scholarly journals Role of Kinins in Hypertension and Heart Failure

2020 ◽  
Vol 13 (11) ◽  
pp. 347
Author(s):  
Suhail Hamid ◽  
Imane A. Rhaleb ◽  
Kamal M. Kassem ◽  
Nour-Eddine Rhaleb
Keyword(s):  
Blood Pressure ◽  
Spontaneous Mutation ◽  
Target Organ Damage ◽  
Regulatory System ◽  
Renin Angiotensin System ◽  
Organ Damage ◽  
Protective Effects ◽  
Kinin System ◽  
Downstream Signaling

The kallikrein–kinin system (KKS) is proposed to act as a counter regulatory system against the vasopressor hormonal systems such as the renin-angiotensin system (RAS), aldosterone, and catecholamines. Evidence exists that supports the idea that the KKS is not only critical to blood pressure but may also oppose target organ damage. Kinins are generated from kininogens by tissue and plasma kallikreins. The putative role of kinins in the pathogenesis of hypertension is discussed based on human mutation cases on the KKS or rats with spontaneous mutation in the kininogen gene sequence and mouse models in which the gene expressing only one of the components of the KKS has been deleted or over-expressed. Some of the effects of kinins are mediated via activation of the B2 and/or B1 receptor and downstream signaling such as eicosanoids, nitric oxide (NO), endothelium-derived hyperpolarizing factor (EDHF) and/or tissue plasminogen activator (T-PA). The role of kinins in blood pressure regulation at normal or under hypertension conditions remains debatable due to contradictory reports from various laboratories. Nevertheless, published reports are consistent on the protective and mediating roles of kinins against ischemia and cardiac preconditioning; reports also demonstrate the roles of kinins in the cardiovascular protective effects of the angiotensin-converting enzyme (ACE) and angiotensin type 1 receptor blockers (ARBs).

scholarly journals Sodium Intake and Target Organ Damage in Hypertension—An Update about the Role of a Real Villain

2020 ◽  
Vol 17 (8) ◽  
pp. 2811 ◽  
Author(s):  
Federica Nista ◽  
Federico Gatto ◽  
Manuela Albertelli ◽  
Natale Musso
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Risk ◽  
Sodium Intake ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Left Ventricular ◽  
Target Organ ◽  
Main Role ◽  
Sodium Consumption

Salt intake is too high for safety nowadays. The main active ion in salt is sodium. The vast majority of scientific evidence points out the importance of sodium restriction for decreasing cardiovascular risk. International Guidelines recommend a large reduction in sodium consumption to help reduce blood pressure, organ damage, and cardiovascular risk. Regulatory authorities across the globe suggest a general restriction of sodium intake to prevent cardiovascular diseases. In spite of this seemingly unanimous consensus, some researchers claim to have evidence of the unhealthy effects of a reduction of sodium intake, and have data to support their claims. Evidence is against dissenting scientists, because prospective, observational, and basic research studies indicate that sodium is the real villain: actual sodium consumption around the globe is far higher than the safe range. Sodium intake is directly related to increased blood pressure, and independently to the enlargement of cardiac mass, with a possible independent role in inducing left ventricular hypertrophy. This may represent the basis of myocardial ischemia, congestive heart failure, and cardiac mortality. Although debated, a high sodium intake may induce initial renal damage and progression in both hypertensive and normotensive subjects. Conversely, there is general agreement about the adverse role of sodium in cerebrovascular disease. These factors point to the possible main role of sodium intake in target organ damage and cardiovascular events including mortality. This review will endeavor to outline the existing evidence.

scholarly journals Eucommia ulmoidesOliv. (Du-Zhong) Lignans Inhibit Angiotensin II-Stimulated Proliferation by Affecting P21, P27, and Bax Expression in Rat Mesangial Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Xian Jing ◽  
Wei-Hua Huang ◽  
Yong-Jun Tang ◽  
Ya-Qin Wang ◽  
Hui Li ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cellular Proliferation ◽  
Mesangial Cells ◽  
Target Organ Damage ◽  
Renin Angiotensin System ◽  
Organ Damage ◽  
Eucommia Ulmoides ◽  
Protective Effects ◽  
Ang Ii ◽  
Hypertensive Nephropathy

