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Hypertensive Nephropathy: Unveiling the Possible Involvement of Hemichannels and Pannexons

Claudia M Lucero1, Juan Prieto-Villalobos2, Lucas Marambio-Ruiz1

  • 1Instituto de Ciencias Biomédicas, Facultad de Ciencias de la Salud, Universidad Autónoma de Chile, El Llano Subercaseaux #2801, Santiago 8910060, Chile.

International Journal of Molecular Sciences
|December 23, 2022
PubMed

Insights

Hypertension damages kidneys by activating mesangial cells and disrupting calcium signaling. Angiotensin II (AngII) and channel activity may create a harmful cycle leading to kidney disease.

Area of Science:

  • Nephrology
  • Cardiovascular Research
  • Cellular Biology

Background:

  • Hypertension is a major risk factor for chronic cardiovascular diseases, notably hypertensive nephropathy.
  • In hypertensive nephropathy, glomerular mesangial cells (MCs) are damaged and activated, releasing vasoactive and proinflammatory factors.
  • Intracellular calcium ([Ca2+]i) signaling dysfunction, particularly via AT1 receptor activation by angiotensin II (AngII), is central to renal damage and inflammation.

Purpose of the Study:

  • To review the role of intracellular calcium ([Ca2+]i) signaling in hypertensive nephropathy.
  • To explore the proposed mechanism involving connexin/pannexin channels, ATP release, and purinergic receptors in AngII-mediated kidney damage.
  • To highlight the potential feed-forward mechanism contributing to renal pathology.

Main Methods:

  • Literature review focusing on cellular and molecular mechanisms of hypertensive nephropathy.
  • Analysis of the role of intracellular calcium ([Ca2+]i) signaling pathways.
  • Examination of the involvement of hemichannels, pannexons, and purinergic signaling.

Main Results:

  • Hypertension-induced MC activation leads to the release of vasoactive and proinflammatory agents.
  • [Ca2+]i signaling deregulation exacerbates cell damage, fibrosis, reduces renal blood flow, and impairs the glomerular filtration barrier.
  • Connexin and pannexin channels, regulated by [Ca2+]i, are implicated in AngII-mediated renal damage.

Conclusions:

  • AngII-mediated activation of AT1 receptors contributes significantly to hypertensive nephropathy pathogenesis via [Ca2+]i signaling.
  • The opening of connexin/pannexin channels by AngII may induce ATP release, activating purinergic receptors and causing calcium overload.
  • This process represents a potential feed-forward mechanism driving progressive kidney damage in hypertension.

Keywords:
Ca2+ dynamicsconnexin 43 hemichannelgap junctionshypertensive nephropathyinflammationoxidative stresspannexins 1 channels

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