Distinct cardio-respiratory response patterns elicited by neuropeptide Y and neuropeptide Y 13-36

• Autorzy: Kaczynska K. , Szereda-Przestaszewska M.
• Języki publikacji: EN

Abstrakty

EN

Neuropeptide Y (NPY) and its receptors have been involved in many physiological functions such as: regulation of cardiovascular system, anxiety, circadian rhythm, pain processing, inflammation, and among others, regulation of breathing. Microinjections of NPY to the dorsal medulla oblongata evoked respiratory and cardiovascular depression (Barraco et al., Brain Res. Bull., 1990; Dunbar et al., Am. J. Physiol., 1992). There is also evidence that respiratory failure or severe dyspnoea in humans was related to a high content of NPY in the infundibular nucleus (Corder et al., Neuroendocrinol., 1990). The objective of this study was to determine and compare the effects of systemic administration of neuropeptide Y and neuropeptide Y 13-36 (NPY 13-36) on the pattern of breathing and cardiovascular function and to evaluate the contribution of vagal input and the role of NPYY1 and/or Y2 receptors in these responses. Anaesthetized, spontaneously breathing rats were used. Tidal volume was measured at tracheostomy. The timing components of the breathing pattern, arterial blood pressure and heart rate were recorded. Intravenous injection of 100µg/kg-1 of NPY before and after midcervical vagotomy induced immediate slowing down of the respiratory rate and decreased tidal volume. Depressed ventilation was accompanied by a significant hypertension and bradycardia. Blockade of NPYY1 receptors with an intravenous dose of 5 mg/kg of BMS 193885, significantly reduced post-NPY cardio-respiratory effects. NPY 13-36, an agonist of NPYY2 receptors, at a dose of 10 mg/ kg provoked completely different respiratory response consisting of increased tidal volume, short-lived acceleration of the respiratory rhythm resulting in hyperventilation. Increased blood pressure but no effect on heart rate were observed. Section of the lung vagi abrogated the increase in respiratory rate thus reducing an enhanced ventilation. The rise in blood pressure was diminished. This study shows that intravenous injection of neuropeptide Y by acting on NPYY1 receptors outside of the lung vagi depresses ventilation by decreasing tidal volume and respiratory rate. Hypertension and bradycardia occur also besides this pathway and might result from the activation of peripheral vascular or heart Y1 receptors. Yet, NPY 13-36 acting through NPYY2 receptors stimulates ventilation augmenting the tidal component of the breathing pattern independent of the vagal pathway. This latter mediates the respiratory timing and hypertensive responses to NPY 13-36.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2011
• Tom: 71
• Numer: 1
• Opis fizyczny: p.150-151

Twórcy

autor

Kaczynska K.

• Laboratory of Respiratory Reflexes, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

autor

Szereda-Przestaszewska M.

• Laboratory of Respiratory Reflexes, Mossakowski Medical Research Centre Polish Academy of Sciences, Warsaw, Poland