title: Immunohistochemical and functional evidence for a noradrenergic regulation in the horse penile deep dorsal vein.
abstract: Our aim was to study the presence of noradrenergic nerves and to characterize the alpha-adrenergic receptors involved in the contractions to electrical field stimulation and to alpha-adrenergic agonists of the horse penile deep dorsal vein. Noradrenergic fibres were visualized by immunohistochemistry using an antibody against dopamine-beta-hydroxylase (DBH). For functional studies, the responses of the venous rings to electrical field stimulation and to alpha-adrenergic agonists (noradrenaline, phenylephrine and BHT 920) were studied in the absence and the presence of noradrenergic transmission- and neuronal sodium channel-blockers (guanethidine and tetrodotoxin, respectively) and of alpha1- and alpha2-adrenergic antagonists (prazosin and rauwolscine, respectively). DBH-immunoreactive fibres were present in the adventitia and in the media layer of the venous rings. Electrical field stimulation (0.5-32 Hz) caused frequency-dependent contractions that were abolished by guanethidine (10(-6) M) and tetrodotoxin (10(-6) M) and reduced by prazosin (10(-9)-10(-7) M) and rauwolscine (3 x 10(-8)-3 x 10(-7) M). Noradrenaline, phenylephrine and BHT 920 induced equipotent contractions of the rings. Prazosin and rauwolscine competitively antagonized the contractions to phenylephrine and BHT 920, respectively. In conclusion, DBH-immunoreactive nerve fibres are present in the horse penile dorsal vein. Both transmural nerve stimulation and alpha-adrenergic agonists induce contraction of the venous rings through a heterogeneous population of alpha1- and alpha2-adrenoceptors.
authors.affiliation: Departamento de Fisiología, Facultad de Farmacia, Universidad Complutense de Madrid, Madrid, Spain. precio@farm.ucm.es
authors.forename: P
authors.initials: P
authors.lastname: Recio
authors.forename: D
authors.initials: D
authors.lastname: Prieto
authors.forename: M P
authors.initials: MP
authors.lastname: Martínez
authors.forename: P
authors.initials: P
authors.lastname: García
authors.forename: L
authors.initials: L
authors.lastname: Rivera
authors.forename: S
authors.initials: S
authors.lastname: Benedito
authors.forename: A C
authors.initials: AC
authors.lastname: Martínez
authors.forename: A G
authors.initials: AG
authors.lastname: Sacristán
authors.forename: L M
authors.initials: LM
authors.lastname: Orensanz
authors.forename: M
authors.initials: M
authors.lastname: Hernández
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D001381:Azepines / Q000494:pharmacology; D004299:Dopamine beta-Hydroxylase / Q000032:analysis; D004558:Electric Stimulation; D006736:Horses / Q000502:physiology*; D007150:Immunohistochemistry; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D009412:Nerve Fibers / Q000201:enzymology / Q000502:physiology; D009638:Norepinephrine / Q000494:pharmacology; D010413:Penis / Q000098:blood supply* / Q000294:innervation*; D010656:Phenylephrine / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*; D014680:Veins / Q000294:innervation*; D015016:Yohimbine / Q000494:pharmacology
chemical_list: D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D001381:Azepines; D011942:Receptors, Adrenergic, alpha; D010656:Phenylephrine; D015016:Yohimbine; C024763:talipexole; D004299:Dopamine beta-Hydroxylase; D009638:Norepinephrine; D011224:Prazosin