Blood pressure is one of the few health numbers almost everyone can measure at home, so it is a natural question for anyone taking fisetin: does it do anything to it? The honest answer is that it lowered blood pressure in hypertensive rats, relaxed isolated arteries through several different routes, and has never been tested for blood pressure in a human trial.
This page walks through that animal and laboratory evidence, including one result where a higher dose made things worse, and explains why none of it is a reason to change how you manage high blood pressure.
Key Takeaways
- In spontaneously hypertensive rats, 28 days of oral fisetin lowered systolic, diastolic and mean arterial pressure [1].
- In isolated rat arteries, fisetin caused relaxation through nitric oxide, potassium channel, calcium channel and other pathways, and also through routes that do not need the endothelium [2].
- In a rat heart-injury study, 10 and 20 mg/kg helped but 40 mg/kg had a deteriorating effect [3].
- There are no human blood pressure trials of fisetin. Do not use it in place of prescribed treatment.
Important: This article describes animal and laboratory research and is not medical advice. Fisetin has not been shown to lower blood pressure in humans. If you take blood pressure medication, do not stop or change it, and ask your doctor before adding fisetin, because a combined effect has not been studied and fisetin can affect drug-metabolising enzymes.
The hypertensive rat study
The most direct evidence is a 2026 study in spontaneously hypertensive rats, a strain bred to develop high blood pressure and a standard model for testing antihypertensive drugs [1]. Daily oral fisetin for 28 days significantly reduced systolic, diastolic and mean arterial pressure. The authors report no overt toxicity based on body weight, blood counts and serum chemistry.
The same paper tested fisetin on isolated rings of rat aorta. It produced concentration-dependent relaxation through several mechanisms at once: nitric oxide and soluble guanylate cyclase signalling, cyclooxygenase and prostacyclin pathways, G-protein-coupled receptor signalling, opening of potassium channels and blocking of calcium channels, with Western blots supporting activation of the Akt/eNOS pathway [1]. The authors describe fisetin as a candidate for development as an antihypertensive adjunct, meaning an add-on, not a replacement.
Relaxation without the endothelium
Most talk about flavonoids and blood vessels centres on the endothelium, the thin lining that releases nitric oxide. An earlier study stripped that lining from rat aortic rings and found fisetin still relaxed contractions triggered by several different agents [2]. The mechanism traced to inhibition of Rho-kinase and MEK signalling in the smooth muscle itself.
A separate line of work found fisetin in mulberry leaves, which are traditionally drunk as tea in parts of Asia for their blood-pressure-regulating reputation. Fisetin was identified as an active component preventing abnormal contraction of human coronary artery smooth muscle cells, and the hydroxyl group at its C-3 position was crucial to the effect [4].
Together these suggest fisetin acts on blood vessels through more than one door. Our page on fisetin and vascular aging covers the separate question of senescent cells in the artery wall.
Heart and artery damage in hypertensive animals
High blood pressure damages the heart and arteries over time, and several studies looked at whether fisetin protects against that damage rather than at pressure itself. In hypertensive rats given 10 mg/kg orally twice a week for six weeks, fisetin reduced apoptosis in heart tissue and raised survival signalling through the IGF-IR, PI3K and Akt pathway [5].
In another hypertensive rat model, fisetin injected at 3 mg/kg daily for two weeks after a balloon injury to the carotid artery reduced the overgrowth of the vessel lining that causes arteries to re-narrow after angioplasty [6]. It did this by raising an antioxidant enzyme, PON2, through PPAR-gamma.
In mice given the chemotherapy drug doxorubicin, which ages blood vessels prematurely, intermittent oral fisetin at 100 mg/kg reversed endothelial dysfunction and aortic stiffening, partly by restoring nitric oxide availability [7]. Stiffer arteries are one of the main drivers of rising blood pressure with age, which is why that result is relevant here.
When a higher dose did worse
One study is worth singling out because it complicates the idea that more is better. Rats were given fisetin at 10, 20 or 40 mg/kg a day for 28 days before a drug-induced heart injury [3]. At 10 and 20 mg/kg, fisetin reversed the harmful changes in blood pressure and left ventricular pressure and reduced markers of heart damage. At 40 mg/kg it had a deteriorating effect similar to the injury group.
