What is behind High Blood Pressure
Blood pressure — the force of blood against the vessel wall, a master cardiovascular gauge. Evidence A — Human trial evidence.
The pressure and fluid-balance system. It has two opposing arms: the classical AT1R axis drives inflammation and stiffening, while the ACE2/Ang-(1-7)/Mas axis actively opposes it. A single arrow into raas averages two systems that fight each other. Evidence A — Human trial evidence.
Nitric-oxide blood-vessel relaxation and flow. Evidence A — Human trial evidence.
The master inflammatory switch — indispensable to defend against threat, corrosive when it never stands down. Evidence B — Preclinical.
Arterial stiffness — pulse wave velocity, central pressure and pulse pressure.
Calcium-channel mediated tone in vascular smooth muscle — how tightly the vessel wall grips. Evidence B — Preclinical.
Gut microbial metabolites — short-chain fatty acids, tmao and community composition. Evidence B — Preclinical.
Hydrogen sulfide, which alongside nitric oxide and carbon monoxide relaxes the muscle of blood vessels. Evidence B — Preclinical.
Dietary nitrate, reduced by oral bacteria to nitrite and then to nitric oxide. Blood-pressure lowering is its best-replicated outcome. Antibacterial mouthwash interrupts the first step — the pathway depends on a bacterial population most people never consider.
Evidence on these pathways
Blood Pressure → Cardiovascular Health. “The randomised, double-blind, placebo-controlled Systolic Hypertension in Europe trial (Syst-Eur 1) proved that blood pressure (BP) lowering therapy starting with nitrendipine reduces the risk of cardiovascular complications in elderly patients with isolated systolic hypertension.” — How well can blood pressure be controlled? Progress report on the Systolic Hypertension in Europe Follow-Up Study (Syst-Eur 2). Current Controlled Trials in Cardiovascular Medicine, 2001, 2(6), 298–306 (the DOAJ record prints the issue and pages; the present-day BioMed Central page shows the journal as Trials, article 298). doi:10.1186/cvm-2-6-298
NF-κB → CD38 NADase. “Regulation of CD38 expression in HASM cells involves the transcription factor NF-κB, and glucocorticoids inhibit this expression through NF-κB-dependent and -independent mechanisms.” — Regulation of the cd38 promoter in human airway smooth muscle cells by TNF-α and dexamethasone. Respiratory Research, 2008, vol 9, 26. doi:10.1186/1465-9921-9-26
NF-κB → COX-2 Induction. “Moreover, the nuclear factor kappa B (NF-κB) inhibitor BAY11‐7085 or the TLR4 neutralizing antibody markedly blocked PM2.5-induced IL-6 and COX-2 expression.” — PM2.5 exposure upregulates pro-inflammatory protein expression in human microglial cells via oxidant stress and TLR4/NF-κB pathway. Ecotoxicology and Environmental Safety, 2024, vol 277, article 116386. doi:10.1016/j.ecoenv.2024.116386
NF-κB → Kynurenine Pathway. “Treatment of vaccinated DCs with pharmacological NF-κB inhibitors ACHP or DHMEQ significantly inhibited IDO1 biosynthesis, suggesting a role for NF-κB signaling in vaccine up-regulation of dendritic cell IDO1.” — Induction of Indoleamine 2, 3-Dioxygenase in Human Dendritic Cells by a Cholera Toxin B Subunit—Proinsulin Vaccine. PLoS ONE, 2015, volume 10, e0118562. doi:10.1371/journal.pone.0118562
Formulas that act on these pathways
Acts on 6 of these pathways: Blood Pressure, Renin-Angiotensin, Arterial Stiffness / PWV, Vascular Calcium Tone, Gut Microbial Metabolites, Dietary Nitrate.
Acts on 2 of these pathways: NF-κB, Gut Microbial Metabolites.
Acts on 2 of these pathways: Blood Pressure, Arterial Stiffness / PWV.
Acts on 2 of these pathways: Blood Pressure, NF-κB.
What this page does not claim
This page names the pathways involved and the published evidence on each. It does not claim that any formula treats, cures or prevents High Blood Pressure. A pathway opens here only on graded, published evidence, under a standard fixed before the evidence was gathered, and every figure above carries its grade.
These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure or prevent any disease.