Cortex Eucommiae (Du-zhong) is the dried bark of theEucommia ulmoidesOliv. The natural products identified fromDu-zhonginclude lignans, iridoids, flavonoids, polysaccharides, terpenes, and proteins, Liu et al. (2012). Lignans, the main bioactive components, were protective against hypertensive renal injury in spontaneous hypertensive rats in our previous study, Li et al. (2012). Moreover,Eucommialignans also diminished aldose reductase (AR) overexpression in the kidney, Li et al. (2012). However, the pathological mechanism underlying the protective effects ofEucommialignans remains unknown. Cellular proliferation was reported to contribute to important pathological changes in hypertensive renal injuries, and increased angiotensin II (Ang II) expression was reported to be essential for target-organ damage during hypertension. Ang II is the main effective peptide in the renin-angiotensin system and is considered to be a key mediator in the development of hypertensive nephropathy, Rüster and Wolf (2011). Our preliminary results showed thatEucommialignans had inhibitory effects on Ang II-induced proliferation of rat mesangial cells. In the present study, we investigated the effects ofEucommia ulmoideson Ang II-induced proliferation and apoptosis of rat mesangial cells. Cell cycle-related genes P21 and P27, and cell apoptosis-related genes Bax and Bcl-2, were determined.

Associations between cardiac target organ damage and microvascular dysfunction: the role of blood pressure

2010 ◽  
Vol 28 (5) ◽  
pp. 952-958 ◽  
Author(s):  
William D Strain ◽  
Nish Chaturvedi ◽  
Alun Hughes ◽  
Petros Nihoyannopoulos ◽  
Christopher J Bulpitt ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Target Organ Damage ◽  
Microvascular Dysfunction ◽  
Organ Damage ◽  
Target Organ

Metabolic syndrome and target organ damage: role of blood pressure

2008 ◽  
Vol 6 (5) ◽  
pp. 731-743 ◽  
Author(s):  
Cesare Cuspidi ◽  
Carla Sala ◽  
Alberto Zanchetti
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Target Organ

Target organ damage in patients with rheumatoid arthritis: The role of blood pressure and heart rate

2010 ◽  
Vol 209 (1) ◽  
pp. 255-260 ◽  
Author(s):  
Vasileios F. Panoulas ◽  
Tracey E. Toms ◽  
Giorgos S. Metsios ◽  
Antonios Stavropoulos-Kalinoglou ◽  
Athanasios Kosovitsas ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Blood Pressure ◽  
Heart Rate ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Target Organ

scholarly journals Role of AT1 receptor-mediated salt retention in angiotensin II-dependent hypertension

2011 ◽  
Vol 301 (5) ◽  
pp. F1124-F1130 ◽  
Author(s):  
Steven D. Crowley ◽  
Jiandong Zhang ◽  
Maria Herrera ◽  
Robert Griffiths ◽  
Phillip Ruiz ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Target Organ Damage ◽  
Kidney Injury ◽  
Systemic Blood Pressure ◽  
Organ Damage ◽  
Sodium Reabsorption ◽  
Blood Pressure Elevation ◽  
Pressure Elevation

Activation of type 1 angiotensin II (AT1) receptors in the kidney promotes blood pressure elevation and target organ damage, but whether renal AT1 receptors influence the level of hypertension by stimulating sodium retention or by raising systemic vascular resistance has not been established. In the current studies, we used a kidney cross-transplantation strategy to determine whether increased sodium reabsorption by AT1 receptors in the kidney mediates the chronic hypertensive response to angiotensin II. We found this to be true. In addition, we also identified a second, nontrivial component of blood pressure elevation induced by activation of renal AT1 receptors that is sodium-independent. As the kidney has the capacity to limit the transmission of elevated systemic blood pressure into the renal microcirculation, prior studies struggled to clearly discriminate the relative contributions of blood pressure elevation vs. activation of AT1 receptors to hypertensive kidney injury. In our model, we found that rapid surges in blood pressure, which may overcome the kidney's capacity to prevent perturbations in renal hemodynamics, correlate closely with kidney damage in hypertension. Moreover, maximal kidney injury in hypertension may require activation of a pool of nonrenal, systemic AT1 receptors. These studies provide insight into precise mechanisms through which AT1 receptor blockade influences the progression of hypertensive kidney disease.

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