title: Prolactin-releasing peptide regulates the cardiovascular system via corticotrophin-releasing hormone.
abstract: Prolactin-releasing peptide (PrRP)-producing neurones are known to be localised mainly in the medulla oblongata and to act as a stress mediator in the central nervous system. In addition, central administration of PrRP elevates the arterial pressure and heart rate. However, the neuronal pathway of the cardiovascular effects of PrRP has not been revealed. In the present study, we demonstrate that PrRP-immunoreactive neurones projected to the locus coeruleus (LC) and the paraventricular nucleus (PVN) of the hypothalamus. The c-fos positive neurones among the noradrenaline cells in the LC, and the parvo- and magnocellular neurones in the PVN, were increased after central administration of PrRP. The arterial pressure and heart rate were both elevated after i.c.v. administration of PrRP. Previous studies have demonstrated that PrRP stimulated the neurones in the PVN [i.e. oxytocin-, vasopressin- and corticotrophin-releasing hormone (CRH)-producing neurones], which suggests that PrRP may induce its cardiovascular effect via arginine vasopressin (AVP) or CRH. Although the elevation of blood pressure and heart rate elicited by PrRP administration were not inhibited by an AVP antagonist, they were completely suppressed by treatment with a CRH antagonist. Thus, we conclude that PrRP stimulated CRH neurones in the PVN and that CRH might regulate the cardiovascular system via the sympathetic nervous system.
authors.affiliation: Department of Regulatory Biology, Graduate School of Science and Engineering, Saitama University, Sakura-ku, Saitama, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Yamada
authors.forename: A
authors.initials: A
authors.lastname: Mochiduki
authors.forename: Y
authors.initials: Y
authors.lastname: Sugimoto
authors.forename: Y
authors.initials: Y
authors.lastname: Suzuki
authors.forename: K
authors.initials: K
authors.lastname: Itoi
authors.forename: K
authors.initials: K
authors.lastname: Inoue
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002319:Cardiovascular System / Q000378:metabolism*; D003346:Corticotropin-Releasing Hormone / Q000037:antagonists & inhibitors / Q000378:metabolism*; D006339:Heart Rate / Q000502:physiology; D007028:Hypothalamic Hormones / Q000235:genetics / Q000378:metabolism*; D007031:Hypothalamus / Q000033:anatomy & histology / Q000378:metabolism; D008125:Locus Coeruleus / Q000166:cytology / Q000378:metabolism; D008297:Male; D009434:Neural Pathways / Q000033:anatomy & histology / Q000502:physiology; D009474:Neurons / Q000166:cytology / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism; D056690:Prolactin-Releasing Hormone; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism; D014667:Vasopressins / Q000378:metabolism
chemical_list: D007028:Hypothalamic Hormones; C534379:Prlh protein, rat; D056690:Prolactin-Releasing Hormone; D016760:Proto-Oncogene Proteins c-fos; D014667:Vasopressins; D003346:Corticotropin-Releasing Hormone; D014446:Tyrosine 3-Monooxygenase; D009638:Norepinephrine