Posted on 11/24/2024 7:30:39 AM PST by ConservativeMind
Commonly prescribed drugs used to treat high blood pressure have been shown to, over time, wreck the kidneys' ability to filter and purify blood, but exactly how that dangerous side effect unfolded has been a riddle. Researchers say they've solved the mystery.
Researchers found that the drugs essentially rewire the kidneys to do something other than the important work of filtering blood. The kidneys start producing more of a hormone called renin; nerve endings grow excessively; cells lining the kidneys' tiny blood vessels get too large; scars form and spread; and inflammation sets in, which "can take a terrible toll on the kidney," according to a news release.
The result is a "silent but serious" vascular disease where the kidneys become zombie-like, changing into something unwanted and unwelcome while abandoning their critical duties.
Now that they know the cause, researchers say the next step is to figure out how to use the effective blood pressure drugs known as renin-angiotensin system inhibitors—often called RAS inhibitors—while stopping the kidney-damaging effects.
RAS inhibitors, which include the generics enalapril, lisinopril, ramipril and others, are commonly prescribed when a patient is first diagnosed with high blood pressure, a condition that affects 120 million people in the U.S., or nearly half of the adult population, according to the Centers for Disease Control and Prevention. High blood pressure can cause heart attacks, strokes and other vascular diseases.
The drugs work by relaxing blood vessels and allowing blood to flow more freely. The medicines are widely used and generally considered safe, researchers say, but are not without risk. Doctors have long warned patients that certain blood pressure medications could cause kidney damage, often first noticed as a reduction in the frequency of urination, swelling in the legs or feet, or seizures.
(Excerpt) Read more at medicalxpress.com ...
Helps explain why people who control their blood pressure to the level demanded by the ‘medical community’ don’t seem to live any longer (or even as long) as people who are somewhat (but not excessively above) those guidelines - as the people who are not controlling BP as tightly take far less meds (usually some meds, but not nearly as much).
Bad news: Eat right. Take the right medications. Get plenty of exercise. YOU WILL STILL DIE OF SOMETHING !
It’s so disappointing to obsess with a healthy lifestyle, exercise regularly, eat only healthy foods, and ultimately still find yourself in the hospital, DYING (of nothing).
There must be a tombstone somewhere with the inscription: “Being dead now anyway, I wish I had eaten a lot more french fries and greasy hamburgers.”
MD’s are the snake oil salesmen that they accused others of being in the 1930’s - BP medicine is derived (sometimes synthesized) using the venow of a pit viper, (you know the deadliest venom known) but it does thin the blood!
venom - typo above...
“Used to be systolic over 150. Then 140. Now they want people of every age to be at 120. “
Blood sugar level recommendations did the same thing.
The lowered numbers mean only ONE thing. Now MORE PEOPLE qualify for these drugs. PERIOD!
I continue to go by the old standards as I think they are more accurate.
I take one prescription drug, lisinopril, which is on the naughty list. Also take those vitamins and others
My friend’s Naturopath reccomended Carditone made by Ayush Herbs and available at AMZ. My blood pressure is usually perfect. 11/76 at doctor’s office last time I went. The more I walk, the better it gets.
Anyway, exercise and Carditone are, I believe, contributing a lot to my health. My MD says he’s never seen anyone as healthy as I am at my seriously advanced age.
Everyone needs to do their homework & not trust the Medical Industrial Complex or Big Pharma; case closed.
High Blood pressure: Why we shouldn’t worry about the number - Dr. Sanjay Gupta
https://www.youtube.com/watch?v=QXE3SO05hxw&t=37s
York Cardiology
https://www.youtube.com/@YorkCardiology
Circulation Research
RESEARCH LETTERTransformation of the Kidney into a Pathological Neuro-lmmune-Endocrine Organ
Manako Yamaguchi, Lucas Ferreira de Almeida, Hiroki Yamaguchi, Xiuyin Liang, Jason P. Smith, Silvia Medrano, Maria Luisa S Sequeira-Lopez, R. Ariel Gomez
Hypertension affects over 1.3 billion people, and it is a major contributor to death and morbidity from cardiovascular disease and stroke. iRAS (inhibitors of the renin-angiotensin system) are used widely and effectively to treat hypertension. However, chronic stimulation of the renin cells, with iRAS or deletion of the renin gene, leads to concentric hypertrophy of the kidney arterioles’ characterized by (1) numerous and enlarged renin cells that surround and encroach the vessel walls, (2) concentric accumulation of small and immature smooth muscle cells (SMCs), and (3) surrounding each arteriole, a cuff of inflammatory cells and fibrosis. Ablation of renin cells with diphtheria toxin prevents the arterial disease indicating that renin cells per se cause the disease. What prompts renin cells to adopt an invasive embryonic-secretory phenotype is unknown. Because renin cells are exquisitely innervated and responsive to sympathetic discharge, we hypothesized that their transformation to an embryonic-secretory phenotype along the renal arterial tree leads to hyperinnervation, accumulation of numerous, immature SMCs, and perivascular immune cell infiltration resulting in a silent but serious vascular disease.
