Regulation of cell volume and water transport – An old fundamental role of the renin angiotensin aldosterone system components at the cellular level

Mello, Walmor C. De

doi:10.1016/j.peptides.2014.06.003

Cited by 8 publications

(6 citation statements)

References 38 publications

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“…37 Similarly, to ACEi treatment, the pathway Ang II/Ang III/AT2-R is also still operative. Thus, even in the event ACEi or ARB are used during the inflammatory phase of SARS-CoV2 pneumonia and ARDS, redundant alternative pathways exist for the activation of AT2 receptors or Mas Receptors [via Angiotensin (1)(2)(3)(4)(5)(6)(7)] to maintain the anti-inflammatory capacity and counteract the cytokines storm (Figure 2B). AT2-R activation counteracts most effects of AT1R by inhibiting cell proliferation and differentiation, promoting vasodilation, and reducing inflammation and oxidative stress.…”

Section: Does the Treatment With Either Acei Or Arbs Facilitate Sars-cov-2 Infectivity?mentioning

confidence: 99%

“…It is involved in the regulation of cardiovascular, metabolic and immune-regulatory homeostasis. 1 The Severe Acute Respiratory Syndrome-Coronavirus (SARS-CoV) and Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2) utilize the ACE2-Receptor (ACE2-R) to invade human cells in alveolar epithelial and in several other tissues where ACE2-R is expressed. [2][3][4] SARS-CoV-2 infection is triggered by binding the spike S protein of the virus to ACE2.…”

Section: Introductionmentioning

confidence: 99%

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Obesity and COVID-19: the ominous duet affecting the renin-angiotensin system

et al. 2021

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Section: Does the Treatment With Either Acei Or Arbs Facilitate Sars-cov-2 Infectivity?mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Obesity and COVID-19: the ominous duet affecting the renin-angiotensin system

et al. 2021

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“…The expression of certain RAAS components even in simple organisms like crustaceans, insects, and leeches underscores the importance of the renin cascade in the control of cell volume and water homeostasis throughout evolution (De Mello 2014). The history of the RAAS and its discovery has recently been retraced with great accuracy in a review paper by Tsukamoto and Kitakaze (2013).…”

Section: A Complex and Highly Regulated Machinerymentioning

confidence: 99%

Chronobiology and Pharmacologic Modulation of the Renin–Angiotensin–Aldosterone System in Dogs: What Have We Learned?

Mochel

Danhof

2015

Reviews of Physiology, Biochemistry and Pharmacology Vol. 169

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Congestive heart failure (CHF) is a primary cause of morbidity and mortality with an increasing prevalence in human and canine populations. Recognition of the role of renin-angiotensin-aldosterone system (RAAS) overactivation in the pathophysiology of CHF has led to significant medical advances. By decreasing systemic vascular resistance and angiotensin II (AII) production, angiotensin-converting enzyme (ACE) inhibitors such as benazepril improve cardiac hemodynamics and reduce mortality in human and dog CHF patients. Although several experiments have pointed out that efficacy of ACE inhibitors depends on the time of administration, little attention is paid to the optimum time of dosing of these medications. A thorough characterization of the chronobiology of the renin cascade has the potential to streamline the therapeutic management of RAAS-related diseases and to help determining the optimal time of drug administration that maximizes efficacy of ACE inhibitors, while minimizing the occurrence of adverse effects. We have developed an integrated pharmacokinetic-pharmacodynamic model that adequately captures the disposition kinetics of the paradigm drug benazeprilat, as well as the time-varying changes of systemic renin-angiotensin-aldosterone biomarkers, without and with ACE inhibition therapy. Based on these chronobiological investigations, the optimal efficacy of ACE inhibitors is expected with bedtime dosing. The data further show that benazepril influences the dynamics of the renin-angiotensin-aldosterone cascade, resulting in a profound decrease in AII and aldosterone (ALD), while increasing renin activity for about 24 h. From the results of recent investigations in human, it is hypothesized that reduction of AII and ALD is one of the drivers of increased survival and improved quality of life in dogs receiving ACE inhibitors. To support and consolidate this hypothesis, additional efforts should be directed toward the collection of circulating RAAS peptides in spontaneous cases of canine CHF. If such a link could be established, profiling of these biomarkers could support determination of the severity of heart failure, complement clinical and echocardiographic findings, and be used for therapeutic drug monitoring purposes.

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“…Evidence provided in recent decades revealed that local expression of renin angiotensin or aldosterone impairs communication between heart cells by altering the gap junction conductance ( 20 – 24 ). Angiotensin II, for instance, plays an important role on the modulation of cell communication, inward calcium current, heart contractility, and cell volume regulation in health and disease through activation of cell surface AT1 receptors as well as PKC or tyrosine kynases ( 22 , 24 , 25 ).…”

Section: Raas Metabolic Cooperation and Organogenesismentioning

confidence: 99%

“…Evidence is now available that the formation of angiotensin ( 1 – 3 , 8 , 9 , 12 , 20 ) [Ang (1–7) elicited by the activation of ACE2 ( 39 )] has beneficial effects in the heart ( 39 , 41 , 42 ), counteracting the harmful effects of Ang II ( 43 ) and re-establishing impulse conduction during myocardial ischemia ( 42 ) as well as after cell swelling ( 44 ). It is then conceivable that Ang (1–7) can play a role in the formation of functional cellular patterns in the adult heart by enhancing gap junction permeability with consequent improvement of metabolic cooperation between cardiac cells.…”

Section: Ace/ang Ii/at1 Receptor Axis Versus Ace2/ang(1-7)/mas Receptmentioning

confidence: 99%

Chemical Communication between Heart Cells is Disrupted by Intracellular Renin and Angiotensin II: Implications for Heart Development and Disease

Mello

Walmor

2015

Front. Endocrinol.

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HighlightsIntracellular renin and angiotensin disrupts chemical communication in heart.Epigenetic modification of renin angiotensin aldosterone system (RAAS) and heart disease.Intracrine renin angiotensin and metabolic cooperation.Gap junction, intracellular renin and angiotensin, cellular patterns, and heart development.The finding that intracellular renin and angiotensin II (Ang II) disrupts chemical communication and impairs metabolic cooperation between cardiomyocytes induced by aldosterone, hyperglycemia, and pathological conditions like myocardial ischemia is discussed. The hypothesis is presented that epigenetic changes of the renin angiotensin aldosterone system (RAAS) are responsible for cardiovascular abnormalities, including the expression of RAAS components inside cardiac myocytes (intracrine RAAS) with serious consequences including inhibition of electrical and chemical communication in the heart, resulting in metabolic disarrangement and cardiac arrhythmias. Moreover, the inhibition of gap junctional communication induced by intracellular Ang II or renin can contribute to the selection of cellular patterns during heart development.

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Regulation of cell volume and water transport – An old fundamental role of the renin angiotensin aldosterone system components at the cellular level

Cited by 8 publications

References 38 publications

Obesity and COVID-19: the ominous duet affecting the renin-angiotensin system

Obesity and COVID-19: the ominous duet affecting the renin-angiotensin system

Chronobiology and Pharmacologic Modulation of the Renin–Angiotensin–Aldosterone System in Dogs: What Have We Learned?

Chemical Communication between Heart Cells is Disrupted by Intracellular Renin and Angiotensin II: Implications for Heart Development and Disease

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