Involvement of the Neurokinin-2 Receptor in Airway Smooth Muscle Stretch-Activated Contractions Assessed in Perfused Intact Bovine Bronchial Segments

Hernandez, Jeremy M.; Cox, Gerard; Janssen, Luke J.

doi:10.1124/jpet.108.141176

Cited by 12 publications

(27 citation statements)

References 40 publications

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“…2A). A more detailed description of this protocol is outlined in our previous study (Hernandez et al, 2008).…”

Section: Resultsmentioning

confidence: 99%

“…Using intact bovine bronchial segments, we have shown that airway R stretch depends on contractile machinery priming and the magnitude of airway stretch. Moreover, in intact bovine bronchi, these responses possess nonmyogenic characteristics caused by the requirement of sensory neuronal input mediated by NK-A acting through the NK 2 receptor (Hernandez et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

“…To evaluate the effects of mechanical stretch on ASM contraction (measured by transmural pressure generation) in the isolated bronchial segment, we followed the protocol outlined in our previous publication (Hernandez et al, 2008). In brief, after the tissue viability test, the airway was allowed 20 min of recovery time under isovolumic conditions.…”

Section: Methodsmentioning

confidence: 99%

“…For a detailed description of our bronchial segment preparation protocol, please refer to our previous study (Hernandez et al, 2008). In brief, after the dissection and excision of the bronchial segment, side branches were tightly ligated.…”

Section: Methodsmentioning

confidence: 99%

“…It is noteworthy that our laboratory has shown, using perfused intact bovine bronchial segments, that airway stretchactivated contractions (R stretch ) depend on baseline airway tone and the magnitude of airway stretch. Moreover, we have shown that in intact bovine bronchi these responses possess nonmyogenic characteristics caused by the requirement of sensory neuronal input mediated by neurokinin (NK)-A acting through the NK 2 receptor (Hernandez et al, 2008). The inflammation present in asthmatic airways may also amplify airway R stretch responses.…”

Section: Introductionmentioning

confidence: 99%

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Thromboxane Prostanoid Receptor Activation Amplifies Airway Stretch-Activated Contractions Assessed in Perfused Intact Bovine Bronchial Segments

Hernandez

Janssen²

2011

J Pharmacol Exp Ther

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A deep inspiration (DI) produces bronchodilation in healthy individuals. Conversely, in asthmatics, DIs are less effective in producing bronchodilation and can cause more rapid airway renarrowing and even bronchoconstriction in moderate to severe asthmatics. It is noteworthy that the manner by which a DI is able to cause bronchoconstriction via a stretch-activated contraction (R stretch ) is thought to correlate positively with airway inflammation. Asthmatic airway inflammation is associated with increased production of thromboxane A 2 (TxA 2 ) and subsequent thromboxane prostanoid (TP) receptor activation, causing the heightened contractility of airway smooth muscle. In this study, we sought to investigate the effect of TxA 2 on airway R stretch by using bovine bronchial segments. In brief, these intact bronchial segments (2 mm in diameter) were dissected, side branches were ligated, and the tissues were mounted horizontally in an organ bath. R stretch was elicited by varying the transmural pressure under isovolumic conditions. Using a pharmacological approach, we showed a reduced R stretch response in tissues pretreated with indomethacin, a cyclooxygenase inhibitor, a result mimicked by pretreatment with the TP-selective receptor antagonist 4-(Z)-6-(2-o-chlorophenyl-4-o-hydroxyphenyl-1,3-dioxan-cis-5-yl)hexenoic acid (ICI 192605) and the selective p42/p44 mitogen-activated protein kinase inhibitor 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one (PD 95089) and by airway epithelial denudation. 9,11-Dideoxy-9␣,11␣-methanoepoxy-prosta-5Z,13E-dien-1-oic acid (U46619), a TP receptor agonist, elicited enhanced R stretch responses in a dose-dependent manner. Pretreatment with 6-isopropoxy-9-oxoxanthene-2-carboxylic acid (AH 6809), a prostaglandin E (EP) receptor 1/prostaglandin D2 (DP)-selective receptor antagonist, and 9␣,15R-dihydroxy-11.␤-fluoro-15-(2,3-dihydro-1H-inden-2-yl)- 16,17,18,19,20-pentanor-prosta-5Z,13E-dien-1-oic acid (AL 8810), a prostaglandin F (FP)-selective receptor antagonist, had no effect, suggesting EP, DP, and FP receptor activation is not involved in amplifying airway smooth muscle R stretch . These data suggest a role for TP receptor activation and epithelial release of TxA 2 in amplifying airway R stretch , thus providing novel insights into mechanisms regulating the DI-induced bronchoconstriction seen in asthmatics.

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“…2A). A more detailed description of this protocol is outlined in our previous study (Hernandez et al, 2008).…”

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Thromboxane Prostanoid Receptor Activation Amplifies Airway Stretch-Activated Contractions Assessed in Perfused Intact Bovine Bronchial Segments

Hernandez

Janssen²

2011

J Pharmacol Exp Ther

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The role of neuropeptides in adverse myocardial remodeling and heart failure

Widiapradja

Chunduri

Levick

2017

Cell. Mol. Life Sci.

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In addition to traditional neurotransmitters of the sympathetic and parasympathetic nervous systems, the heart also contains numerous neuropeptides. These neuropeptides not only modulate the effects of neurotransmitters, but also have independent effects on cardiac function. While in most cases the physiological actions of these neuropeptides are well defined, their contributions to cardiac pathology are less appreciated. Some neuropeptides are cardioprotective, some promote adverse cardiac remodeling and heart failure, and in the case of others their functions are unclear. Some have both cardioprotective and adverse effects depending on the specific cardiac pathology and progression of that pathology. In this review, we briefly describe the actions of several neuropeptides on normal cardiac physiology, before describing in more detail their role in adverse cardiac remodeling and heart failure. It is our goal to bring more focus toward understanding the contribution of neuropeptides to the pathogenesis of heart failure, and to consider them as potential therapeutic targets.

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L-type Ca2+ channels, Ca2+-induced Ca2+ release, and BKCa channels in airway stretch-induced contraction

Hernandez

Janssen

2012

European Journal of Pharmacology

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Involvement of the Neurokinin-2 Receptor in Airway Smooth Muscle Stretch-Activated Contractions Assessed in Perfused Intact Bovine Bronchial Segments

Cited by 12 publications

References 40 publications

Thromboxane Prostanoid Receptor Activation Amplifies Airway Stretch-Activated Contractions Assessed in Perfused Intact Bovine Bronchial Segments

Thromboxane Prostanoid Receptor Activation Amplifies Airway Stretch-Activated Contractions Assessed in Perfused Intact Bovine Bronchial Segments

The role of neuropeptides in adverse myocardial remodeling and heart failure

L-type Ca2+ channels, Ca2+-induced Ca2+ release, and BKCa channels in airway stretch-induced contraction

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