Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (807 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Isopropyl analog of epinephrine; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Isopropylarterenol; Isopropylnoradrenaline; Isoprenaline; 4-(1-Hydroxy-2-((1-methylethyl)amino)ethyl)-1,2-benzenediol; Isopropyl Noradrenaline; Noradrenaline, Isopropyl; Isopropylnorepinephrine; Isoproterenol Hydrochloride.
Where it fits in the MeSH classification
- Broader topics
- Ethanolamines; Catecholamines
Related concepts
Research landscape
PubMed indexes 31,354 records tagged with the MeSH heading “Isoproterenol” (counts retrieved 2026-10-31). 1,217 of them (3.9%) were published from 2020 onward, and the busiest period so far is through 1999 with 24,296 records.
Reviews account for 586 records (1.9%) and meta-analyses for 0. Randomized controlled trials number 288 (0.9%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 24,296 |
| 2000-2009 | 3,415 |
| 2010-2019 | 2,426 |
| 2020 onward | 1,217 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 586 | 1.9% |
| Meta-analyses | 0 | 0.0% |
| Randomized controlled trials | 288 | 0.9% |
Method: PubMed query "Isoproterenol"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| CaMKII induces permeability transition through Drp1 phosphorylation during chronic β-AR stimulation | 2016 | Research article Design not recorded in structured metadata | 194 | cc by PMID 27739424 · DOI · PMC5067512 |
| Toxic tau oligomer formation blocked by capping of cysteine residues with 1,2-dihydroxybenzene groups | 2015 | Research article Design not recorded in structured metadata | 101 | cc by PMID 26671725 · DOI · PMC4703892 |
| Effects of Curcumin Nanoparticles in Isoproterenol-Induced Myocardial Infarction | 2019 | Research article Design not recorded in structured metadata | 76 | cc by PMID 31205590 · DOI · PMC6530192 |
| Verteporfin Mitigates Isoproterenol-Induced Myocardial Hypertrophy by Attenuating IL-6/STAT3 in Cardiac Fibroblasts | 2025 | Research article Design not recorded in structured metadata | 1 | cc by PMID 40919415 · DOI · PMC12411024 |
CaMKII induces permeability transition through Drp1 phosphorylation during chronic β-AR stimulation [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Mitochondrial permeability transition pore (mPTP) is involved in cardiac dysfunction during chronic β-adrenergic receptor (β-AR) stimulation.
- Closing excerpt
- These results uncover a pathway downstream of chronic β-AR stimulation that links CaMKII, Drp1 and mPTP to bridge cytosolic stress signal with mitochondrial dysfunction in the heart.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (140 words)
Mitochondrial permeability transition pore (mPTP) is involved in cardiac dysfunction during chronic β-adrenergic receptor (β-AR) stimulation. The mechanism by which chronic β-AR stimulation leads to mPTP openings is elusive. Here, we show that chronic administration of isoproterenol (ISO) persistently increases the frequency of mPTP openings followed by mitochondrial damage and cardiac dysfunction. Mechanistically, this effect is mediated by phosphorylation of mitochondrial fission protein, dynamin-related protein 1 (Drp1), by Ca2+/calmodulin-dependent kinase II (CaMKII) at a serine 616 (S616) site. Mutating this phosphorylation site or inhibiting Drp1 activity blocks CaMKII- or ISO-induced mPTP opening and myocyte death in vitro and rescues heart hypertrophy in vivo. In human failing hearts, Drp1 phosphorylation at S616 is increased. These results uncover a pathway downstream of chronic β-AR stimulation that links CaMKII, Drp1 and mPTP to bridge cytosolic stress signal with mitochondrial dysfunction in the heart.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 27739424 · DOI · PMC5067512
Toxic tau oligomer formation blocked by capping of cysteine residues with 1,2-dihydroxybenzene groups [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Neurofibrillary tangles, composed of hyperphosphorylated tau fibrils, are a pathological hallmark of Alzheimer's disease; the neurofibrillary tangle load correlates strongly with clinical progression of the disease.
