ArticleNaunyn-Schmiedeberg's archives of pharmacology2008
Noradrenergic vasoconstriction of pig prostatic small arteries.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Role of α- and β-adrenergic signaling in phenotypic targeting: significance in benign and malignant urologic disease.Cell communication and signaling : CCS · 2021Review
- Are blood vessels a target to treat lower urinary tract dysfunction?Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
- A vascular mechanistic approach to understanding Raynaud phenomenon.Nature reviews. Rheumatology · 2015Review
- Suppression of peripheral sympathetic activity underlies protease-activated receptor 2-mediated hypotension.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2014Article
- Effect of tamsulosin on iris vasculature and morphology.Journal of cataract and refractive surgery · 2014Article
- Perivascular innervation: a multiplicity of roles in vasomotor control and myoendothelial signaling.Microcirculation (New York, N.Y. : 1994) · 2013Review
- Mechanisms involved in the adenosine-induced vasorelaxation to the pig prostatic small arteries.Purinergic signalling · 2011Article
- Role of the α-adrenergic system in femoral vascular reactivity in neonatal llamas and sheep: a comparative study between highland and lowland species.American journal of physiology. Regulatory, integrative and comparative physiology · 2011Article
- Mechanisms involved in the nitric oxide-induced vasorelaxation in porcine prostatic small arteries.Naunyn-Schmiedeberg's archives of pharmacology · 2011Article
- Subtypes of functional alpha1-adrenoceptor.Cellular and molecular life sciences : CMLS · 2010Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The 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 alpha1-adrenoceptors blockers, respectively) and by the alpha2-adrenoceptor agonist UK 14,304. The alpha2-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 alpha1A-adrenoceptor antagonist N-[2-(2-cyclopropylmethoxyphenoxy)ethyl]-5-chloro-alpha-alpha-dimethyl-1H-indole-3-ethanamine (RS 17053). The alpha1A-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 alpha1L-adrenoceptors, and the alpha1L-adrenoceptor antagonist tamsulosin, which also has high affinity for alpha1A- and alpha1D-adrenoceptors, induced rightward shifts with high affinity of the contraction-response curve to NA. The alpha1D-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 alpha2-adrenoceptors, evokes contraction mainly through activation of muscle alpha1L-adrenoceptors coupled to extracellular Ca2+ entry via voltage (L-type)- and non-voltage-activated Ca2+ channels.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.