Modulatory role of endothelial calcium level in vascular tension of canine depolarized coronary arteries

1998 ◽  
Vol 274 (2) ◽  
pp. H494-H499 ◽  
Author(s):  
Kazuo Sato ◽  
Jun Yamazaki ◽  
Taku Nagao
Keyword(s):  
Smooth Muscle ◽  
Coronary Arteries ◽  
Muscle Tone ◽  
Typical Characteristic ◽  
Entry Pathway ◽  
High K ◽  
Intracellular Ca ◽  
The Relationship ◽  
Low K

The vascular tension in the coronary artery is modulated by factors released by endothelial cells. We investigated the relationship between the Ca2+ level in endothelium and endothelium-mediated changes in smooth muscle tone in high K+-depolarized canine coronary arteries by measuring intracellular Ca2+ concentration fluorimetrically with the Ca2+indicator fura 2. Addition of Ca2+(1 mM) caused an increase in endothelial Ca2+ and relaxed the 30 mM K+-depolarized arteries following inhibition of Ca2+ influx in the smooth muscle with diltiazem. This relaxation was inhibited by N G-monomethyl-l-arginine. As extracellular K+ concentration was decreased, increases of endothelial Ca2+ were augmented, whereas the relaxation was decreased. Basal muscle tone was found to be decreased in low K+ by measuring relaxation by sodium nitroprusside. These results suggest the importance of Ca2+ level in the endothelium in playing a modulatory role in coronary tension through the production of nitric oxide. The correlation of extracellular K+ to Ca2+ level in the endothelium indicates a typical characteristic of the passive Ca2+ entry pathway in the endothelium, whereas the resultant relaxation appears to be restricted by the basal muscle tone.

Long-term regulation of contractility and calcium current in smooth muscle

1997 ◽  
Vol 273 (5) ◽  
pp. C1714-C1720 ◽  
Author(s):  
Maria Gomez ◽  
Karl Swärd
Keyword(s):  
Smooth Muscle ◽  
Calf Serum ◽  
Cell Voltage ◽  
High K ◽  
Intracellular Ca ◽  
The Right ◽  
The Relationship ◽  
Cell Capacitance

Longitudinal smooth muscle strips from guinea pig ileum were cultured in vitro for 5 days, and the relationship between extracellular Ca2+ and force in high-K+ medium was evaluated. In strips cultured with 10% fetal calf serum (FCS), this relationship was shifted to the right (50% effective concentration changed by 2–3 mM) compared with strips cultured without FCS. The shift was prevented by inclusion of verapamil (1 μM) during culture and mimicked by ionomycin in the absence of FCS. The intracellular Ca2+ concentration ([Ca2+]i) during stimulation with high-K+solution or carbachol was reduced after culture with FCS, whereas the [Ca2+]i-force relationship was unaffected. Cells were isolated from cultured strips, and whole cell voltage-clamp experiments were performed. Maximum inward Ca2+ current (10 mM Ba2+), normalized to cell capacitance, was almost three times smaller in cells isolated from strips cultured with FCS. Culture with 1 μM verapamil prevented this reduction. These results suggest that increased [Ca2+]iduring culture downregulates Ca2+current density, with associated effects on contractility.

Trabecular smooth muscle modulates the capacitor function of the penis. Studies on a rabbit model

1991 ◽  
Vol 260 (5) ◽  
pp. H1590-H1595 ◽  
Author(s):  
I. Saenz de Tejada ◽  
P. Moroukian ◽  
J. Tessier ◽  
J. J. Kim ◽  
I. Goldstein ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Muscle Tone ◽  
Infusion Pump ◽  
Rabbit Model ◽  
Feedback Mechanism ◽  
Outflow Resistance ◽  
Venous Outflow ◽  
High K ◽  
Pressure Feedback