- Closing excerpt
- Thus, compounds that target the cysteine residues of tau may prove useful in halting the progression of Alzheimer's disease and other tauopathies.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (144 words)
Neurofibrillary tangles, composed of hyperphosphorylated tau fibrils, are a pathological hallmark of Alzheimer's disease; the neurofibrillary tangle load correlates strongly with clinical progression of the disease. A growing body of evidence indicates that tau oligomer formation precedes the appearance of neurofibrillary tangles and contributes to neuronal loss. Here we show that tau oligomer formation can be inhibited by compounds whose chemical backbone includes 1,2-dihydroxybenzene. Specifically, we demonstrate that 1,2-dihydroxybenzene-containing compounds bind to and cap cysteine residues of tau and prevent its aggregation by hindering interactions between tau molecules. Further, we show that orally administered DL-isoproterenol, an adrenergic receptor agonist whose skeleton includes 1,2-dihydroxybenzene and which penetrates the brain, reduces the levels of detergent-insoluble tau, neuronal loss and reverses neurofibrillary tangle-associated brain dysfunction. Thus, compounds that target the cysteine residues of tau may prove useful in halting the progression of Alzheimer's disease and other tauopathies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26671725 · DOI · PMC4703892
Effects of Curcumin Nanoparticles in Isoproterenol-Induced Myocardial Infarction [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Curcumin has anti-inflammatory, antioxidative, anticarcinogenic, and cardiovascular protective effects.
- Closing excerpt
- Therefore, improving the bioactivity of curcumin by nanotechnology may help limit cardiac injury after myocardial infarction.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (234 words)
Curcumin has anti-inflammatory, antioxidative, anticarcinogenic, and cardiovascular protective effects. Our study is aimed at evaluating the effects of pretreatment with curcumin nanoparticles (CCNP) compared to conventional curcumin (CC) on isoproterenol (ISO) induced myocardial infarction (MI) in rats. Fifty-six Wistar-Bratislava white rats were randomly divided into eight groups of seven rats each. Curcumin and curcumin nanoparticles were given by gavage in three different doses (100 mg/kg body weight (bw), 150 mg/kg bw, and 200 mg/kg bw) for 15 days. The MI was induced on day 13 using 100 mg/kg bw ISO administered twice, with the second dose 24 h after the initial dose. The blood samples were taken 24 h after the last dose of ISO. The antioxidant, anti-inflammatory, and cardioprotective effects were evaluated in all groups. All doses of CC and CCNP offered a cardioprotective effect by preventing creatine kinase-MB leakage from cardiomyocytes, with the best result for CCNP. All the oxidative stress parameters were significantly improved after CCNP compared to CC pretreatment. CCNP was more efficient than CC in limiting the increase in inflammatory cytokine levels (such as TNF-α, IL-6, IL-1α, IL-1β, MCP-1, and RANTES) after MI. MMP-2 and MMP-9 levels decreased more after pretreatment with CCNP than with CC. CCNP better prevented myocardial necrosis and reduced interstitial edema and neutrophil infiltration than CC, on histopathological examination. Therefore, improving the bioactivity of curcumin by nanotechnology may help limit cardiac injury after myocardial infarction.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31205590 · DOI · PMC6530192
Verteporfin Mitigates Isoproterenol-Induced Myocardial Hypertrophy by Attenuating IL-6/STAT3 in Cardiac Fibroblasts [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Background: Yes-associated protein (YAP) is a major downstream nuclear coactivator of the Hippo pathway and is activated during myocardial hypertrophy.
