ArticleAmerican journal of physiology. Heart and circulatory physiology2013
Suppression of endoplasmic reticulum stress improves endothelium-dependent contractile responses in aorta of the spontaneously hypertensive rat.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 89 citations in OpenAlex.
- Administration of tauroursodeoxycholic acid prevents endothelial dysfunction caused by an oral glucose load.Clinical science (London, England : 1979) · 2016Trial
- Inositol Requiring Enzyme 1α Mediates Hypertension and Vascular Remodeling.Hypertension (Dallas, Tex. : 1979) · 2026Article
- Disparate Mechanical and Functional Properties of Spontaneously Hypertensive Rat and Spontaneously Hypertensive Heart Failure Rat Penetrating Arterioles.Journal of cardiovascular pharmacology · 2026Article
- Narrative review of mitochondrial dysfunction in aging-related salt-sensitive hypertension: outcomes, mechanisms, and therapeutic implications.Aging advances · 2025Article
- Reactive oxygen species in hypertension.Nature reviews. Cardiology · 2025Review
- Endoplasmic Reticulum Stress in Hypertension and Salt Sensitivity of Blood Pressure.Current hypertension reports · 2024Review
- Milestone Papers on Signal Transduction Mechanisms of Hypertension and Its Complications.Hypertension (Dallas, Tex. : 1979) · 2024Review
- Lipotoxicity, ER Stress, and Cardiovascular Disease: Current Understanding and Future Directions.Cardiovascular & hematological agents in medicinal chemistry · 2024Review
- Implications of endoplasmic reticulum stress and autophagy in aging and cardiovascular diseases.Frontiers in pharmacology · 2024Review
- Huaju Xiaoji Formula Regulates ERS-lncMGC/miRNA to Enhance the Renal Function of Hypertensive Diabetic Mice with Nephropathy.Journal of diabetes research · 2024Article
- Endoplasmic reticulum protein 5 attenuates platelet endoplasmic reticulum stress and secretion in a mouse model.Blood advances · 2023Article
- Endoplasmic Reticulum Chemical Chaperone 3-Hydroxy-2-Naphthoic Acid Reduces Angiotensin II-Induced Vascular Remodeling and Hypertension In Vivo and Protein Synthesis In Vitro.Journal of the American Heart Association · 2022Article
- Non-alcoholic fatty liver disease and liver secretome.Archives of pharmacal research · 2022Review
- Inhibition of Endoplasmic Reticulum Stress Improves Acetylcholine-Mediated Relaxation in the Aorta of Type-2 Diabetic Rats.Molecules (Basel, Switzerland) · 2022Article
- The Effect of Tauroursodeoxycholic Acid (TUDCA) Treatment on Pregnancy Outcomes and Vascular Function in a Rat Model of Advanced Maternal Age.Antioxidants (Basel, Switzerland) · 2022Article
- Roles and Therapeutic Implications of Endoplasmic Reticulum Stress and Oxidative Stress in Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- Endoplasmic reticulum stress and unfolded protein response in cardiovascular diseases.Nature reviews. Cardiology · 2021Review
- Oxidative Stress and Hypertension.Circulation research · 2021Review
- Impaired UTP-induced relaxation in the carotid arteries of spontaneously hypertensive rats.Purinergic signalling · 2020Article
- 78 kDa Glucose-Regulated Protein Attenuates Protein Aggregation and Monocyte Adhesion Induced by Angiotensin II in Vascular Cells.International journal of molecular sciences · 2020Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
A contributing factor to increased peripheral resistance seen during hypertension is an increased production of endothelium-derived contractile factors (EDCFs). The main EDCFs are vasoconstrictor prostanoids, metabolites of arachidonic acid (AA) produced by Ca(2+)-dependent cytosolic phospholipase A2 (cPLA2) following phosphorylation (at Ser(505)) mediated by extracellular signal-regulated kinase (ERK1/2) and cyclooxygenase (COX) activations. Although endoplasmic reticulum (ER) stress has been shown to contribute to pathophysiological alterations in cardiovascular diseases, the relationship between ER stress and EDCF-mediated responses remains unclear. We tested the hypothesis that ER stress plays a role in EDCF-mediated responses via activation of the cPLA2/COX pathway in the aorta of the spontaneously hypertensive rat (SHR). Male SHR and Wistar-Kyoto rats (WKY) were treated with ER stress inhibitor, tauroursodeoxycholic acid or 4-phenlybutyric acid (TUDCA or PBA, respectively, 100 mg·kg(-1)·day(-1) ip) or PBS (control, 300 μl/day ip) for 1 wk. There was a decrease in systolic blood pressure in SHR treated with TUDCA or PBA compared with control SHR (176 ± 3 or 181 ± 5, respectively vs. 200 ± 2 mmHg). In the SHR, treatment with TUDCA or PBA normalized aortic (vs. control SHR) 1) contractions to acetylcholine (ACh), AA, and tert-butyl hydroperoxide, 2) ACh-stimulated releases of prostanoids (thromboxane A2, PGF2α, and prostacyclin), 3) expression of COX-1, 4) phosphorylation of cPLA2 and ERK1/2, and 5) production of H2O2. Our findings demonstrate a novel interplay between ER stress and EDCF-mediated responses in the aorta of the SHR. Moreover, ER stress inhibition normalizes such responses by suppressing the cPLA2/COX pathway.
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