α-Adrenoceptor stimulation of porcine pulmonary arteries
European Journal of Pharmacology, ISSN: 0014-2999, Vol: 235, Issue: 2, Page: 169-175
1993
- 23Citations
- 13Captures
Metric Options: CountsSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations23
- Citation Indexes23
- 23
- CrossRef22
- Captures13
- Readers13
- 13
Article Description
The effects of α 1 - and α 2 -adrenoceptors stimulants on vascular tone of 188 isolated rings of pulmonary arteries from 24 pigs have been studied. The rings were pretreated with indomethacin, to inhibit cyclo-oxygenase. Isometric tension was recorded and concentrations of cyclic 3′5′-guanosine monophosphate (cGMP) and cyclic 3′5′-adenosine monophosphate (cAMP) were measured. Rings with endothelium contracted with phenylephrine (10 −5 M) (n = 41) and the α-adrenocpetor agonist methoxamine (10 −3 M) (n = 24). cGMP did not change with methoxamine, but rose with phenylephrine, peaking at 30 to 45 s. This preceded the maximum rise in tension with phenylephrine which occured later at 120 to 360 s. The α 2 -adrenoceptor agonist, clonidine (10 −5 M) (n = 33) and the muscarinic receptor agonist acetylcholine (10 −5 M) (n= 30) relaxed precontracted pulmonary arterial rings, minimum tension occuring after 120 s, whilst cGMP rose after 30–45 s. After removal of endothelium (n = 24), the tension after phenylephrine (10 −5 M) was higher and the rise in cGMP was abolished. The cAMP levels did not change with phenylephrine (10 −5 M), acetylcholine (10 −5 M), clonidine (10 −5 M) nor methoxamine (10 −3 M). Activation of α 1 -adrenoceptors on pulmonary arteries smooth muscle cause contraction, whilst activation of α 2 -adrenoceptors on endothelial cells cause relaxation probably through a release of nitric oxide and a rise in cGMP.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/0014299993901333; http://dx.doi.org/10.1016/0014-2999(93)90133-3; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0027246208&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/8389712; https://linkinghub.elsevier.com/retrieve/pii/0014299993901333; http://dx.doi.org/10.1016/0014-2999%2893%2990133-3; https://dx.doi.org/10.1016/0014-2999%2893%2990133-3
Elsevier BV
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