Abstract

There is no sufficiently investigation about the effects of novokinin, AT2 receptor agonist, on target molecules associated with organ pathology including ADMA, NADPH oxidase and Rho kinase. In this study we investigated the effects of novokinin, perindopril and losartan on Rho kinase, ADMA, NADPH oxidase at renal tissue blood pressure, in L-NAME and salt induced hypertension. Additionally, a1-adrenergic-induced contraction, ach-induced dilator responses in vessels obtained from hypertensive and pharmacological therapy groups were studied.In this study we investigated the effects of novokinin, perindopril and losartan on blood pressure, Rho kinase, ADMA, NADPH oxidase at renal tissue in L-NAME and salt induced hypertension. Additionally, a1-adrenergic-induced contraction, ach-induced dilator responses in vessels obtained from hypertensive and pharmacological therapy groups were studied. To develop hypertension, L-NAME was administrated intraperitoneally and drinking water with salt (1%) for 4 weeks. Perindopril, losartan, novokinin were administrated intraperitoneally for 2 weeks. Blood pressure was measured by using tail-cuff method; Rho kinase, ADMA and NADPH oxidase were measured by ELA°SA at renal tissues.Values are presented as means ± S.E.M.; compared by one way anova. Novokinin, perindopril and losartan diminished the level of NADPH oxidase and ADMA at renal tissue compared to hypertension group. Novokinin, perindopril and losartan decreased blood pressure. The greatest reduction of blood pressure was determined in perindopril treatment group In the hypertensive group, the acetylcholine EC50 value was significantly higher than in the control group and Emax value was significantly lower in hypertensive group compared to control. The application of novokinin, perindopril and losartan were improved the ach induced dilator responses in L-NAME and salt induced hypertension model. AT2 receptor agonist novokinin may offer protection of target organs such as the kidney. In this regard, further experimental studies are needed to exhibit potential benefits of novokinin in hypertension and end organ damage treatment for advanced clinical research.

Highlights

  • Hypertension correlates with renal function and is associated with renal pathology

  • For the first time the present study showed that treatment of novokinin diminished the level of Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and ADMA at renal tissue, decreased blood pressure and improved ach induced dilator responses in L-NAME and salt a ADMA level

  • It has been demonstrated that the application of perindopril and losartan was decreased ADMA and NADPH oxidase at renal tissue in the current experimental hypertension model

Read more

Summary

Introduction

Hypertension correlates with renal function and is associated with renal pathology. The renin-angiotensin-aldosterone system (RAAS) plays crucial roles in the pathogenesis of progression of arterial hypertension, cardiovascular disease and chronic kidney disease [1]. Long lasting stimulation of circulatory and tissue RAAS can cause the development and progression of renal pathophysiology. In this regard, making RAAS blockage is a logical therapeutic way in the prevention of renal diseases in hypertensive patients. Angiotensin-converting enzyme inhibitors (ACEis) and an­ giotensin II AT-1 receptor blockers (ARBs) are major approach to decelerate and treat hypertension, cardiovascular and renal diseases [2]. Despite this therapy, the progression of renal disease is not completely inhibited and residual proportion of hospitalisation and death in patients with cardiovascular pathology remain high. Novel alter­native RAAS related strategies are currently being attempted to improve patient outcomes

Methods
Results
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.