorylation, RhoA activation, and transforming growth factor (TGF)-β1 upregulation and finally leads to matrix upregulation in mesangial cells (MCs). It has been reported that glucose-induced PKC-β1 activation is dependent on caveolin-1 and the presence of intact caveolae in MCs; however, whether activated PKC-β1 regulates caveolin-1 expression and phosphorylation are unknown. Here, we showed that, although the caveolin-1 protein level had no significant change, the PKC-β-specific inhibitor LY-333531 blocked caveolin-1 Y14 phosphorylation in high glucose (HG)-treated MCs and in the renal cortex of diabetic rats. The Src-specific inhibitor SU-6656 prevented the HG-induced association between PKC-β1 and caveolin-1 and PKC-β1 membrane translocation, whereas PKC-β1 small interfering RNA failed to block Src activation, indicating that Src kinase is upstream of PKC-β1 activation. Although LY-333531 blocked PKC-β1 membrane translocation, it had no effect on the PKC-β1/caveolin-1 association, suggesting that PKC-β1 activation requires the interaction of caveolin-1 and PKC-β1. PKC-β1-mediated Akt S473 phosphorylation, RhoA activation, and fibronectin upregulation in response to HG were prevented by SU-6656 and nonphosphorylatable mutant caveolin-1 Y14A. In conclusion, Src activation by HG mediates the PKC-β1/caveolin-1 association and PKC-β1 activation, which assists in caveolin-1 Y14 phosphorylation by Src kinase. The downstream effects, including Akt S473 phosphorylation, RhoA activation, and fibronectin upregulation, require caveolin-1 Y14 phosphorylation. Caveolin-1 is thus an important mediator of the profibrogenic process in diabetic renal disease.

Cardiac transplantation and resistance artery myogenic tone

2004 ◽  
Vol 82 (10) ◽  
pp. 840-848 ◽  
Author(s):  
Farzad Moien-Afshari ◽  
Peter L Skarsgard ◽  
Bruce M McManus ◽  
Ismail Laher
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Contractile Function ◽  
Myogenic Tone ◽  
Resistance Arteries ◽  
Interstitial Edema ◽  
Functional Changes ◽  
Ventricular Compliance ◽  
Myogenic Regulation ◽  
Oxide Synthase

Transplantation is an effective treatment for end-stage heart disease; however, most grafts eventually fail by progressive cardiac failure. Primarily, failure is ischemic due to the occlusive nature of transplant vascular disease (TVD). Early after transplantation and preceding TVD, alterations in coronary physiology such as reduced vascular myogenic tone occur. Resistance arteries possess an inherent ability to constrict in response to transmural pressure; this constrictive response (myogenic tone) is important in fluid homeostasis. Recent evidence suggests that a decline in myogenic tone leads to deficits in cardiac contractility. Factors that reduce myogenic tone in transplantation include constitutive nitric oxide synthase and inducible nitric oxide synthase catalyzed, NO-mediated vasodilation as well as deficits in arterial contractile function. Reduced myogenic tone in allograft resistance arteries increases coronary blood flow such that hydrostatic pressure surpasses oncotic pressure, causing cardiac interstitial edema. This generalized edema decreases ventricular compliance leading to heart failure during the course of acute immune rejection of the graft. Cyclosporine A treatment reduces immune mediated dysregulation of myogenic tone, resulting in reduced interstitial edema and improved cardiac function. In this review, we discuss aspects of TVD and myogenic tone signaling mechanisms and how aberrations in myogenic regulation of arterial tone contribute to functional changes observed in cardiac transplant.Key words: myogenic tone, smooth muscle, nitric oxide, transplantation, edema.

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