Lowers blood pressure
RAAS↓
Also searched as RAAS.
Acute vs chronic: the renin-angiotensin system defends blood pressure when you are dry or bleeding. Chronically active it is hypertension and cardiac remodeling — which is why blocking it is first-line therapy. Vital to hold pressure steady, damaging when chronically driven — you want it regulated, not overactive.
In depth
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.
What drives it
Stress & cortisol increases it.
10.3390/vetsci9100539 — SNS/renin-angiotensin review — sympathetic activation (a core stress response) stimulates renin release from juxtaglomerular cells via β1-adrenoceptors, activating the renin-angiotensin system. doi 10.3390/vetsci9100539 · PMID 1382170
Blood pressure hormone increases it.
Verbatim: 'It plays an essential role in the rate-limiting step of the renin-angiotensin-aldosterone system (RAAS), responsible for blood volume homeostasis and mean arterial blood pressure.'. PMC7152415
Sodium load reduces it.
Verbatim: 'During high sodium intake, the renin-angiotensin-aldosterone system is downregulated and nitric oxide signaling is upregulated in order to remain in sodium balance.' (10.1161/JAHA.117.006896). What was measured: Plasma aldosterone concentration, plasma renin concentration, intrarenal angiotensin II, intrarenal angiotensinogen, ACE activity, ENaC activity and sodium transporter abundance. doi 10.1161/JAHA.117.006896
What it drives
It increases Blood pressure.
Angiotensin II plays a critical role in both the acute and chronic regulation of blood pressure: it is a potent vasoconstrictor, stimulates adrenal zona glomerulosa to secrete aldosterone, alters renal sodium and water handling, enhances thirst and drives ADH release. Pathological high blood pressure is mediated principally by the AT1 receptor. PMID 10619573
It increases Supports heart function.
Angiotensin II activates fibroblasts and cardiac myocytes to promote cardiac remodeling, driving maladaptive myocardial hypertrophy and fibrosis; a local intracardiac renin-angiotensin system exists and is differentially expressed in pressure-overload and post-infarction remodeling (PMC9356743; PMID 7495212). The sign depends on duration: acute RAAS activation supports perfusion in low-output states, while sustained engagement drives adverse remodeling, heart-failure progression and arrhythmogenesis. And the therapy is population-specific: RAAS blockade improves mortality and hospitalization in systolic heart failure and acute MI but has not shown the same benefit in preserved ejection fraction. Provenance: previously cited PMID 8583476 could not be confirmed and has been replaced. PMID 7495212 · PMC9356743
It reduces Muscle.
Angiotensin II induces skeletal muscle wasting — the effect that muscle-specific IGF-1 was built to block. Angiotensin infusion reduces phospho-Akt in muscle, which disinhibits FoxO and drives the MuRF1/Atrogin-1 ubiquitin-proteasome program, and IGF1 transgenic mice ARE resistant to muscle atrophy induced by angiotensin treatment. What this adds: the renin-angiotensin system is usually read as purely cardiovascular. It is also a catabolic driver of muscle, which means a hormone system managed for blood pressure has a body-composition cost. The evidence is rodent infusion models and transgenic rescue; the human arm is inference from ACE-inhibitor observational data and is not claimed here. doi 10.1172/JCI22324 · PMC7564605
It reduces Cardiac output.
Neurohormonal dysregulation with angiotensin II, endothelin-1, and sympatho-adrenergic overactivation, which occurs in heart failure, stimulates ventricular cardiomyocyte hypertrophy and aggravates the cellular damage. And this is the rare case where the intervention arm is the standard of care: the understanding of the important role of neurohormonal activation in the pathophysiology of heart failure has paved the way for the current medical treatment to improve morbidity and mortality. Inappropriate activation of the renin-angiotensin-aldosterone system is also named among the routes by which metabolic disease produces cardiac stiffening and diastolic dysfunction. Note: the same hormone system is catabolic for skeletal muscle and hypertrophic for cardiac muscle — opposite structural effects in two striated tissues, both shown on the map. doi 10.1016/j.jacc.2006.07.007 · PMC10932393
It reduces Kidney.
Named across five reviews of the cardiovascular-renal-hepatic-metabolic syndrome as part of the shared mechanism set: ectopic fat accumulation triggered by metabolic reprogramming, oxidative stress and inflammation induced by energy overload, modified lipids, UREMIC toxins, and senescence, as well as insulin resistance pathways activated by pro-inflammatory factors and lipotoxic products, collectively exacerbate simultaneous hepatic and renal injury. doi 10.1038/s41581-026-01066-0 · PMC11725408
It reduces Insulin sensitivity.
insulin, fasting insulin, type 2 diabetes and blood lipids share one literature: heart, kidney, liver, and metabolic diseases share interlinked pathological mechanisms, including inflammation, oxidative stress, insulin resistance, and endothelial health issues. These four overlap by nature: fasting insulin is the level, insulin is the signaling, type 2 diabetes is the diagnosis and blood lipids are the substrate. The same driver legitimately reaches all four, and a reader should not mistake four arrows for four independent findings. doi 10.1038/s41581-026-01066-0 · PMC11725408
It increases Fasting insulin.
insulin, fasting insulin, type 2 diabetes and blood lipids share one literature: heart, kidney, liver, and metabolic diseases share interlinked pathological mechanisms, including inflammation, oxidative stress, insulin resistance, and endothelial health issues. These four overlap by nature: fasting insulin is the level, insulin is the signaling, type 2 diabetes is the diagnosis and blood lipids are the substrate. The same driver legitimately reaches all four, and a reader should not mistake four arrows for four independent findings. doi 10.1038/s41581-026-01066-0 · PMC11725408
It increases Type 2 diabetes.
insulin, fasting insulin, type 2 diabetes and blood lipids share one literature: heart, kidney, liver, and metabolic diseases share interlinked pathological mechanisms, including inflammation, oxidative stress, insulin resistance, and endothelial health issues. These four overlap by nature: fasting insulin is the level, insulin is the signaling, type 2 diabetes is the diagnosis and blood lipids are the substrate. The same driver legitimately reaches all four, and a reader should not mistake four arrows for four independent findings. doi 10.1038/s41581-026-01066-0 · PMC11725408
It reduces Lowers cholesterol.
insulin, fasting insulin, type 2 diabetes and blood lipids share one literature: heart, kidney, liver, and metabolic diseases share interlinked pathological mechanisms, including inflammation, oxidative stress, insulin resistance, and endothelial health issues. These four overlap by nature: fasting insulin is the level, insulin is the signaling, type 2 diabetes is the diagnosis and blood lipids are the substrate. The same driver legitimately reaches all four, and a reader should not mistake four arrows for four independent findings. doi 10.1038/s41581-026-01066-0 · PMC11725408
It reduces Hydration & electrolytes.
RAAS is the principal hormonal control of sodium and volume. PMC7005133
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.