Download Acute and Chronic Cough (Lung Biology in Health and Disease, by Anthony E. Redington, Alyn H. Morice PDF

By Anthony E. Redington, Alyn H. Morice

A entire evaluation of the clinical and medical points of acute and protracted cough, this reference makes a speciality of fresh advancements in our realizing of the molecular biology of putative cough receptors, the neural mechanisms all for the afferent and efferent limbs, the primary processing of the cough reflex, and peptides and different elements that could mediate or modulate the cough reflex. With chapters wriitenby said professionals within the box, this guide covers present and strength healing brokers, a variety of methodologies to degree cough reflex sensitivity, and medical techniques for the evaluate of power cough in adults and youngsters.

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Additional resources for Acute and Chronic Cough (Lung Biology in Health and Disease, Volume 205)

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46. Kuzhikandathil EV, Wang H, Szabo T, Morozova N, Blumberg PM, Oxford GS. Functional analysis of capsaicin receptor (vanilloid receptor subtype 1) multimerization and agonist responsiveness using a dominant negative mutation. J Neurosci 2001; 21:8697–8706. 47. Jordt S-E, Julius D. Molecular basis for species-specific sensitivity to ‘‘hot’’ chili peppers. Cell 2002; 108:421–430. 48. Jung J, Lee S-Y, Hwang SW, Cho H, Shin J, Kang Y-S, Kim S, Oh U. Agonist recognition sites in the cytosolic tails of vanilloid receptor 1.

Bronchospasm evoked by 14 Hwang CysLTs is thought to be mediated by the release of tachykinins such as SP from vagal afferent nerves (80,119,120). The biological effects of LTC4 and LTD4 are mediated by CysLT receptors, such as CysLT1 (121). The signaling pathways downstream of the CysLT receptors in the respiratory system are not known; however, LTD4 has been shown to activate PLC in intestinal epithelial cells (122). Therefore, it is conceivable that PLC sensitization of TRPV1 via PKC-dependent or PIP2-dependent pathways could underlie the bronchoconstrictor effects of CysLTs.

Activation of the channel results in sufficient Naþ and Ca2þ influx to depolarize sensory nerve terminals, generate action potentials, transmit signals to the brain via ascending connections, and cause the antidromic release of tachykinins from the peripheral terminals. Excessive Ca2þ influx through the channel caused by chronic exposure to relevant stimuli desensitizes the afferent as well as the channel itself and sometimes leads to reversible degeneration of the nerve by complex mechanisms (7,17).

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