Functional consequences of contrasting properties of α1/α2 systems

1985 ◽  
Vol 68 (s10) ◽  
pp. 93s-97s ◽  
Author(s):  
Pieter B. M. W. M. Timmermans ◽  
Martin J. M. C. Thoolen ◽  
Adriaan De Jonge ◽  
Bob Wilffert ◽  
Pieter A. Van Zwieten
Keyword(s):  
Smooth Muscle ◽  
Experimental Evidence ◽  
Diastolic Pressure ◽  
Previous Treatment ◽  
Pithed Rat ◽  
Pithed Rats ◽  
Functional Consequences ◽  
Adrenoceptor Agonists

Ample experimental evidence supports the existence of two distinct types of vasoconstrictor α-adrenoceptors in vascular smooth muscle at postjunctional sites, showing similarities with α1 and α2-adrenoceptors. Especially in vivo, the characterization of an α2-adrenoceptor mediating an increase in diastolic pressure has been most successful. In this respect the model of the pithed rat has been employed most frequently (for reviews see [1, 2]). At present, the agents cirazoline, (−) phenylephrine, (±)-erythro-methoxamine, (−)-amidephrine, SKF89748, St587 and Sgd 101/75 fulfil the criteria for selective α1-adrenoceptor agonists; their log dose-vasopressor effect curves are virtually unaffected by previous treatment with yohimbine or rauwolscine (selective dose in pithed rats: 1 mg/kg), whereas prazosin (selective dose in pithed rats: 0.1 mg/kg) causes an appreciable parallel rightward displacement. The reverse holds true for the stimulants B-HT 920, B-HT 933, B-HT 958, UK-14304, xylazine, TL-99, M-7 and DP-6,7-ADTN, which all have been classified as preferential agonists of vascular postjunctional α-adrenoceptors.

Characterization of the airway smooth muscle muscarinic receptor in vivo

1991 ◽  
Vol 197 (1-2) ◽  
pp. 109-112 ◽  
Author(s):  
Ralph E. Howell ◽  
Keith Laemont ◽  
Raymond Gaudette ◽  
Maureen Raynor ◽  
Abby Warner ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Muscarinic Receptor ◽  
Airway Smooth Muscle

scholarly journals Molecular Characterization of HOXA2 and HOXA3 Binding Properties

2021 ◽  
Vol 9 (4) ◽  
pp. 55
Author(s):  
Joshua Mallen ◽  
Manisha Kalsan ◽  
Peyman Zarrineh ◽  
Laure Bridoux ◽  
Shandar Ahmad ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Molecular Characterization ◽  
Sequence Motif ◽  
Body Parts ◽  
Binding Affinities ◽  
Binding Properties ◽  
Functional Consequences

The highly conserved HOX homeodomain (HD) transcription factors (TFs) establish the identity of different body parts along the antero–posterior axis of bilaterian animals. Segment diversification and the morphogenesis of different structures is achieved by generating precise patterns of HOX expression along the antero–posterior axis and by the ability of different HOX TFs to instruct unique and specific transcriptional programs. However, HOX binding properties in vitro, characterised by the recognition of similar AT-rich binding sequences, do not account for the ability of different HOX to instruct segment-specific transcriptional programs. To address this problem, we previously compared HOXA2 and HOXA3 binding in vivo. Here, we explore if sequence motif enrichments observed in vivo are explained by binding affinities in vitro. Unexpectedly, we found that the highest enriched motif in HOXA2 peaks was not recognised by HOXA2 in vitro, highlighting the importance of investigating HOX binding in its physiological context. We also report the ability of HOXA2 and HOXA3 to heterodimerise, which may have functional consequences for the HOX patterning function in vivo.

scholarly journals Characterization of cystic fibrosis airway smooth muscle cell proliferative and contractile activities

2019 ◽  
Vol 317 (5) ◽  
pp. L690-L701
Author(s):  
Joyce Hojin Jang ◽  
Alice Panariti ◽  
Michael J. O’Sullivan ◽  
Melissa Pyrch ◽  
Chris Wong ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Airway Remodeling ◽  
Airway Smooth Muscle Cell ◽  
Cystic Fibrosis Airway ◽  
Contractile Activation ◽  
Pathological Behavior

Cystic fibrosis (CF) is a genetic disease that causes multiple airway abnormalities. Two major respiratory consequences of CF are airway hyperresponsiveness (AHR) and airway remodeling. Airway smooth muscle (ASM) is hypothesized to be responsible for the airway dysfunction, since their thickening is involved in remodeling, and excessive contraction by the ASM may cause AHR. It is unclear whether the ASM is intrinsically altered to favor increased contractility or proliferation or if microenvironmental influences induce pathological behavior in vivo. In this study, we examined the contractile and proliferative properties of ASM cells isolated from healthy donor and CF transplant lungs. Assays of proliferation showed that CF ASM proliferates at a higher rate than healthy cells. Through calcium analysis, no differences in contractile activation in response to histamine were found. However, CF ASM cells lagged in their reuptake of calcium in the sarcoplasmic reticulum. The combination CFTR corrector and potentiator, VX-809/770, used to restore CFTR function in CF ASM, resulted in a reduction in proliferation and in a normalization of calcium reuptake kinetics. These results show that impaired CFTR function in ASM cells causes intrinsic changes in their proliferative and contractile properties.

