ArticleBritish journal of pharmacology2011
Effects of systemic inhibition of Rho kinase on blood pressure and renal haemodynamics in diabetic rats.
Article in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- The core mechanism of hypertension-linked renal fibrosis: "RAAS-ROS-inflammation-fibrosis" axis.iScience · 2026Review
- Rho/ROCK Signaling Pathway in Kidney Diseases: Mechanisms and Therapeutic Perspectives.Biomedicines · 2026Review
- Harnessing ROCK biology to revolutionize diabetic nephropathy: decoding mechanisms, designing therapies.Diabetology international · 2026Review
- Shared signaling pathways and comprehensive therapeutic approaches among diabetes complications.Frontiers in medicine · 2024Review
- NLRP3-mediated pyroptosis in diabetic nephropathy.Frontiers in pharmacology · 2022Review
- Activin A and Cell-Surface GRP78 Are Novel Targetable RhoA Activators for Diabetic Kidney Disease.International journal of molecular sciences · 2021Article
- Biologically active isoquinoline alkaloids covering 2014-2018.Medicinal research reviews · 2020Review
- Druggable targets in the Rho pathway and their promise for therapeutic control of blood pressure.Pharmacology & therapeutics · 2019Review
- Vascular smooth muscle contraction in hypertension.Cardiovascular research · 2018Review
- Blocking VEGF/Caveolin-1 signaling contributes to renal protection of fasudil in streptozotocin-induced diabetic rats.Acta pharmacologica Sinica · 2015Article
- Targeting of Rho kinase ameliorates impairment of diabetic endothelial function in intrarenal artery.International journal of molecular sciences · 2013Article
- Potential benefits of rho-kinase inhibition in arterial hypertension.Current hypertension reports · 2013Review
- Rho kinase inhibition in diabetic kidney disease.British journal of clinical pharmacology · 2013Review
- Activated Rho kinase mediates diabetes-induced elevation of vascular arginase activation and contributes to impaired corpora cavernosa relaxation: possible involvement of p38 MAPK activation.The journal of sexual medicine · 2013Article
- Prevention of diabetes-induced arginase activation and vascular dysfunction by Rho kinase (ROCK) knockout.Cardiovascular research · 2013Article
- Myosin light chain kinase is involved in the mechanism of gastrointestinal dysfunction in diabetic rats.Digestive diseases and sciences · 2012Article
- The ADF/Cofilin-Pathway and Actin Dynamics in Podocyte Injury.International journal of cell biology · 2012Article
- Pathophysiology of the diabetic kidney.Comprehensive Physiology · 2011Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeThe RhoA/Rho associated kinases (ROCK) pathway has been implicated in the pathophysiology of diabetic nephropathy (DN). Early stages of diabetes are associated with renal haemodynamic changes, contributing to later development of DN. However, the role of RhoA/ROCK, known regulators of vascular tone, in this process has not been studied. EXPERIMENTAL APPROACH: Blood pressure (BP), glomerular filtration (GFR), effective renal plasma flow and filtration fraction (FF) in response to the ROCK inhibitors Y27632 (0.1 and 0.5 mg·kg(-1) ) and fasudil (0.3 and 1.5 mg·kg(-1) ) were examined in streptozotocin-diabetic rats and non-diabetic controls. KEY
resultsDiabetic rats demonstrated baseline increases in GFR and FF. In contrast to similar decreases in BP in diabetic and control rats, renal vasodilator effects and a decrease in FF, following ROCK inhibition were observed only in diabetic rats. The vasodilator effects of Y27632 and a further decrease in FF, were also detected in diabetic rats pretreated with the angiotensin antagonist losartan. The effects of ROCK inhibitors in diabetic rats were modulated by prior protein kinase C (PKC)β inhibition with ruboxistaurin, which abolished their effects on FF. Consistent with the renal vasodilator effects, the ROCK inhibitors reduced phosphorylation of myosin light chain in diabetic kidneys. CONCLUSIONS AND IMPLICATIONS: The results indicate greater dependence of renal haemodynamics on RhoA/ROCK and beneficial haemodynamic effects of ROCK inhibitors in diabetes, which were additive to the effects of losartan. In this process, the RhoA/ROCK pathway operated downstream of or interacted with, PKCβ in some segments of the renal vascular tree.
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