Investigation of changes in apelin receptor mRNA and protein expression in the myocardium and aorta of rats with two-kidney, one-clip (2K1C) Goldblatt hypertension

Najafipour, Hamid; Vakili, Abedin; Shahouzehi, Beydolah; Hekmat, Ava Soltani; Masoomi, Yaser; Yeganeh-Hajahmadi, Mahboobeh; Esmaeli-Mahani, Saeed

doi:10.1007/s13105-015-0394-z

Cited by 22 publications

(17 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent findings suggest that the apelin/APJ system may be involved in the pathophysiology of cardiovascular diseases . For the first time, Földes and colleagues reported that apelin may be involved in the pathogenesis of heart failure in the human .…”

Section: Introductionmentioning

confidence: 99%

Chronic treatment with apelin, losartan and their combination reduces myocardial infarct size and improves cardiac mechanical function

Abbasloo

Najafipour

Vakili

2019

Clin Exp Pharma Physio

Self Cite

View full text Add to dashboard Cite

The renin–angiotensin system (RAS) has a deleterious and apelin/APJ system has protective effect on the ischaemic heart. The collaboration between these systems in the pathophysiology of myocardial infarction is not clear. We determined the effect of chronic pretreatment with apelin, losartan and their combination on ischaemia–reperfusion (IR) injury in the isolated perfused rat heart and on the expression of apelin‐13 receptor (APJ) and angiotensin type 1 receptor (AT1R) in the myocardium. During 5 days before the induction of IR, saline (vehicle), apelin‐13 (Apl), F13A (apelin antagonist), losartan (Los, AT1R antagonist) and the combination of Apl and Los were administered intraperitoneally in rats. Ischaemia was induced by left anterior descending (LAD) artery occlusion for 30 minutes followed by reperfusion for 55 minutes in the Langendorff isolated heart perfusion system. Pretreatment with Apl, Los and the combination of Apl + Los significantly reduced infarct size by about 30, 33 and 48 percent respectively; and significantly improved the left ventricular function indices such as left ventricular developed pressure (LVDP), left ventricular end‐diastolic pressure (LVEDP) and rate pressure product (RPP). IR increased AT1R protein level but it did not change APJ significantly. AT1R expression was reduced in groups treated with Apl, Los and Apl + Los. Findings showed that chronic pretreatment with apelin along with AT1R antagonist had more protective effects against IR injury. Combination therapy may diminish the risk of IR‐induced heart damage, by reducing AT1R expression, in the heart of patients with coronary artery disease that are at the risk of MI and reperfusion injury.

show abstract

Section: Introductionmentioning

confidence: 99%

Chronic treatment with apelin, losartan and their combination reduces myocardial infarct size and improves cardiac mechanical function

Abbasloo

Najafipour

Vakili

2019

Clin Exp Pharma Physio

Self Cite

View full text Add to dashboard Cite

show abstract

“…The skin and abdominal layers were sutured using 4-0 silk threads and 5-0 chromic catgut, respectively. 11, 12 After the animals recovered from the anesthesia, they were kept in individual cages under standard conditions. After 4 weeks, the 2K1C rats, along with the normotensive rats, were anesthetized using sodium thiopental (50 mg/kg, i.p.).…”

mentioning

confidence: 99%

Differences in Cardiovascular Responses to Alamandine in Two-Kidney, One Clip Hypertensive and Normotensive Rats

Javanmardi

Kouhpayeh

et al. 2017

Circ J

Self Cite

View full text Add to dashboard Cite

angiotensin II type 1 receptor (AT1R) blockers. These drugs block angiotensin II (Ang II) -the primary active peptide in the RAS, which has many effects on blood vessels, the heart, the brain and the kidneys -from activating AT1R. AT1R is one of the two well-characterized receptors that Ang II activates (in addition to angiotensin II type 2 receptor (AT2R)). 3 Losartan is an angiotensin receptor blocker, 4 which mainly antagonizes AT1R, while PD123319 can block AT2R and Mas-related G protein-coupled receptor D (MrgD) receptors. 5 Recently, numerous researchers have shown that the RAS has additional complex multifunctional peptides, enzymes and receptors. The discovery of the ACE2/angiotensin-(1-7) [Ang-(1-7)]/Mas receptor axis, 6,7 which counterbalances several functions of the ACE/Ang II/AT1R axis, has highlighted the complexity of the RAS. The ACE2/Ang-(1-7)/ Mas receptor axis acts as a counter-regulatory axis. 7 It involves the heptapeptide peptide known as Ang-(1-7), which acts through a G-protein-coupled receptor called Mas. 7 Ang-(1-7) can be hydrolyzed from Ang II by the action of peptidases such as ACE2 and prolyl endopepti-D espite major progress in the research on the pathogenesis and management of hypertension and other aspects of cardiometabolic disease, these conditions underlie a significant number cases of morbidity and mortality due to cardiovascular and chronic kidney disease. It is predicted that there will be an increase in the hypertension prevalence rate in the United States (US). Currently, this condition affects 29% of the population in this country; that is, ~65 million individuals. 1 The significance of the renin-angiotensin system (RAS) in the development of hypertension and cardiovascular disease is well known. 2 Chronic RAS activation is a significant causal factor associated with the gradual malfunction of organs such as blood vessels, the kidneys and the heart. 2 These consequences of RAS activation have encouraged the development of medicines that can deactivate the RAS and thereby prevent the associated pathologies. The first class of drugs aimed at RAS inhibition are known as angiotensin-converting enzyme (ACE1) inhibitors, and they came on the market in the late 1970 s. Background: Alamandine is a newly discovered component of the renin-angiotensin system, which regulates blood pressure. In this study, the effect of alamandine on cardiovascular parameters in two-kidney, one clip (2K1C) hypertensive rats and normotensive rats, and the possible roles of the angiotensin II type 1 receptor (AT1R) and the PD123319-sensitive receptors in mediating this effect was investigated.

show abstract

“…Whereas the kidney plays a central role in the regulation of long-term blood pressure, aiming to improve this situation, the experimental model of renovascular hypertension has also been widely used [10].…”

Section: Introductionmentioning

confidence: 99%

History of vascular reactivity models and their involvement in hypertension pathogenesis

Conceição-Vertamatti

Borghi

Canova

et al. 2017

Vasa

View full text Add to dashboard Cite

Summary:Hypertension is a silent and multifactorial disease. Over two centuries ago, the fi rst device to record blood pressure was developed, making it possible to determine normotension and to establish criteria for hypertension. Since then, several studies have contributed to advance knowledge in this area, promoting signifi cant advances in pharmacological treatments and, as a result, increasing survival of hypertensive people. The main models developed for the study of hypertension and the main fi ndings in the vascular area are included in this review. We considered aspects related to vascular reactivity, changes in the population, and action of beta adrenergic receptors in the pathogenesis of hypertension.

show abstract

Investigation of changes in apelin receptor mRNA and protein expression in the myocardium and aorta of rats with two-kidney, one-clip (2K1C) Goldblatt hypertension

Cited by 22 publications

References 32 publications

Chronic treatment with apelin, losartan and their combination reduces myocardial infarct size and improves cardiac mechanical function

Chronic treatment with apelin, losartan and their combination reduces myocardial infarct size and improves cardiac mechanical function

Differences in Cardiovascular Responses to Alamandine in Two-Kidney, One Clip Hypertensive and Normotensive Rats

History of vascular reactivity models and their involvement in hypertension pathogenesis

Contact Info

Product

Resources

About