We investigated the role of trabecular smooth muscle tone in regulation of intracavernosal pressure, venous outflow resistance, and penile capacitance. In an isolated rabbit whole penis model, corpora cavernosa were infused with either contracting (high K(+)-norepinephrine combination) or relaxing (no added Ca(2+)-papaverine combination) physiological salt solutions while intracavernosal pressure was recorded. An infusion pump regulated by an intracavernosal pressure feedback mechanism enabled the measurement of flow necessary to maintain intracavernosal pressures at 30, 60, 90, 120, and 150 mmHg under steady-state conditions (inflow = outflow). These experiments allowed resistance to outflow from corpora to be calculated when trabecular smooth muscle was either constricted or relaxed. Decay in intracavernosal pressure over time from various predetermined intracavernosal pressures (150, 120, 90, 60, and 30 mmHg) was studied under conditions of zero inflow following contraction or relaxation of trabecular smooth muscle. This permitted calculation of the time constant, which together with the outflow resistance, permitted the calculation of penile capacitance. When smooth muscle is relaxed, venous outflow resistance is high, constant, and independent of intracavernosal pressure. Furthermore, relaxation of smooth muscle allows expansion of corpora with accumulation of volume under pressure, enabling the penis to act as a capacitor. This capacitor function is limited in the presence of constant high outflow resistance by stiffness of the fibroelastic elements of penis, tunica, and fibroelastic frame, which exhibit nonlinear deflection trends. Analysis of these variables has led us to propose a model for penile erection.

Electron Probe Analysis of Vertebrate Smooth Muscle: Distribution of Ca and Ci

1976 ◽  
Vol 34 ◽  
pp. 334-335 ◽  
Author(s):  
Avril V. Somlyo ◽  
H. Shuman ◽  
A.P. Somlyo
Keyword(s):  
Smooth Muscle ◽  
Electron Probe ◽  
Preliminary Report ◽  
Cell Damage ◽  
Electron Probe Analysis ◽  
Perinuclear Space ◽  
Probe Analysis ◽  
High K ◽  
Low K ◽  
Initial Results

This is a preliminary report of electron probe analysis of rabbit portal-anterior mesenteric vein (PAMV) smooth muscle cryosectioned without fixation or cryoprotection. The instrumentation and method of electron probe quantitation used (1) and our initial results with cardiac (2) and skeletal (3) muscle have been presented elsewhere.In preparations depolarized with high K (K2SO4) solution, significant calcium peaks were detected over the sarcoplasmic reticulum (Fig 1 and 2) and the continuous perinuclear space. In some of the fibers there were also significant (up to 200 mM/kg dry wt) calcium peaks over the mitochondria. However, in smooth muscle that was not depolarized, high mitochondrial Ca was found in fibers that also contained elevated Na and low K (Fig 3). Therefore, the possibility that these Ca-loaded mitochondria are indicative of cell damage remains to be ruled out.

Role of capacitative Ca2+ entry in bronchial contraction and remodeling

2002 ◽  
Vol 92 (4) ◽  
pp. 1594-1602 ◽  
Author(s):  
Michele Sweeney ◽  
Sharon S. McDaniel ◽  
Oleksandr Platoshyn ◽  
Shen Zhang ◽  
Ying Yu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Transient Receptor Potential ◽  
Bronchial Hyperresponsiveness ◽  
Receptor Potential ◽  
Transient Receptor Potential Channel ◽  
Wall Thickening ◽  
Bronchial Wall ◽  
Intracellular Ca ◽  
Transient Receptor

Asthma is characterized by airway inflammation, bronchial hyperresponsiveness, and airway obstruction by bronchospasm and bronchial wall thickening due to smooth muscle hypertrophy. A rise in cytosolic free Ca2+ concentration ([Ca2+]cyt) may serve as a shared signal transduction element that causes bronchial constriction and bronchial wall thickening in asthma. In this study, we examined whether capacitative Ca2+ entry (CCE) induced by depletion of intracellular Ca2+ stores was involved in agonist-mediated bronchial constriction and bronchial smooth muscle cell (BSMC) proliferation. In isolated bronchial rings, acetylcholine (ACh) induced a transient contraction in the absence of extracellular Ca2+ because of Ca2+ release from intracellular Ca2+ stores. Restoration of extracellular Ca2+in the presence of atropine, an M-receptor blocker, induced a further contraction that was apparently caused by a rise in [Ca2+]cyt due to CCE. In single BSMC, amplitudes of the store depletion-activated currents ( I SOC) and CCE were both enhanced when the cells proliferate, whereas chelation of extracellular Ca2+ with EGTA significantly inhibited the cell growth in the presence of serum. Furthermore, the mRNA expression of TRPC1, a transient receptor potential channel gene, was much greater in proliferating BSMC than in growth-arrested cells. Blockade of the store-operated Ca2+channels by Ni2+ decreased I SOC and CCE and markedly attenuated BSMC proliferation. These results suggest that upregulated TRPC1 expression, increased I SOC, enhanced CCE, and elevated [Ca2+]cyt may play important roles in mediating bronchial constriction and BSMC proliferation.