- Closing excerpt
- Conclusions: Verteporfin protects the heart against ISO-induced myocardial hypertrophy by regulating IL-6/STAT3 in cardiac fibroblasts.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (289 words)
Background: Yes-associated protein (YAP) is a major downstream nuclear coactivator of the Hippo pathway and is activated during myocardial hypertrophy. Verteporfin, a YAP inhibitor, may serve as a potential treatment for myocardial hypertrophy. Aim: This study was aimed at exploring the role and underlying mechanisms of verteporfin in isoproterenol (ISO)-induced myocardial hypertrophy both in vivo and in vitro. Methods: GSE18801 directs our focus toward the Hippo pathway role in myocardial hypertrophy. Using an ISO-induced myocardial hypertrophy rat model, YAP expression and localization were observed through Western blot and immunofluorescence. Histopathological analysis was performed to evaluate cardiomyocyte cross-sectional area, and echocardiographic examinations were conducted to assess cardiac function. In vitro, primary neonatal rat cardiomyocytes (NRCMs) were cultured with conditioned medium from cardiac fibroblasts (CF-CM) treated with ISO to observe cell hypertrophy. Mechanistically, GSE203358 dataset analysis, enzyme-linked immunosorbent assay (ELISA), and Western blot were utilized to investigate the effects of ISO and verteporfin on IL-6, STAT3, and p-STAT3 levels in CFs. Subsequently, the changes in the IL-6/STAT3 pathway were evaluated in CFs treated with ISO and verteporfin. Additionally, recombinant IL-6 and IL-6 inhibitor were applied to CMs treated with CF-CM to observe changes in cardiomyocyte size. Results: Verteporfin improved cardiac performance in rats receiving ISO. In cultured NRCM, both ISO and CF-CM treated with ISO could induce cardiomyocyte hypertrophy. Verteporfin did not attenuate ISO-induced cardiomyocyte hypertrophy. However, it could attenuate hypertrophy induced by the CF-CM treated with ISO. GSE203358 indicated the involvement of the IL-6/STAT3 pathway in the presence of verteporfin in CFs. Additionally, verteporfin reduces IL-6 production in cultured CFs subjected to ISO treatment. Notably, the effects of verteporfin on NRCM were reversed by IL-6. Conclusions: Verteporfin protects the heart against ISO-induced myocardial hypertrophy by regulating IL-6/STAT3 in cardiac fibroblasts.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40919415 · DOI · PMC12411024
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Isoproterenol-induced cardiac ischemia and fibrosis: Plant-based approaches for intervention [5]
- Research article Morphological and functional characteristics of models of experimental myocardial injury induced by isoproterenol [6]
- Research article Molecular understanding of the protective role of natural products on isoproterenol-induced myocardial infarction: A review [7]
- Research article How to ablate long-standing persistent atrial fibrillation? [8]
- Research article STUDIES ON INFARCT-LIKE MYOCARDIAL NECROSIS PRODUCED BY ISOPROTERENOL: A REVIEW [9]
- Research article Caudal epidural block: a review of test dosing and recognition of systemic injection in children [10]
References
- Xu S, Wang P, Zhang H, Gong G, Gutierrez Cortes N, Zhu W, et al.. CaMKII induces permeability transition through Drp1 phosphorylation during chronic β-AR stimulation. . 2016. PMID 27739424 · DOI · PMC5067512
- Soeda Y, Yoshikawa M, Almeida OF, Sumioka A, Maeda S, Osada H, et al.. Toxic tau oligomer formation blocked by capping of cysteine residues with 1,2-dihydroxybenzene groups. . 2015. PMID 26671725 · DOI · PMC4703892
- Boarescu PM, Chirilă I, Bulboacă AE, Bocșan IC, Pop RM, Gheban D, et al.. Effects of Curcumin Nanoparticles in Isoproterenol-Induced Myocardial Infarction. . 2019. PMID 31205590 · DOI · PMC6530192
- Sheng S, Ding L, Lai J, Ye Z, Zhao R, Chen S, et al.. Verteporfin Mitigates Isoproterenol-Induced Myocardial Hypertrophy by Attenuating IL-6/STAT3 in Cardiac Fibroblasts. . 2025. PMID 40919415 · DOI · PMC12411024
- Allawadhi P, Khurana A, Sayed N, Kumari P, Godugu C. Isoproterenol-induced cardiac ischemia and fibrosis: Plant-based approaches for intervention. Phytother Res. 2018. PMID 30009418 · DOI
- Nichtova Z, Novotova M, Kralova E, Stankovicova T. Morphological and functional characteristics of models of experimental myocardial injury induced by isoproterenol. Gen Physiol Biophys. 2012. PMID 22781817 · DOI
- Wong ZW, Thanikachalam PV, Ramamurthy S. Molecular understanding of the protective role of natural products on isoproterenol-induced myocardial infarction: A review. Biomed Pharmacother. 2017. PMID 28826162 · DOI
- Di Biase L, Santangeli P, Natale A. How to ablate long-standing persistent atrial fibrillation?. Curr Opin Cardiol. 2013. PMID 23207492 · DOI
- RONA G, KAHN DS, CHAPPEL CI. STUDIES ON INFARCT-LIKE MYOCARDIAL NECROSIS PRODUCED BY ISOPROTERENOL: A REVIEW. Rev Can Biol. 1963. PMID 14143355
- Tobias JD. Caudal epidural block: a review of test dosing and recognition of systemic injection in children. Anesth Analg. 2001. PMID 11682386 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.