Peripheral vascular neuroeffector mechanisms in experimental cholestasis

1993 ◽  
Vol 265 (3) ◽  
pp. G579-G586 ◽  
Author(s):  
G. Jacob ◽  
O. Said ◽  
J. Finberg ◽  
A. Bomzon
Keyword(s):  
Electrical Stimulation ◽  
Bile Duct ◽  
Vascular Reactivity ◽  
Bile Duct Ligation ◽  
Norepinephrine Uptake ◽  
Pithed Rats ◽  
Duct Ligation ◽  
Adrenoceptor Agonists

Jaundiced patients have systemic hypotension and are more susceptible to hemorrhagic shock than nonjaundiced individuals. We have hypothesized that the mechanism whereby these cardiovascular complications arise is linked to a disturbance of the vascular neuroeffector process in the cardiovascular system. With the use of 3-day bile duct-manipulated (sham-operated) and bile duct-ligated rats, we have evaluated alpha-adrenoceptor function and amine uptake using in vivo and in vitro techniques. Blunted pressor responsiveness to norepinephrine, electrical stimulation, and the alpha 1-adrenoceptor agonists, methoxamine and phenylephrine, was observed in the bile duct-ligated pithed rats. In contrast, normal responsiveness to BHT-933 and clonidine, the alpha 2-adrenoceptor agonists, was seen in these animals. The uptake 1 blocker, cocaine, caused potentiation of equal magnitudes of the pressor responsiveness to electrical stimulation and norepinephrine in the sham-operated and bile duct-ligated pithed rats. In aortic rings prepared from the bile duct-ligated rats, blunted in vitro vascular reactivity to norepinephrine and the same alpha 1-adrenoceptor agonists was seen. Bile duct ligation had no effect on norepinephrine uptake or its kinetics in stressed and unstressed arterial rings and portal veins. We have thus concluded that bile duct ligation induces a defect in the functional expression of cardiovascular alpha 1-adrenoceptors without any effects on the activity of alpha 2-adrenoceptors or norepinephrine uptake.

scholarly journals CHARACTERIZATION OF A UNIQUE MUSCLE CELL LINE

1974 ◽  
Vol 61 (2) ◽  
pp. 398-413 ◽  
Author(s):  
David Schubert ◽  
A. John Harris ◽  
Carrick E. Devine ◽  
Stephen Heinemann
Keyword(s):  
Smooth Muscle ◽  
Cell Line ◽  
Action Potentials ◽  
Creatine Phosphokinase ◽  
Clonal Cell Line ◽  
Excitable Membranes ◽  
Hyperpolarizing Response ◽  
Electrically Excitable Membranes

A clonal cell line derived from a mouse neoplasm is described which shares many properties with smooth muscle. The cells have electrically excitable membranes capable of generating overshooting action potentials, and they contract both spontaneously and with electrical stimulation. They respond to the iontophoretic application of acetylcholine with a depolarizing response, and to norepinephrine with a hyperpolarizing response. Electron microscopy reveals that the cells have a morphology similar in many, but not all, respects to that of smooth muscle cells in vivo. The cells secrete soluble collagen-like molecules in addition to several proteins of undefined function. Finally, there is an increase in the specific activities of creatine phosphokinase and myokinase associated with increased cell density and the cessation of cell division.

Phenotypic and Functional Characterization of In Vivo Tissue Engineered Smooth Muscle From Normal and Pathological Bladders

2002 ◽  
pp. 1853-1858 ◽  
Author(s):  
JIN-YAO LAI ◽  
CHEOL YONG YOON ◽  
JAMES J. YOO ◽  
TINA WULF ◽  
ANTHONY ATALA
Keyword(s):  
Smooth Muscle ◽  
Functional Characterization

Phenotypic and Functional Characterization of In Vivo Tissue Engineered Smooth Muscle From Normal and Pathological Bladders

2002 ◽  
Vol 168 (4 Part 2) ◽  
pp. 1853-1858 ◽  
Author(s):  
Jin-Yao Lai ◽  
Cheol Yong Yoon ◽  
James J. Yoo ◽  
Tina Wulf ◽  
Anthony Atala
Keyword(s):  
Smooth Muscle ◽  
Functional Characterization

scholarly journals Measuring Arterial Stiffness in Animal Experimental Studies

2020 ◽  
Vol 40 (5) ◽  
pp. 1068-1077
Author(s):  
Mark Butlin ◽  
Isabella Tan ◽  
Bart Spronck ◽  
Alberto P. Avolio
Keyword(s):  
Smooth Muscle ◽  
Arterial Stiffness ◽  
Animal Studies ◽  
Ex Vivo ◽  
Experimental Studies ◽  
Full Characterization ◽  
Invasive Techniques

The arterial wall is a composite material of elastin, collagen, and extracellular matrix with acutely modifiable material properties through the action of smooth muscle cells. Therefore, arterial stiffness is a complex parameter that changes not only with long-term remodeling of the wall constituents but also with acute contraction or relaxation of smooth muscle or with changes in the acute distending pressure to which the artery is exposed. It is not possible to test all these aspects using noninvasive or even invasive techniques in humans. Full characterization of the mechanical properties of the artery and the specific arterial factors causing changes to stiffness with disease or modified lifestyle currently require animal studies. This article summarizes the major in vivo and ex vivo techniques to measure the different aspects of arterial stiffness in animal studies.

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