Angiotensin II Revisited: New Roles In Inflammation, Immunology And Aging

md_a

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If we win this fight with the `coronavirus` using ARB inhibitors (blocking AT1), or something else by natural means, we have the chance to become younger and healthier as a side effect. (ACE inhibitors are not good)

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Angiotensin II: A Key Player In Oxidative Stress Toxicity and Aging

We have previously referred to the impact of Ang II in ROS production. In fact, Ang II robustly stimulates the production of molecular oxygen species that trigger mitochondrial dysfunction and cellular injury (de Cavanagh et al, 2007; Wilson, 1990). Ang II via AT1 receptor stimulation can activate NAD(P)H oxidase to produce ROS, resulting in oxidative stress damage (Griendling et al, 1994). Harman has proposed that ROS are the most prominent molecular species involved in the aging process (Harman, 1956). According to his theory, ROS contribute significantly to various age-associated organ failures, including hypertension, cardiovascular diseases and renal damage (de Cavanagh et al, 2007). Hence, Ang II could be involved in organ senescence given its ability to mediate the release of oxidant species. Supporting this hypothesis, Ang II-induced ROS production via AT1 receptor promotes the onset of vascular senescence associated with functional and structural changes of blood vessels that contribute to age-related vascular diseases (Min et al, 2009). Interestingly, homozygous mice deficient for AT1A grow-up normally and outlive their wild-type littermates by 26% (Benigni et al, 2009). These AT1A−/− mice also develop fewer aortic atherosclerotic lesions and less cardiac injury during aging. Oxidative stress is reduced in cardiomyocytes, aortas and kidneys from mice lacking AT1A receptor with respect to aged wild-type mice and ultrastructural analysis of mitochondria in proximal renal tubular cells show that AT1A−/− mice have an increased number of mitochondria (Benigni et al, 2009). Extension of lifespan is associated with upregulation of pro-survival genes including nicotinamide phosphoribosyltransferase (Nampt) and Sirtuin 3 (Sirt3) (but not Sirtuin 1) in the kidney from these mice (Benigni et al, 2009). Importantly, candesartan prevents Ang II-induced Nampt and Sirt3 mRNA down-regulation in cultured tubular epithelial cells indicating a possible molecular link between Ang II, AT1A and these survival genes. The effects in longevity observed in AT1A-deficient mice are likely the consequence of reduced mitochondrial damage due to attenuation of oxidative stress and the increased expression of Nampt and Sirt3 survival genes (Fig 3). Our results shed light on early reports that showed favourable effects of chronic long-term Ang II inhibition by either ACEi or ARBs in protecting rats from the deleterious effects of aging on cardiovascular system and prolonging life span (Basso et al, 2007). Other studies implicate the AT1 receptors in ROS-induced damage and aging; old mice lacking AT1 receptors also do not develop age-related cerebral circulation damage caused by the accumulation of oxygen radicals (Modrick et al, 2009). The inhibition of RAS reverses age-related advanced myocardiac hypertrophy and fibrosis in aged spontaneously hypertensive rats, and the protective effect presumably involves the attenuation of Ang II-mediated oxidative stress, as documented by reduced expression of NAD(P)H oxidative components in the hearts of aged animals (Ito et al, 2007). Chronic treatment with ACEi or ARB reduces kidney damage associated with age, and the beneficial effect of RAS inhibition involves the preservation of renal mitochondria (Ferder et al, 2002). Enalapril and losartan treatments prevent the age-associated decline in the renal mitochondrial capacity for energy production and attenuate the age-associated increase in mitochondrial oxidant production (de Cavanagh et al, 2003). RAS inhibition exerts a similar protective effect in the liver from old rats through the maintenance of an adequate mitochondrial function due to enhanced expression of genes responsible for mitochondrial respiration and biogenesis (de Cavanagh et al, 2008).

Angiotensin II revisited: new roles in inflammation, immunology and aging
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Serum ACE levels have been found to be significantly elevated in AIDS patients, patients in the intermediate stage of HIV infection, and patients with Pneumocystis carinii pneumonia.

Thiamine attenuates hypertension and metabolic abnormalities in spontaneously hypertensive rats (SHRs). Thiamine repletion downregulates the expression of angiotensinogen (−80%), ACE (−77%), and angiotensin type 1 receptor (−72%) mRNAs in SHRs.34 These observations suggest that thiamine affects ACE activity in HIV-infected patients.

The role of thiamine in HIV infection - ScienceDirect
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LeeLemonoil

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B1 is one of Peats Corona-Recommendations.

Thanks for the quality posts once again @md_a

Did you do medical training / have med-Duty in your Professional life ?
 
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md_a

md_a

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B1 is one of Peats Corona-Recommendations.

Thanks for the quality posts once again @md_a

Did you do medical training / have med-Duty in your Professional life ?
Thank you, I'm only a seaman, but I stopped navigation and now I work as a videographer, but I was out of work because of the `virus`. I have no medical training, just what I have read about Ray Peat stuff since 2009.
 

S.Seneff

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Without energetic immune system due to thiamine defficiency, the body try desesperately to kill pathogens with oxidative stress ?
 

peateats1

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Anyone know of vitamins that completely block angiotensin?
I know of vitamin d but I think my vitamin d status is good and I'm still having trouble with angiotensin.(poor circulation)
 
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Peatness

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