title: Depression by relaxin of neurally induced contractile responses in the mouse gastric fundus.
abstract: The peptide hormone relaxin, which attains high circulating levels during pregnancy, has been shown to depress small-bowel motility through a nitric oxide (NO)-mediated mechanism. In the present study we investigated whether relaxin also influences gastric contractile responses in mice. Female mice in proestrus or estrus were treated for 18 h with relaxin (1 microg s.c.) or vehicle (controls). Mechanical responses of gastric fundal strips were recorded via force-displacement transducers. Evaluation of the expression of nitric oxide synthase (NOS) isoforms was performed by immunohistochemistry and Western blot. In control mice, neurally induced contractile responses elicited by electrical field stimulation (EFS) were reduced in amplitude by addition of relaxin to the organ bath medium. In the presence of the NO synthesis inhibitor l-NNA, relaxin was ineffective. Direct smooth muscle contractile responses were not influenced by relaxin or l-NNA. In strips from relaxin-pretreated mice, the amplitude of neurally induced contractile responses was also reduced in respect to the controls, while that of direct smooth muscle contractions was not. Further addition of relaxin to the bath medium did not influence EFS-induced responses, whereas l-NNA did. An increased expression of NOS I and NOS III was observed in gastric tissues from relaxin-pretreated mice. In conclusion, the peptide hormone relaxin depresses cholinergic contractile responses in the mouse gastric fundus by up-regulating NO biosynthesis at the neural level.
authors.affiliation: Departments of Physiological Sciences and Anatomy,4, University of Florence, Florence, Italy. mcaterina.baccari@unifi.it
authors.forename: Maria Caterina
authors.initials: MC
authors.lastname: Baccari
authors.forename: Silvia
authors.initials: S
authors.lastname: Nistri
authors.forename: Silvia
authors.initials: S
authors.lastname: Quattrone
authors.forename: Mario
authors.initials: M
authors.lastname: Bigazzi
authors.forename: Tatiana
authors.initials: T
authors.lastname: Bani Sacchi
authors.forename: Franco
authors.initials: F
authors.lastname: Calamai
authors.forename: Daniele
authors.initials: D
authors.lastname: Bani
mesh_terms: D000818:Animals; D029742:Caenorhabditis elegans Proteins / Q000378:metabolism; D002799:Cholinergic Fibers / Q000502:physiology; D004558:Electric Stimulation; D030762:Estrous Cycle; D005260:Female; D005748:Gastric Fundus / Q000187:drug effects* / Q000294:innervation / Q000502:physiology*; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D051379:Mice; D009119:Muscle Contraction / Q000187:drug effects*; D009130:Muscle, Smooth / Q000187:drug effects / Q000294:innervation / Q000502:physiology; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052248:Nitric Oxide Synthase Type I; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; D011359:Proestrus; D012065:Relaxin / Q000494:pharmacology*
chemical_list: D029742:Caenorhabditis elegans Proteins; C400703:nos-2 protein, C elegans; D012065:Relaxin; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; C496321:Nos1 protein, mouse; C496315:Nos3 protein, mouse