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Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
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Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
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Hypertension, the most common cardiovascular disease, is diagnosed through repeated measurements of elevated blood pressure. Its risks, including damage to the kidney, heart, and brain, are directly proportional to blood pressure levels. Starting from 115/75 mm Hg, the risk of cardiovascular disease doubles with each increment of 20/10 mm Hg. The diagnosis relies on blood pressure measurements, not on patient symptoms, as hypertension is often asymptomatic until end-organ damage is imminent or...
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In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
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Related Experiment Video

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Inositol Requiring Enzyme 1α Mediates Hypertension and Vascular Remodeling.

Keiichi Torimoto1, Yuki Nakayama2, Yuka Terada2

  • 1Cardiovascular Research Center, Lewis Katz School of Medicine at Temple University, Philadelphia, PA (K.T., K.O., S.C., S.E.).

Hypertension (Dallas, Tex. : 1979)
|December 30, 2025
PubMed
Summary

Inhibiting inositol-requiring enzyme 1α (IRE1α) reduces high blood pressure and vascular changes caused by angiotensin II. This targets endoplasmic reticulum stress, offering a potential therapy for hypertension.

Keywords:
aortablood pressurefibrosishypertensioninositol

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Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Endoplasmic Reticulum Stress

Background:

  • Endoplasmic reticulum (ER) stress and chronic unfolded protein response (UPR) are implicated in hypertension.
  • Inositol-requiring enzyme 1α (IRE1α) is a key mediator of the UPR.
  • IRE1α is a potential therapeutic target for managing hypertension and associated vascular complications.

Purpose of the Study:

  • To investigate if inhibiting IRE1α mitigates hypertension and vascular remodeling.
  • To evaluate the effects of IRE1α inhibition on vascular smooth muscle cell function.
  • To explore the role of IRE1α in angiotensin II-induced cardiovascular changes.

Main Methods:

  • Angiotensin II infusion in C57BL6 mice with or without the IRE1α inhibitor KIRA6.
  • Assessment of blood pressure, cardiovascular remodeling, and vascular reactivity.
  • Analysis of IRE1α activation, intracellular calcium, and secretory phenotype in rat vascular smooth muscle cells.

Main Results:

  • KIRA6 treatment significantly lowered angiotensin II-induced hypertension.
  • Vascular thickening and perivascular fibrosis were prevented by KIRA6.
  • IRE1α inhibition attenuated vasoconstriction, reduced intracellular Ca2+ elevation, and mitigated a unique secretory phenotype in vascular smooth muscle cells.

Conclusions:

  • Targeting IRE1α is a promising therapeutic strategy for hypertension.
  • IRE1α inhibition reduces vascular resistance and smooth muscle cell Ca2+ signaling.
  • Inhibiting IRE1α protects against detrimental secretory phenotypes in vascular smooth muscle cells, ameliorating vascular remodeling.