Rho-kinase as a therapeutic target in vascular diseases: Striking nitric oxide signaling

Nitric Oxide ◽  
2014 ◽  
Vol 43 ◽  
pp. 45-54 ◽  
Author(s):  
Gopi Krishna Kolluru ◽  
Syamantak Majumder ◽  
Suvro Chatterjee
Keyword(s):  
Nitric Oxide ◽  
Therapeutic Target ◽  
Rho Kinase ◽  
Vascular Diseases ◽  
Nitric Oxide Signaling

scholarly journals Inhibition of Rho-Kinase Improves Erectile Function, Increases Nitric Oxide Signaling and Decreases Penile Apoptosis in a Rat Model of Cavernous Nerve Injury

2013 ◽  
Vol 189 (3) ◽  
pp. 1155-1161 ◽  
Author(s):  
Johanna L. Hannan ◽  
Maarten Albersen ◽  
Omer Kutlu ◽  
Christian Gratzke ◽  
Christian G. Stief ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nerve Injury ◽  
Rat Model ◽  
Erectile Function ◽  
Rho Kinase ◽  
Cavernous Nerve ◽  
Nitric Oxide Signaling ◽  
Cavernous Nerve Injury

scholarly journals Effects of AGXT2 variants on blood pressure and blood sugar among 750 older Japanese subjects recruited by the complete enumeration survey method

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Yuta Yoshino ◽  
Hiroshi Kumon ◽  
Takaaki Mori ◽  
Taku Yoshida ◽  
Ayumi Tachibana ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Sugar ◽  
Vascular Diseases ◽  
Survey Method ◽  
Nucleotide Polymorphisms ◽  
Complete Enumeration ◽  
Plasma Adma ◽  
Oxide Synthase ◽  
Japanese Subjects

Abstract Background Alanine:glyoxylate aminotransferase 2 (AGXT2; EC 2.6.1.44) is the only enzyme that degrades the R-form of 3-aminoisobutyrate, an intermediate metabolite of thymine. AGXT2, as well as diaminoarginine dimethylaminohydrolase 1 (DDAH1; EC 3.5.3.18), works as an enzyme that degrades asymmetric dimethylarginine (ADMA), which competitively inhibits the nitric oxide synthase family. Thus, these two enzyme activities may change vascular vulnerability for a lifetime via the nitric oxide (NO) system. We investigated the association between vascular conditions and diseases such as hypertension and diabetes mellitus and polymorphisms of these two genes in 750 older Japanese subjects (mean age ± standard deviation, 77.0 ± 7.6 years) recruited using the complete enumeration survey method in the Nakayama study. Demographic and biochemical data, such as blood pressure (BP) and casual blood sugar (CBS), were obtained. Four functional single nucleotide polymorphisms (SNPs; rs37370, rs37369, rs180749, and rs16899974) of AGXT2 and one functional insertion/deletion polymorphism in the promotor region with four SNPs (rs307894, rs669173, rs997251, and rs13373844) of DDAH1 were investigated. Plasma ADMA was also analyzed in 163 subjects. Results The results of multiple regression analysis showed that a loss of the functional haplotype of AGXT2, CAAA, was significantly positively correlated with BP (systolic BP, p = 0.034; diastolic BP, p = 0.025) and CBS (p = 0.021). No correlation was observed between DDAH1 and either BP or CBS. ADMA concentrations were significantly elevated in subjects with two CAAA haplotypes compared with subjects without the CAAA haplotype (p = 0.033). Conclusions Missense variants of AGXT2, but not DDAH1, may be related to vulnerability to vascular diseases such as hypertension and DM via the NO system.

scholarly journals Role of β-Adrenergic Receptors and Nitric Oxide Signaling in Exercise-Mediated Cardioprotection

Physiology ◽  
2013 ◽  
Vol 28 (4) ◽  
pp. 216-224 ◽  
Author(s):  
John W. Calvert ◽  
David J. Lefer
Keyword(s):  
Nitric Oxide ◽  
Risk Factors ◽  
Adrenergic Receptors ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nitric Oxide Signaling ◽  
Factors Associated ◽  
Cardioprotective Effects ◽  
Β Adrenergic Receptors

Exercise promotes cardioprotection in both humans and animals not only by reducing risk factors associated with cardiovascular disease but by reducing myocardial infarction and improving survival following ischemia. This article will define the role that nitric oxide and β-adrenergic receptors play in mediating the cardioprotective effects of exercise in the setting of ischemia-reperfusion injury.

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