MicroRNA-Dependent Control of Serotonin-Induced Pulmonary Arterial Contraction

2017 ◽  
Vol 54 (4) ◽  
pp. 246-256 ◽  
Author(s):  
Diana Dahan ◽  
Tran Thi Hien ◽  
Philip Tannenberg ◽  
Mari Ekman ◽  
Catarina Rippe ◽  
...  
Keyword(s):  
Arterial Contraction ◽  
Pulmonary Arterial

Blockade Of Either Alpha-5 And Beta-1 Integrin Inhibits Pulmonary Arterial Contraction: Possible Role In PAH

2012 ◽  
Author(s):  
Kealan O'Neill ◽  
Austin Reece ◽  
Abdallah Alzoubi ◽  
Michie Toba ◽  
Masahiko Oka ◽  
...  
Keyword(s):  
Arterial Contraction ◽  
Beta 1 Integrin ◽  
Pulmonary Arterial

Regional contractile responses in pulmonary artery to α- and β-adrenoceptor agonists

1987 ◽  
Vol 65 (6) ◽  
pp. 1165-1170 ◽  
Author(s):  
Ralph C. Kolbeck ◽  
William A. Speir Jr.
Keyword(s):  
Pulmonary Artery ◽  
Contractile Response ◽  
Pulmonary Arteries ◽  
Regional Heterogeneity ◽  
Receptor Sites ◽  
Arterial Contraction ◽  
Adrenoceptor Agonists ◽  
Vascular Sensitivity ◽  
Pulmonary Arterial ◽  
Arterial Reactivity

Contractile sensitivity and reactivity to α- and β-adrenoceptor stimulation was studied in incubated rabbit pulmonary artery cylindrical segments of differing diameters. Distinct differences were noted between the responses of extra- and intra-pulmonary pulmonary arteries to norepinephrine and isoproterenol. The sensitivity to norepinephrine was largest in the intrapulmonary pulmonary arteries. Arterial reactivity to norepinephrine was greatest in the larger of the intrapulmonary vessel segments, diminishing considerably as the vessels became smaller. Cocaine did not cause substantial alterations in the response of any of the arterial segments to the α-agonist. Phentolamine, however, exerted its influence primarily in the smaller arterial segments. Vascular sensitivity to isoproterenol was least in the intrapulmonary pulmonary arteries. These smaller vessel segments, however, were more reactive to isoproterenol than were the extrapulmonary pulmonary arterial segments. Propranolol, at a concentration of 10−8 M, was an effective antagonist of the β-agonist; at a concentration of 10−7 M, however, this antagonist was related to isoproterenol-induced arterial contraction, apparently by stimulation of α-receptor sites. The results of this study demonstrated a regional heterogeneity in the contractile response of the pulmonary artery to α- and β-stimulation. The extrapulmonary arterial segments were found to be more sensitive to β-stimulation than were the smaller, intrapulmonary, segments. The intrapulmonary arterial segments, on the other hand, were found to be more sensitive to α-stimulation than were the extrapulmonary segments.

Hypoxia-induced pulmonary arterial contraction appears to be dependent on myosin light chain phosphorylation

1996 ◽  
Vol 271 (5) ◽  
pp. L768-L774 ◽  
Author(s):  
Y. Zhao ◽  
R. A. Rhoades ◽  
C. S. Packer
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Kinase Inhibitor ◽  
Tension Development ◽  
Arterial Contraction ◽  
Pulmonary Arterial ◽  
Mlc20 Phosphorylation ◽  
Arterial Muscle

The signal transduction pathway of hypoxic pulmonary arterial contraction has not been elucidated. Phosphorylation of the 20-kDa myosin light chain (MLC20) is thought to be essential for vascular muscle contraction. However, there are reports that smooth muscle will contract in response to nonphysiological stimuli such as phorbol esters without the involvement of MLC20 phosphorylation. The purpose of this study was to determine if hypoxia-induced pulmonary arterial contraction is dependent on MLC20 phosphorylation. Isolated rat pulmonary and carotid (for comparative purposes) arterial strips were contracted with 80 mM KCl to establish maximum active tension in response to membrane depolarization. The strips were then stimulated with one of the following: 30 mM KCl, 1 microM phenylephrine, 0.01 microM angiotensin II, 1 microM phorbol 12-myristate 13-acetate (PMA), or hypoxia (95% N2-5% CO2). In some experiments ML-9, a myosin light chain kinase inhibitor, or calphostin C, a protein kinase C (PKC) inhibitor, was introduced into the bath before hypoxia. Isometric tension was recorded as a function of time. Muscle strips were freeze-clamped (liquid N2) at various time points during the course of responses to the various stimuli. MLC20 phosphorylation levels were measured by ureaglycerol gel electrophoresis followed by Western blot procedure. Results show that increased MLC20 phosphorylation correlates with initiation of pulmonary arterial smooth muscle contraction in response to all agonists with the exception of PMA, a known activator of PKC. The MLC20 phosphorylation levels correlate with tension development in response to hypoxia, and ML-9 abolished the hypoxic contractions. In contrast, hypoxia relaxed carotid arterial muscle, and there was a corresponding decrease in the MLC20 phosphorylation level. In conclusion, hypoxia appears to result in MLC20 phosphorylation-mediated contraction in conduit pulmonary arterial muscle and in MLC20 dephosphorylation-mediated relaxation in systemic arterial muscle.

Inositol trisphosphate is involved in norepinephrine- but not in hypoxia-induced pulmonary arterial contraction

1993 ◽  
Vol 264 (2) ◽  
pp. L160-L164 ◽  
Author(s):  
N. Jin ◽  
C. S. Packer ◽  
D. English ◽  
R. A. Rhoades
Keyword(s):  
Time Course ◽  
Inositol Phosphates ◽  
Second Messengers ◽  
Acute Hypoxia ◽  
Inositol Trisphosphate ◽  
Pulmonary Arteries ◽  
Signal Transduction Pathway ◽  
Pulmonary Vasoconstriction ◽  
Arterial Contraction ◽  
Pulmonary Arterial

The role that second messengers play in pulmonary vasoconstriction is not understood. The purpose of this study was to directly measure inositol phosphates in isolated pulmonary arterial preparations before and during norepinephrine (NE) stimulation and acute hypoxia. Rat main pulmonary arteries were isolated and incubated with myo-[3H]-inositol. After incubation, control tissue was stimulated with 0.5 microM NE or 30 mM KCl. Test preparations were precontracted with 30 mM KCl and then exposed to hypoxia. Samples were homogenized and applied to a high-pressure liquid chromatography column for analysis of inositol phosphates. Results show that inositol trisphosphate (IP3) increases twofold at 5 s following NE stimulation. Thirty micromolars of KCl results in a slight but significant increase in IP3 formation at 5 min following the stimulation. Phentolamine inhibits the KCl-induced increase in IP3 formation, whereas A23187 has no effect on IP3 levels. Hypoxia caused a biphasic contraction in the precontracted isolated rat pulmonary artery. IP3 levels did not change during the hypoxic period. In conclusion, NE causes a rapid increase in IP3 formation consistent with the time course of production of an excitation-contraction coupling second messenger. However, inositol trisphosphate is not involved in the signal transduction pathway leading to pulmonary arterial contraction induced by hypoxia.

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