Vascular smooth muscle contraction in hypertension

Topic: Brain proteins, microglia and lab models

Hypertension is a major risk factor for many common chronic diseases, such as heart failure, myocardial infarction, stroke, vascular dementia, and chronic kidney disease. Pathophysiological mechanisms contributing to the development of hypertension include increased vascular resistance, determined in large part by reduced vascular diameter due to increased vascular contraction and arterial remodelling. These processes are regulated by complex-interacting systems such as the renin-angiotensin-aldosterone system, sympathetic nervous system, immune activation, and oxidative stress, which influence vascular smooth muscle function. Vascular smooth muscle cells are highly plastic and in pathological conditions undergo phenotypic changes from a contractile to a proliferative state. Vascular smooth muscle contraction is triggered by an increase in intracellular free calcium concentration ([Ca2+]i), promoting actin-myosin cross-bridge formation. Growing evidence indicates that contraction is also regulated by calcium-independent mechanisms involving RhoA-Rho kinase, protein Kinase C and mitogen-activated protein kinase signalling, reactive oxygen species, and reorganization of the actin cytoskeleton. Activation of immune/inflammatory pathways and non-coding RNAs are also emerging as important regulators of vascular function. Vascular smooth muscle cell [Ca2+]i not only determines the contractile state but also influences activity of many calcium-dependent transcription factors and proteins thereby impacting the cellular phenotype and function. Perturbations in vascular smooth muscle cell signalling and altered function influence vascular reactivity and tone, important determinants of vascular resistance and blood pressure. Here, we discuss mechanisms regulating vascular reactivity and contraction in physiological and pathophysiological conditions and highlight some new advances in the field, focusing specifically on hypertension.

Key findings

• Growing evidence indicates that contraction is also regulated by calcium-independent mechanisms involving RhoA-Rho kinase, protein Kinase C and mitogen-activated protein kinase signalling, reactive oxygen species, and reorganization of the actin cytoskeleton.

Why it matters

This review describes mechanisms of vascular smooth muscle contraction in hypertension, a condition listed as a risk factor for vascular dementia. It does not test or report any treatment, cure, or prevention for Alzheimer's disease.

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Study details

• Evidence strengthLow

Read the original

• DOI: 10.1093/cvr/cvy023
• PubMed: 29394331
• Original source →
• Free full text: Cardiovascular Research →

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

@article{touyz2018-29394331,
  author  = {Touyz, R. M. and Alves-Lopes, R. and Rios, F. J. and Camargo, L. L. and Anagnostopoulou, A. and Arner, A. and Montezano, A. C.},
  title   = {{Vascular smooth muscle contraction in hypertension}},
  journal = {Cardiovascular research},
  year    = {2018},
  doi     = {10.1093/cvr/cvy023},
  pmid    = {29394331},
  url     = {https://doi.org/10.1093/cvr/cvy023}
}

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