ReviewBritish journal of pharmacology2012
The pharmacology of adrenomedullin 2/intermedin.
Review in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
66 citing papers in PubMed, 145 citations in OpenAlex.
- Intermedin prevents acute heart failure following acute kidney injury by alleviating inflammatory responses.Renal failure · 2025Article
- Intermedin Inhibits DNA Damage-Promoted Senescent Phenotype Transition of Vascular Smooth Muscle Cells in Aorta by Activating NAMPT/PARP1 in Mice.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Expression and regulation of adrenomedullin 2 gene in ovarian follicles and its effect on follicular granulosa cells in chicken.Poultry science · 2025Article
- CXCL12/CXCR4 axis mediates CD8Journal of translational medicine · 2025Article
- IntermedinJournal of inflammation research · 2025Article
- Intermedin Alleviates Diabetic Cardiomyopathy by Up-Regulating CPT-1β through Activation of the Phosphatidyl Inositol 3 Kinase/Protein Kinase B Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Variable CGRP family peptide signaling durations and the structural determinants thereof.Biochemical pharmacology · 2024Article
- Adrenomedullin Improves Hypertension and Vascular Remodeling partly through the Receptor-Mediated AMPK Pathway in Rats with Obesity-Related Hypertension.International journal of molecular sciences · 2023Article
- Adrenomedullin 2/intermedin is a slow off-rate, long-acting endogenous agonist of the adrenomedullinbioRxiv : the preprint server for biology · 2023Article
- Elucidating the Interactome of G Protein-Coupled Receptors and Receptor Activity-Modifying Proteins.Pharmacological reviews · 2023Review
- Sustained Activation of CLR/RAMP Receptors by Gel-Forming Agonists.International journal of molecular sciences · 2022Article
- Intermedin Alleviates Vascular Calcification in CKD through Sirtuin 3-Mediated Inhibition of Mitochondrial Oxidative Stress.Pharmaceuticals (Basel, Switzerland) · 2022Article
- miR-1297 sensitizes glioma cells to temozolomide (TMZ) treatment through targeting adrenomedullin (ADM).Journal of translational medicine · 2022Article
- Pharmacological characterisation of mouse calcitonin and calcitonin receptor-like receptors reveals differences compared with human receptors.British journal of pharmacology · 2022Article
- IMD/ADM2 operates as a secretory factor that controls cumulus-oocyte complexes (COCs) conformation for oocytes in vitro maturation.In vitro cellular & developmental biology. Animal · 2022Article
- Beyond CGRP: The calcitonin peptide family as targets for migraine and pain.British journal of pharmacology · 2022Review
- Gel-forming antagonist provides a lasting effect on CGRP-induced vasodilation.Frontiers in pharmacology · 2022Article
- Adrenomedullin increases cAMP accumulation and BDNF expression in rat DRG and spinal motor neurons.Iranian journal of basic medical sciences · 2021Article
- IntermedinCell death & disease · 2021Article
- Mono and dual agonists of the amylin, calcitonin, and CGRP receptors and their potential in metabolic diseases.Molecular metabolism · 2021Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 4 countries.
Funding
Abstract
Adrenomedullin 2 (AM2) or intermedin is a member of the calcitonin gene-related peptide (CGRP)/calcitonin family of peptides and was discovered in 2004. Unlike other members of this family, no unique receptor has yet been identified for it. It is extensively distributed throughout the body. It causes hypotension when given peripherally, but when given into the CNS, it increases blood pressure and causes sympathetic activation. It also increases prolactin release, is anti-diuretic and natriuretic and reduces food intake. Whilst its effects resemble those of AM, it is frequently more potent. Some characterization of AM2 has been done on molecularly defined receptors; the existing data suggest that it preferentially activates the AM(2) receptor formed from calcitonin receptor-like receptor and receptor activity modifying protein 3. On this complex, its potency is generally equivalent to that of AM. There is no known receptor-activity where it is more potent than AM. In tissues and in animals it is frequently antagonised by CGRP and AM antagonists; however, situations exist in which an AM2 response is maintained even in the presence of supramaximal concentrations of these antagonists. Thus, there is a partial mismatch between the pharmacology seen in tissues and that on cloned receptors. The only AM2 antagonists are peptide fragments, and these have limited selectivity. It remains unclear as to whether novel AM2 receptors exist or whether the mismatch in pharmacology can be explained by factors such as metabolism.
Indexed as
Identifiers
What OpenQuestion holds
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.