Role of extracellular calcium and calmodulin in prolactin secretion induced by hyposmolarity, thyrotropin-releasing hormone, and high K+ in GH4C1 cells

1990 ◽  
Vol 123 (2) ◽  
pp. 218-224 ◽  
Author(s):  
Xiangbing Wang ◽  
Noriyuki Sato ◽  
Monte A. Greer ◽  
Susan E. Greer ◽  
Staci McAdams
Keyword(s):  
Smooth Muscle ◽  
Muscle Relaxant ◽  
Prolactin Secretion ◽  
Thyrotropin Releasing Hormone ◽  
Dependent Manner ◽  
Cell Toxicity ◽  
High K ◽  
Dose Dependent ◽  
Smooth Muscle Relaxant

Abstract. The mechanism by which 30% medium hyposmolarity induces PRL secretion by GH4C1 cells was compared with that induced by 100 nmol/l TRH or 30 mmol/l K+. Removing medium Ca2+, blocking Ca2+ channels with 50 μmol/l verapamil, or inhibiting calmodulin activation with 20 μmol/l trifluoperazine, 10 μmol/l chlorpromazine or 10 μmol/l pimozide almost completely blocked hyposmolarity-induced secretion. The smooth muscle relaxant, W-7, which is believed relatively specific in inhibiting the Ca2+-calmodulin interaction, depressed hyposmolarity-induced PRL secretion in a dose-dependent manner (r = −0.991, p<0.01 ). The above drugs also blocked or decreased high K+-induced secretion, but had much less effect on TRH-induced secretion. Secretion induced by TRH, hyposmolarity, or high K+ was optimal at pH 7.3-7.65 and was significantly depressed at pH 6.0 or 8.0, indicating that release of hormone induced by all 3 stimuli is due to an active cell process requiring a physiologic extracellular pH and is not produced by nonspecific cell toxicity. The data suggest hyposmolarity and high K+ may share some similarities in their mechanism of stimulating secretion, which is different from that of TRH.

Abstract P334: The Relationship Between Urinary Sodium-to-Potassium Ratio And High Blood Pressure: TMM CommCohort Study

Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Mana Kogure ◽  
Tomohiro Nakamura ◽  
Naho Tsuchiya ◽  
Takumi Hirata ◽  
Akira Narita ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Alcohol Intake ◽  
Positive Association ◽  
Cross Sectional Study ◽  
Analysis Of Covariance ◽  
Cross Sectional ◽  
High K ◽  
Prevention Of Hypertension ◽  
The Relationship ◽  
Low K

Introduction: Recently, the balance between sodium and potassium intake, i.e. sodium-to-potassium (Na/K) ratio, has received significant attention for prevention of hypertension. Previous studies reported the positive association between urinary Na/K (uNa/K) ratio and hypertension. However, even the same uNa/K ratio value, there might be high Na/ high K ratio or low Na/ low K ratio. Hypothesis: We assessed the hypothesis that blood pressure (BP) is higher in high Na/ high K group than that in low Na/ low K group even at the same uNa/K ratio in general population in cross-sectional study. Methods: The subjects were 20 to 74 years old who participated in The Tohoku Medical Megabank Project Community-based Cohort Study. Of these participants, we targeted 54,011 subjects (men: 20,505 women: 33,506 mean age: 59.9 years) who had information of BP, urinary Na and K. We estimated 24-h urinary excretion of Na and K using Tanaka formula. Urinary Na and K were each classified into quartiles (Na; Q1~Q4, K; Q1~Q4), and set all 16 groups of uNa/K ratio by combining Na and K respectively. To assess the relationship between casual uNa/K ratio and BP, we performed an analysis of covariance to calculate the adjusted mean systolic BP (SBP). We included covariate factors as age, sex, BMI and alcohol intake. We also assessed the relationship between uNa/K ratio and SBP using multiple regression analyses adjusted for covariate factors. We stratified the participants into two groups: ‘under treatment for hypertension’ (n=17,091) and ‘without treatment for hypertension (n=36,920)’. Results: The mean of uNa/K ratio for each group of Na (Q1)/K(Q1), Na (Q2)/K(Q2), Na (Q3)/K(Q3) and Na (Q4)/K(Q4) was all 4.0. As previous report showed, higher uNa/K ratio group showed higher SBP and lower uNa/K group showed lower BP. When we compared adjusted mean SBP of Na (Q1)/K(Q1) and Na (Q4)/K(Q4) the value were comparable, but the value were significantly higher in Na (Q4)/K(Q4) group (The adjusted mean SBP of Na (Q1)/K(Q1), Na (Q2)/K(Q2), Na (Q3)/K(Q3) and Na (Q4)/K(Q4) was 123.6, 124.9, 124.7 and 125.5 mmHg, respectively). The uNa/K was significantly positively associated with SBP independently of age, sex, BMI, and alcohol intake. The finding was unchanged the results in under treatment group. Conclusions: BP was significantly higher in high Na/ high K group than in low Na/ low K group even at the same uNa/K ratio. We suggested that not only increasing K intake but also reducing salt is important for preventing hypertension.

