Key Benefits

• Check nitric oxide balance for healthy blood vessel function.
• Spot early endothelial stress that can raise long-term cardiovascular risk.
• Explain contributors to hypertension or arterial stiffness linked to reduced nitric oxide.
• Guide intensity of lifestyle and risk-factor management to improve endothelial function.
• Track improvement after exercise, weight loss, or smoking cessation targeting vascular health.
• Flag elevated risk in chronic kidney disease, where ADMA commonly accumulates.
• Clarify erectile concerns related to endothelial dysfunction and reduced nitric oxide.
• Best interpreted with L-arginine or L-arginine/ADMA ratio and kidney function.

What is ADMA?

ADMA is a small, naturally occurring molecule made during normal protein turnover. It forms inside cells when arginine pieces within proteins are tagged with two methyl groups and later released as those proteins are broken down. This methyl tagging (protein arginine methylation) is done by specific enzymes (protein arginine methyltransferases, PRMTs). Once freed, ADMA circulates in blood and tissues, and the body normally keeps it in check by breaking it down with enzymes (dimethylarginine dimethylaminohydrolase, DDAH) and removing it via the kidneys.

ADMA acts as an internal brake on nitric oxide production. It competes with the usual substrate, L-arginine, at the enzyme that makes nitric oxide (nitric oxide synthase, NOS), reducing nitric oxide (NO) availability. Because NO is the key signal that relaxes blood vessels, limits platelet and white-cell sticking, and supports healthy microvascular flow, ADMA helps set vascular tone and endothelial behavior. In essence, it reflects the balance between protein methylation and clearance and serves as a window into the body’s NO signaling capacity.

Why is ADMA important?

ADMA (asymmetric dimethylarginine) is the body’s internal “brake” on nitric oxide production. Because nitric oxide governs vessel tone, blood flow, platelet quieting, oxygen delivery, insulin signaling, and kidney filtration, ADMA becomes a whole‑system readout of endothelial health. Higher ADMA means less nitric oxide and stiffer, under‑perfused tissues; lower ADMA within normal supports flexible, well‑perfused organs.

Most adults fall within a relatively tight reference range, with values near the lower end generally considered more favorable for vascular function. Levels tend to creep up with age; children usually run lower. In healthy pregnancy, ADMA declines to help open the placental circulation.

When ADMA is low, it reflects minimal blockade of nitric oxide synthase and robust endothelial signaling. People are often asymptomatic, with easier vasodilation—sometimes manifesting as naturally lower blood pressure, warm extremities, or better exercise tolerance. In pregnancy this physiology supports placental flow; in youth it aligns with resilient vessels.

When ADMA is high, nitric oxide generation is restrained. Arteries become less compliant, microcirculation underperforms, and kidneys filter less efficiently. This can track with higher blood pressure, exertional fatigue, cold hands and feet, chest pressure in coronary disease, and erectile difficulties in men. Elevated ADMA is seen in chronic kidney disease, diabetes and metabolic syndrome, smoking exposure, and systemic inflammation, and is associated with higher risks of heart attack, stroke, heart failure, and adverse pregnancy outcomes such as preeclampsia.

Big picture: ADMA sits at the crossroads of the nitric oxide pathway, oxidative stress, and renal clearance, interacting with L‑arginine availability, homocysteine, and lipid and inflammatory status. As a marker of endothelial integrity, it helps connect day‑to‑day vascular function with long‑term cardiometabolic and renal outcomes.

What Insights Will I Get?

ADMA (asymmetric dimethylarginine) is an endogenous blocker of nitric oxide synthase, the enzyme that makes nitric oxide (NO). Because NO governs vascular tone, microcirculation, mitochondrial efficiency, insulin signaling, platelet reactivity, and endothelial immunity, ADMA functions as a systems-level marker of NO bioavailability and endothelial health. It is produced during protein turnover and cleared by DDAH enzymes and the kidneys.

Low values usually reflect strong DDAH activity and renal clearance with lower NOS inhibition, supporting flexible blood vessels, steady blood pressure regulation, and good tissue perfusion. They are common in younger adults and during healthy pregnancy when NO signaling rises. Very low results are rarely pathologic on their own.

Being in range suggests balanced NO-cGMP signaling and stable endothelial function. Across studies, values toward the low end of the reference interval tend to associate with better cardiometabolic profiles and vascular resilience.

High values usually reflect reduced degradation or clearance (notably kidney impairment), increased production, or DDAH inhibition by oxidative stress, inflammation, or elevated homocysteine. The result is less NO, endothelial dysfunction, higher vascular resistance, and impaired microvascular flow, with downstream effects on exercise capacity, cognition (via cerebral perfusion), and sexual or placental blood flow. Higher ADMA is more common with aging, hypertension, diabetes, metabolic syndrome, dyslipidemia, and chronic kidney or liver disease. In pregnancy, rising ADMA is linked to preeclampsia risk. Men may run slightly higher than women.

Notes: Interpretation is assay- and lab-dependent (mass spectrometry methods are most specific). Renal function, inflammatory status, thyroid status, and sex hormones can shift ADMA. Consider concurrent arginine and homocysteine when available to contextualize NO pathway balance.