ArticleNaunyn-Schmiedeberg's archives of pharmacology2011
Rat intermedin1-47 does not improve functional recovery in postischemic hearts.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
4 citing papers in PubMed, 5 citations in OpenAlex.
- Adrenomedullin 2 increases cardiac sympathetic nerve activity in parallel to heart rate in normal conscious sheep.Physiological reports · 2019Article
- Adrenomedullin 2/intermedin: a putative drug candidate for treatment of cardiometabolic diseases.British journal of pharmacology · 2018Review
- Intermedin protects against myocardial ischemia-reperfusion injury in diabetic rats.Cardiovascular diabetology · 2013Article
- Reverse myocardial effects of intermedin in pressure-overloaded hearts: role of endothelial nitric oxide synthase activity.The Journal of physiology · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intermedin, a novel member of the calcitonin/calcitonin gene-related peptide family identified from vertebrate genomes, may directly affect cardiac function but current studies revealed no clear picture. The aims of our study were to compare direct contractile effects of intermedin on cardiomyocytes to that on the whole organ and to investigate whether intermedin improves postischemic recovery independent of an effect on acute reperfusion injury. Isolated adult rat ventricular cardiomyocytes were electrically paced and cell shortening was monitored as a readout associated to cardiac performance. Calcium transients were analyzed by Fura-2AM loading of these cells. Isolated rat hearts were investigated by Langendorff perfusion under nonischemic conditions and after 45-min no-flow ischemia followed up by 30-min reperfusion prior to drug testing. Intermedin caused a positive contractile effect on cardiomyocytes that was mediated by protein kinase A activation and accompanied by improved calcium transients. In contrast, intermedin reduced left ventricular developed pressure in Langendorff-perfused rat hearts. This negative inotropic effect was attenuated by inhibition of nitric oxide synthesis. In postischemic hearts (impaired nitric oxide synthesis), the negative inotropic effect was attenuated but no positive inotropic effect occurred. However, intermedin caused robust vasodilation in nonischemic and postischemic hearts. Our findings suggest that the peptide binds preferentially to vascular cells in the intact organ. The loss of nitric oxide induction in postischemic hearts attenuates a negative inotropic effect of intermedin but does not improve cardiac performance independent of acute reperfusion injury.
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