Role of cyclic ADP-ribose in the regulation of [Ca2+]i in porcine tracheal smooth muscle

1998 ◽  
Vol 274 (6) ◽  
pp. C1653-C1660 ◽  
Author(s):  
Y. S. Prakash ◽  
Mathur S. Kannan ◽  
Timothy F. Walseth ◽  
Gary C. Sieck
Keyword(s):  
Smooth Muscle ◽  
Second Messenger ◽  
Ruthenium Red ◽  
Tracheal Smooth Muscle ◽  
Cyclic Adp Ribose ◽  
Intracellular Ca ◽  
Subsequent Exposure ◽  
Trisphosphate Receptor ◽  
Dose Dependent Increase

The purpose of the present study was to determine whether cyclic ADP-ribose (cADPR) acts as a second messenger for Ca2+ release through ryanodine receptor (RyR) channels in tracheal smooth muscle (TSM). Freshly dissociated porcine TSM cells were permeabilized with β-escin, and real-time confocal microscopy was used to examine changes in intracellular Ca2+ concentration ([Ca2+]i). cADPR (10 nM–10 μM) induced a dose-dependent increase in [Ca2+]i, which was blocked by the cADPR receptor antagonist 8-amino-cADPR (20 μM) and by the RyR blockers ruthenium red (10 μM) and ryanodine (10 μM), but not by the inositol 1,4,5-trisphosphate receptor blocker heparin (0.5 mg/ml). During steady-state [Ca2+]ioscillations induced by acetylcholine (ACh), addition of 100 nM and 1 μM cADPR increased oscillation frequency and decreased peak-to-trough amplitude. ACh-induced [Ca2+]ioscillations were blocked by 8-amino-cADPR; however, 8-amino-cADPR did not block the [Ca2+]iresponse to a subsequent exposure to caffeine. These results indicate that cADPR acts as a second messenger for Ca2+ release through RyR channels in TSM cells and may be necessary for initiating ACh-induced [Ca2+]ioscillations.

Activation of Rho signaling contributes to lysophosphatidic acid-induced contraction of intact ileal smooth muscle of guinea-pig

2000 ◽  
Vol 78 (9) ◽  
pp. 729-736 ◽  
Author(s):  
Mayumi Mori ◽  
Hiromi Tsushima
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Lysophosphatidic Acid ◽  
Membrane Fraction ◽  
Smooth Muscles ◽  
Rho Kinase ◽  
Specific Inhibitor ◽  
High K ◽  
Rho A

To elucidate the possible role of Rho A/Rho-kinase on lysophosphatidic acid (LPA)-induced contraction in intact guinea-pig ileal smooth muscle, we examined effects of pretreatment with a specific inhibitor of Rho-kinase (Y-27632) on the LPA-induced contraction and MLC20 phosphorylation. In addition, we investigated whether LPA actually elicits an activation of Rho A by studying subcellular distribution of Rho A in unstimulated and stimulated smooth muscles by LPA. LPA induced a less intense, but sustained, contraction compared with ACh, and was accompanied by significant increases in MLC20 phosphorylation. The effects of LPA on tension and MLC20 phosphorylation were inhibited by Y-27632. The ACh-induced contraction, but not increases in MLC20 phosphorylation, was partially inhibited by Y-27632. High K+-induced contraction was unaffected by the inhibitor. LPA stimulated translocation of Rho A from the cytosol to the membrane fraction of the muscle. Translocation of Rho A was also induced by ACh and high K+. These results suggest that LPA-induced contraction of intact ileal smooth muscle is dominated through activation of Rho A and Rho-kinase and subsequent increases in MLC20 phosphorylation.Key words: lysophosphatidic acid, Rho, Rho-kinase, ileal smooth muscle.

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