To test this hypothesis, we used 2 mouse models of RAS (renin-angiotensin system) inhibition: (1) Ren***; Ren1***; Ren26R**** mice and (2) SMMHQ******; R26R******; Ren1**** mice. In the first model, the renin gene is deleted and the Renin*** cells are labeled with green fluorescent protein (GFP). The SMCs are stained with a fluorescently labeled anti-alpha-smooth muscle actin (aSMA) antibody. In the second model, mice are
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injected with tamoxifen at 2 months of age and treated with captopril for 6 months. Here, SMCs are labeled with tdTomato, while renin cells are labeled with yellow fluorescent protein (YFP). We performed tissue-clearing and 3-dimensional imaging of kidneys from both models. Axons were stained by a fluorescently labeled anti-tublin-03 (TUBB3) antibody. In control mice, axon branches run along the renal vascular tree, reach the renin cells, and extend toward the glomeruli (Figure [A]). Both iRAS interventions resulted in marked hyperinnervation of a distorted and hypertrophic kidney vasculature. In Ren1***; Ren1***; R26R**** mice, axons became thicker and tightly bound with numerous branches around hypertrophic GFP-labeled Reni*** cells that surrounded the thickened vessels and extended toward the glomeruli (Figure [A]). A similar hypertrophy and hyperinnervation of the kidney arterioles were observed after a 6-month treatment with captopril (Figure [A]). Immunostaining for tyrosine hydroxylase in both models confirmed that the hyperinnervation was composed of sympathetic fibers (Figure [B]).
To determine the factors responsible for the hyperinnervation, we examined the expression of neurogenesis-related genes in renin-lineage cells using single-cell RNA-seq from embryonic and adult FoxD1**; R26R**** mouse kidneys.(2) FoxD1* cells are progenitors for all the mural cells of the kidney vasculature, including renin precursor cells, which differentiate into reninproducing juxtaglomerular cells, SMCs, mesangial cells, and pericytes. Nerve growth factor (NGF), which is . . . . . . . . .
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Key Words: arterioles ■ hypertrophy ■ mmune system ■ kidney ■ myocyte, smooth musde ■ neurons ■ renin-angiotensin systemCirculation Research. 2024;135:1025-1027. DOI: 10.1161/CIRCRESAHA 124.325305
They only did that to prove the cause.
It’s a very common approach to identify genes or other intrinsic issues you can’t have a human or human fetus do, and we don’t want human fetuses in research.
Drink a glass of water for every cup of coffee (whose substances are good for other reasons) that supplies enough liquid to keep your circulatory system properly. Otherwise, the coffee's diuretic activity will cause you to to excrete more water (and its electrolytes) than the amount in the coffee. Without the extra water, your body will adjust a lower blood volume to adapt to its lower total amount of electrolytes to keep the concentration constant.
Lower blood volume causes the heart to pulse faster to get enough nutrients in to your cells and waste out from them.
If you want to restore blood volume from the harmful low-volume condition while keeping electrolytes at the body's self-governed constant level, drink a cup or a pint of pediatric electrolyte, whereupon your body will take in and keep enough water to keep the blood volume at the optimum level, at which point the blood pressure and pulse rate will also be optimized.
The right amount to fill will not over-pressurize the circulatory system.
+1
Steve86, this is _not_ to criticize what you wrote, but...
To everyone, a caution around ChatGPT and other AI chat bots: please always double-check all answers it provides, with Internet search engines! Also, consider asking ChatGPT to provide references, and to “explain things step-by-step” - so you can verify its responses.
Please sanity check EVERYTHING it gives you! It’s a tool that will blithely spew out plausible garbage.
I do. And have a good sense for ferreting out bogus info.
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