ArticleJournal of the American Heart Association2015
Calcium/calmodulin-dependent kinase II inhibition in smooth muscle reduces angiotensin II-induced hypertension by controlling aortic remodeling and baroreceptor function.
Article in Journal of the American Heart Association, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 46 citations in OpenAlex.
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- Proteomics analysis of empagliflozin in patients without diabetes or overt heart failure from empagliflozin and cardiac remodeling in people without diabetes CardioLink-7 randomized clinical trial.Cardiovascular endocrinology & metabolism · 2026Article
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- Plasma Calmodulin as a Biomarker of Subclinical Cardiovascular Disease in Pediatric Chronic Kidney Disease.Children (Basel, Switzerland) · 2025Article
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- Orally administered sodium nitrite prevents the increased α-1 adrenergic vasoconstriction induced by hypertension and promotes the S-nitrosylation of calcium/calmodulin-dependent protein kinase II.Biochemical pharmacology · 2023Article
- CaMKII as a Therapeutic Target in Cardiovascular Disease.Annual review of pharmacology and toxicology · 2023Review
- AGTR1rs5186 Polymorphism Is Associated with the Risk of Restenosis after Percutaneous Coronary Intervention: A Meta-Analysis.Journal of cardiovascular development and disease · 2022Review
- CaMKII Splice Variants in Vascular Smooth Muscle Cells: The Next Step or Redundancy?International journal of molecular sciences · 2022Review
- Sex-Specific Differences in Endothelial Function Are Driven by Divergent Mitochondrial CaJournal of the American Heart Association · 2022Article
- The circSPON2/miR-331-3p axis regulates PRMT5, an epigenetic regulator of CAMK2N1 transcription and prostate cancer progression.Molecular cancer · 2022Article
- Pleiotropic, non-cell death-associated effects of inhibitors of receptor-interacting protein kinase 1 in the heart.Molecular and cellular biochemistry · 2021Article
- Activation of Orexin System Stimulates CaMKII Expression.Frontiers in physiology · 2021Article
- A GSK3-SRF Axis Mediates Angiotensin II Induced Endothelin Transcription in Vascular Endothelial Cells.Frontiers in cell and developmental biology · 2021Article
- Article
- An Overview of the Role of Calcium/Calmodulin-Dependent Protein Kinase in Cardiorenal Syndrome.Frontiers in physiology · 2020Review
- Camk2n1 Is a Negative Regulator of Blood Pressure, Left Ventricular Mass, Insulin Sensitivity, and Promotes Adiposity.Hypertension (Dallas, Tex. : 1979) · 2019Article
- Cellular and Molecular Mechanisms Underlying Arterial Baroreceptor Remodeling in Cardiovascular Diseases and Diabetes.Neuroscience bulletin · 2019Review
- Maladaptive aortic remodeling in hypertension associates with dysfunctional smooth muscle contractility.American journal of physiology. Heart and circulatory physiology · 2019Article
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMultifunctional calcium/calmodulin-dependent kinase II (CaMKII) is activated by angiotensin II (Ang II) in cultured vascular smooth muscle cells (VSMCs), but its function in experimental hypertension has not been explored. The aim of this study was to determine the impact of CaMKII inhibition selectively in VSMCs on Ang II hypertension. METHODS AND
resultsTransgenic expression of a CaMKII peptide inhibitor in VSMCs (TG SM-CaMKIIN model) reduced the blood pressure response to chronic Ang II infusion. The aortic depressor nerve activity was reset in hypertensive versus normotensive wild-type animals but not in TG SM-CaMKIIN mice, suggesting that changes in baroreceptor activity account for the blood pressure difference between genotypes. Accordingly, aortic pulse wave velocity, a measure of arterial wall stiffness and a determinant of baroreceptor activity, increased in hypertensive versus normotensive wild-type animals but did not change in TG SM-CaMKIIN mice. Moreover, examination of blood pressure and heart rate under ganglionic blockade revealed that VSMC CaMKII inhibition abolished the augmented efferent sympathetic outflow and renal and splanchnic nerve activity in Ang II hypertension. Consequently, we hypothesized that VSMC CaMKII controls baroreceptor activity by modifying arterial wall remodeling in Ang II hypertension. Gene expression analysis in aortas from normotensive and Ang II-infused mice revealed that TG SM-CaMKIIN aortas were protected from Ang II-induced upregulation of genes that control extracellular matrix production, including collagen. VSMC CaMKII inhibition also strongly altered the expression of muscle contractile genes under Ang II.
conclusionsCaMKII in VSMCs regulates blood pressure under Ang II hypertension by controlling structural gene expression, wall stiffness, and baroreceptor activity.
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