I always thought it was the plaque reducing the diameter of the arteries which then increases blood pressure. But it is a self-reinforcing negative cycle as each begets the other.
I don’t know what the research says. My own experience has quite volatile blood pressure because when I apply a systemic change to mitochondria the homestatic feedback system in the cardiovascular system needs to adjust and that does not happen instantenously.
Also the vasodilation that occurs with drinking reduces arterial blood pressure quite substantially and this also then causes the homeostatic feedback system to adjust whilst the acetate is systemic and then it has to readjust when the acetate has gone (in around 2 days).
I would think, therefore, it is not the reduction of the diameter that matters so much, but the reduction in elasticity. I do think this will have an effect, but also higher BP can cause further endothelial problems.
I would be interested in reading any papers on this.
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My N=1 is a decade ago, I had a CAC of almost 500, so it’s sure to be higher now, and I have good blood pressure.
Perhaps this means I have plaque but decent elasticity?
That may be true.
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Here is a list of the causes of high blood pressure:
Biological Etiology of Hypertension
Essential hypertension (comprising 90–95% of clinical cases) does not have a singular biological cause. It is a polygenic, multifactorial syndrome driven by the dysregulation of interacting neurohormonal, vascular, and renal systems. Secondary hypertension (5–10% of cases) has discrete, identifiable etiologies, such as primary aldosteronism, pheochromocytoma, or renal artery stenosis.
Core Pathophysiological Mechanisms
Current clinical and scientific evidence identifies several primary, interacting biological drivers in essential hypertension:
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Endothelial Dysfunction and eNOS Uncoupling: The healthy endothelium regulates vascular tone via the production of nitric oxide (NO) by endothelial nitric oxide synthase (eNOS). In hypertension, elevated oxidative stress (reactive oxygen species, ROS) depletes tetrahydrobiopterin (BH4), a crucial eNOS cofactor. This leads to eNOS uncoupling, where the enzyme produces superoxide instead of NO, creating a pro-inflammatory, pro-thrombotic, and vasoconstrictive state.
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Renin-Angiotensin-Aldosterone System (RAAS) Overactivation: Chronic upregulation of the RAAS pathway leads to excessive Angiotensin II production. Angiotensin II is a potent vasoconstrictor that also stimulates aldosterone secretion (driving renal sodium and water retention) and activates NADPH oxidase, further exacerbating oxidative stress and endothelial dysfunction.
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Sympathetic Nervous System (SNS) Hyperactivity: A disturbed basal sympathetic tone, originating in the hypothalamus and influenced by cortical signaling, drives elevated resting peripheral resistance and cardiac output.This is often the most consistently observed abnormality in the early development of essential hypertension.
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Vascular Remodeling and Arterial Stiffness: Chronic mechanical stress and low-grade systemic inflammation lead to structural changes in resistance arteries. This includes vascular smooth muscle cell (VSMC) hypertrophy, extracellular matrix (ECM) alteration (collagen deposition, elastin degradation), and increased vascular stiffness, which creates a positive feedback loop sustaining high blood pressure.
Scholarly Debates and Knowledge Gaps
- The Initiating Event: A major ongoing debate in cardiovascular pathology is whether essential hypertension originates fundamentally as a renal defect in sodium excretion (the Guytonian hypothesis) or as a neurogenic disorder driven by central sympathetic overdrive.
- Data Needed: Full elucidation of the condition requires longitudinal multi-omic data (genomic, metabolomic, and proteomic) to track the exact sequence of molecular events that precede clinical blood pressure elevation in asymptomatic humans. Current animal models fail to fully replicate the complexity of human polygenic essential hypertension.
Longevity Implications and Actionable Pathways
Chronic hypertension accelerates biological aging by inducing vascular cellular senescence, driving mitochondrial dysfunction in VSMCs, and precipitating end-organ damage (renal failure, cognitive decline, cardiac hypertrophy). Intervening in these specific biological pathways is critical for extending human healthspan and lifespan.
Targeted molecular interventions include:
- Restoring eNOS Coupling: Compounds that replete BH4 or enhance NO bioavailability (e.g., L-citrulline, high-nitrate dietary protocols) can theoretically reverse early endothelial dysfunction and lower the trajectory of vascular aging.
- RAAS Inhibition with Pleiotropic Effects: Angiotensin II Receptor Blockers (ARBs), specifically Telmisartan, not only block RAAS but also act as partial agonists of PPAR-γ. This dual action improves insulin sensitivity and reduces vascular inflammation, offering actionable longevity benefits beyond simple hemodynamic control.
- Downregulating Systemic Inflammation and ROS: Interventions targeting upstream oxidative stress—such as specific mitochondrial antioxidants or Nrf2 activators—may prevent the initial oxidative trigger that uncouples eNOS and initiates vascular remodeling.
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Thanks @RapAdmin I’m thankful that the longevity interventions I’ve adopted have brought my SBP down from 120-130 to 100-110. Any further reduction is dangerous (risk of passing out) IMHO (and based on personal experience!)
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Methotrexate has been a staple treatment for rheumatoid arthritis for decades, valued for its ability to calm an overactive immune system and reduce painful joint inflammation. Now, researchers say it may deliver an unexpected bonus that matters far beyond the joints: lower blood pressure, a change that could translate into meaningful protection against heart attacks and strokes for some patients.
https://scitechdaily.com/common-arthritis-drug-found-to-lower-blood-pressure-and-boost-heart-health/