ArticleBioMed research international2017
Basal and Activated Calcium Sensitization Mediated by RhoA/Rho Kinase Pathway in Rats with Genetic and Salt Hypertension.
Article in BioMed research international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- Altered Balance between Vasoconstrictor and Vasodilator Systems in Experimental Hypertension.Physiological research · 2024Review
- A Novel Single-Color FRET Sensor for Rho-Kinase Reveals Calcium-Dependent Activation of RhoA and ROCK.Sensors (Basel, Switzerland) · 2024Article
- Cooperation of augmented calcium sensitization and increased calcium entry contributes to high blood pressure in salt-sensitive Dahl rats.Hypertension research : official journal of the Japanese Society of Hypertension · 2021Article
- Characterization of Contractile Machinery of Vascular Smooth Muscles in Hypertension.Life (Basel, Switzerland) · 2021Review
- Pathophysiology of Hypertension: The Mosaic Theory and Beyond.Circulation research · 2021Review
- Role of Rho in Salt-Sensitive Hypertension.International journal of molecular sciences · 2021Review
- Association between gene polymorphisms of voltage-dependent CaBMC medical genetics · 2020Article
- Exaggerated blood pressure response to fasudil or nifedipine in hypertensive Ren-2 transgenic rats: role of altered baroreflex.Hypertension research : official journal of the Japanese Society of Hypertension · 2019Article
- Vascular smooth muscle contraction in hypertension.Cardiovascular research · 2018Review
- Inositol 1,4,5-Trisphosphate Receptors in Hypertension.Frontiers in physiology · 2018Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcium sensitization mediated by RhoA/Rho kinase pathway can be evaluated either in the absence (basal calcium sensitization) or in the presence of endogenous vasoconstrictor systems (activated calcium sensitization). Our aim was to compare basal and activated calcium sensitization in three forms of experimental hypertension with increased sympathetic tone and enhanced calcium entry-spontaneously hypertensive rats (SHR), heterozygous Ren-2 transgenic rats (TGR), and salt hypertensive Dahl rats. Activated calcium sensitization was determined as blood pressure reduction induced by acute administration of Rho kinase inhibitor fasudil in conscious rats with intact sympathetic nervous system (SNS) and renin-angiotensin system (RAS). Basal calcium sensitization was studied as fasudil-dependent difference in blood pressure response to calcium channel opener BAY K8644 in rats subjected to RAS and SNS blockade. Calcium sensitization was also estimated from reduced development of isolated artery contraction by Rho kinase inhibitor Y-27632. Activated calcium sensitization was enhanced in all three hypertensive models (due to the hyperactivity of vasoconstrictor systems). In contrast, basal calcium sensitization was reduced in SHR and TGR relative to their controls, whereas it was augmented in salt-sensitive Dahl rats relative to their salt-resistant controls. Similar differences in calcium sensitization were seen in femoral arteries of SHR and Dahl rats.
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