ArticleBritish journal of pharmacology1993
Evidence that depletion of internal calcium stores sensitive to noradrenaline elicits a contractile response dependent on extracellular calcium in rat aorta.
Article in British journal of pharmacology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 34 citations in OpenAlex.
- α1D-Adrenoceptors are responsible for the high sensitivity and the slow time-course of noradrenaline-mediated contraction in conductance arteries.Pharmacology research & perspectives · 2013Article
- Functional characterization of alpha 1-adrenoceptor subtypes in vascular tissues using different experimental approaches: a comparative study.British journal of pharmacology · 2003Article
- Pathological role of a constitutively active population of alpha(1D)-adrenoceptors in arteries of spontaneously hypertensive rats.British journal of pharmacology · 2002Article
- Functional evidence of inverse agonism in vascular smooth muscle.British journal of pharmacology · 1996Article
- Ca2+ entry activated by emptying of intracellular Ca2+ stores in ileal smooth muscle of the rat.British journal of pharmacology · 1995Article
- Mechanism of the cardiovascular activity of laudanosine: comparison with papaverine and other benzylisoquinolines.British journal of pharmacology · 1994Article
- Actions of alpha-adrenoceptor blocking agents on two types of intracellular calcium stores mobilized by noradrenaline in rat aorta.Naunyn-Schmiedeberg's archives of pharmacology · 1993Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Noradrenaline 1 microM induced a contractile response in rat isolated aorta in the presence or in the absence of extracellular Ca2+ with depletion of intracellular Ca2+ stores. Thereafter, during incubation in the presence of Ca2+, an increase in the resting tone was observed. Such a contractile response did not occur after exposure to caffeine or 5-hydroxytryptamine. 2. This increase in tension was inhibited in a concentration-dependent manner by alpha-adrenoceptor antagonists (prazosin, phentolamine and yohimbine), the non-specific relaxing compound, papaverine and by the Ca(2+)-entry blocker, nifedipine. Therefore, this contractile process is related to depletion of Ca2+ stores sensitive to noradrenaline and is linked to Ca2+ entry through voltage-operated Ca2+ channels and alpha-adrenoceptors. 3. Phentolamine and yohimbine did not block the Ca2+ refill pathway; prazosin and nifedipine inhibited the reuptake of Ca2+ by an internal store sensitive only to noradrenaline; papaverine inhibited the refilling of caffeine- and noradrenaline-sensitive Ca(2+)-stores.
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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.