Abstract not available

Bibliography: leaves 217-244. Tachykinins are implicated in the mediation of airway inflammatory responses and may have roles in airway remodeling and healing. The actions of tachykinins are mediated by specific receptors, designated NK1, NK2 and NK3. Tachykinin degredation, an important mechanism for limiting the effects of these peptides, is principally mediated by neutral endopeptidase (NEP). This thesis investigates the role of tachykinins, in vivo, in an ovine model and in human airway epithelium. Results show that the nett effect of tachykinins in the airway will depend on the relative balance between the expression of receptors, tachykinins and NEP. Assessment of these molecules in the airway epithelium from subjects with normal lungs or chronic bronchitis showed that preprotachykinin-A gene expression was relatively higher in the disease group whereas NEP and NK1 receptor levels were unchanged. These studies provide new insights into the role of tachykinins in airways disease.

abstract / Biological Sciences / Doctoral / Doctor of Philosophy

Bibliography: leaves 217-244. / x, 246 leaves : ill. (chiefly col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Tachykinins are implicated in the mediation of airway inflammatory responses and may have roles in airway remodeling and healing. The actions of tachykinins are mediated by specific receptors, designated NK1, NK2 and NK3. Tachykinin degredation, an important mechanism for limiting the effects of these peptides, is principally mediated by neutral endopeptidase (NEP). This thesis investigates the role of tachykinins, in vivo, in an ovine model and in human airway epithelium. Results show that the nett effect of tachykinins in the airway will depend on the relative balance between the expression of receptors, tachykinins and NEP. Assessment of these molecules in the airway epithelium from subjects with normal lungs or chronic bronchitis showed that preprotachykinin-A gene expression was relatively higher in the disease group whereas NEP and NK1 receptor levels were unchanged. These studies provide new insights into the role of tachykinins in airways disease. / Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 1999

Thesis (Ph.D.) -- University of Adelaide, Dept. of Medicine, 1999. / Bibliography: leaves 217-244.

Thesis (M.S.)--University of Wyoming, 2007. / Title from PDF title page (viewed on June 10, 2009). Includes bibliographical references (p. 40-55).

No description available.

This study investigated the cellular basis for the enhanced ganglionic responsiveness to NK1 agonists in the spontaneously hypertensive rat (SHR) in comparison to their normotensive counterpart, the Wistar-Kyoto (WKY) rat. Rats for in vivo studies were anesthetized with pentobarbital and treated with chlorisondamine (10.5 μmol/kg). Extracellular recordings from the external carotid nerve showed a greater responsiveness of decentralized SHR superior cervical ganglia (SCG) to intravenous injection of SP (32 nmol/kg). Blood pressure and heart rate were increased in SHRs, whereas WKY rats responded with a decrease in blood pressure and only slight tachycardia. Membrane properties of SCG neurons, as shown by intracellular microelectrode recordings, were similar between strains. Picospritzer application of the NK1 agonist GR-73632 (100 μM, 1 s) evoked slow depolarization and increased neuron excitability. Spontaneous firing was evoked only in some neurons. Depolarization amplitudes were similar between strains; however, the NK1 agonist depolarized a greater number of neurons in hypertensive rats. In conclusion, SHRs are more responsive to ganglion stimulation by NK1 agonists due to a greater number of responsive cells within the SCG rather than an enhanced responsiveness of individual neurons.

No description available.

No description available.