Recio Visedo, María PazOrensanz Muñoz, Luis MiguelMartínez Sainz, María Del PilarNavarro Dorado, JorgeBustamante Alarma, SalvadorGarcía Sacristán, AlbinoPrieto Ocejo, DoloresHernández Rodríguez, Medardo Vicente2024-02-092024-02-092008-01-03Recio P, Orensanz LM, Martínez MP, Navarro-Dorado J, Bustamante S, García-Sacristán A, et al. Noradrenergic vasoconstriction of pig prostatic small arteries. Naunyn-Schmied Arch Pharmacol 2008;376:397–406. https://doi.org/10.1007/s00210-007-0227-x.0028-129810.1007/s00210-007-0227-xhttps://hdl.handle.net/20.500.14352/100824The current study investigated the distribution of adrenergic nerves and the action induced by noradrenaline (NA) in pig prostatic small arteries. Noradrenergic innervation was visualized using an antibody against dopamine-beta-hydroxylase (DBH), and the NA effect was studied in small arterial rings mounted in microvascular myographs for isometric force recordings. DBH-immunoreactive nerve fibers were located at the adventitia and the adventitia-media border of the vascular wall. Electrical field stimulation (EFS, 1-32 Hz) evoked frequency-dependent contractions that were reduced by guanethidine and prazosin (adrenergic neurotransmission and α1-adrenoceptors blockers, respectively) and by the α2-adrenoceptor agonist UK 14,304. The α2-adrenoceptor antagonist rauwolscine reversed the UK 14,304-produced inhibition. NA produced endothelium-independent contractions that were antagonized with low estimated affinities and Schild slopes different from unity by prazosin and the α1A-adrenoceptor antagonist N-[2-(2-cyclopropylmethoxyphenoxy) ethyl]-5-chloro-α-α-dimethyl-1H-indole-3-ethanamine (RS 17053). The α1A-adrenoceptor antagonist 5-methyl-3-[3-[4-[2-(2,2,2,-trifluoroethoxy) phenyl]-1-piperazinyl]propyl]-2,4-(1H)-pyrimidinedione (RS 100329), which also displays high affinity for α1L-adrenoceptors, and the α1L-adrenoceptor antagonist tamsulosin, which also has high affinity for α1A- and α1D-adrenoceptors, induced rightward shifts with high affinity of the contraction-response curve to NA. The α1D-adrenoceptor antagonist 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]-ethyl]8-azaspiro[4,5]decane-7,9-dione dihydrochloride (BMY 7378) failed to modify the NA contractions that were inhibited by extracellular Ca2+ removal and by voltage-activated (L-type) Ca2+ channel blockade. These data suggest that pig prostatic resistance arteries have a rich noradrenergic innervation; and NA, whose release is modulated by prejunctional α2-adrenoceptors, evokes contraction mainly through activation of muscle α1L-adrenoceptors coupled to extracellular Ca2+ entry via voltage (L-type)- and non-voltage-activated Ca2+ channels.engjournal article1432-1912https://doi.org/10.1007/s00210-007-0227-xrestricted access612.019591.1Pig prostatic small arteriesNoradrenergicinnervationPrejunctional α2-adrenoceptorsMuscle α1L-adrenoceptorsNoradrenalineVoltage (L-type)- and non-voltage-activated Ca2+ channelsFarmacología (Farmacia)Fisiología24 Ciencias de la Vida