One rat study cannot set a human dose, and the injury model is not ordinary hypertension. But it is a concrete example of a dose-response that turns over, and it is a reason to be wary of protocols that assume a bigger dose is always a stronger effect. Our dosage guide sets out what the human trials have actually used.
Lung blood pressure is a separate question
Pulmonary arterial hypertension is high pressure in the arteries of the lungs, a different and serious disease. In rats with chemically induced pulmonary arterial hypertension, fisetin reduced right ventricular systolic pressure, right heart enlargement and remodelling of the lung vessels, apparently by suppressing TGF-beta1/Smad2/3 signalling [8]. That says nothing about ordinary blood pressure, and it is not a basis for anyone with the condition to use fisetin. Our page on fisetin and lung health covers the related fibrosis research.
What is missing
There are no human trials of fisetin and blood pressure. A 2021 review of flavonoids from Chinese herbal medicine reached the same conclusion for the flavonoid class as a whole: despite substantial animal evidence, it is not enough to support clinical use as an adjuvant or core drug, and more pharmacokinetic, clinical and safety work is needed [9].
One rat study of fisetin in a preeclampsia-like model, published in 2022, has since been retracted. It still turns up in searches, and it is not cited here.
There is also an interaction question nobody has studied. If fisetin does lower blood pressure in people, adding it to blood pressure medication could add to the effect. Fisetin also affects enzymes that clear many drugs, which our page on fisetin drug interactions explains. Until there is human data, the safe course is to keep managing blood pressure with proven treatment and tell your doctor about any supplement you add.
Common questions
Does fisetin lower blood pressure?
In spontaneously hypertensive rats, 28 days of oral fisetin lowered systolic, diastolic and mean arterial pressure [1]. It has not been tested for blood pressure in humans.
How does fisetin relax blood vessels?
In isolated rat arteries it acted through nitric oxide signalling, prostacyclin pathways, potassium channel opening and calcium channel blocking [1], and it also relaxed arteries with the endothelium removed [2].
Can I take fisetin with blood pressure medication?
The combination has not been studied. Ask your doctor first, and never stop or reduce prescribed blood pressure medication in favour of a supplement.
Is a higher fisetin dose better for the heart?
Not necessarily. In one rat study, 10 and 20 mg/kg protected against heart injury while 40 mg/kg had a deteriorating effect [3].
Does fisetin help pulmonary hypertension?
It reduced lung artery pressure and right heart enlargement in a rat model [8], but there is no human evidence, and the condition needs specialist treatment.
References
- Comprehensive vasodilatory and antihypertensive effects of 3,7,3′,4′-tetrahydroxyflavone (fisetin): Ex vivo and in vivo evidence. Biomed Pharmacother (2026). PMID 42341591
- Endothelium-Independent Effect of Fisetin on the Agonist-Induced Regulation of Vascular Contractility. Biomol Ther (Seoul) (2016). PMID 26759702
- Fisetin attenuates isoproterenol-induced cardiac ischemic injury in vivo by suppressing RAGE/NF-kB mediated oxidative stress, apoptosis and inflammation. Phytomedicine (2019). PMID 30668335
- Fisetin, a major component derived from mulberry (Morus australis Poir.) leaves, prevents vascular abnormal contraction. Biofactors (2022). PMID 34687255
- Protective effect of Fisetin against angiotensin II-induced apoptosis by activation of IGF-IR-PI3K-Akt signaling in H9c2 cells and spontaneous hypertension rats. Phytomedicine (2019). PMID 30668312
- Fisetin Alleviates Neointimal Hyperplasia via PPARgamma/PON2 Antioxidative Pathway in SHR Rat Artery Injury Model. Oxid Med Cell Longev (2021). PMID 33968295
- Fisetin Supplementation Attenuates Premature Vascular Aging Induced by Doxorubicin via Suppression of Cellular Senescence and Mitochondrial Oxidative Stress. Aging Cell (2026). PMID 42144546
- Fisetin alleviates pulmonary arterial hypertension by inhibiting the TGF-beta1/Smad 2/3 signaling pathway. Saudi Pharm J (2026). PMID 42347890
- The antihypertensive potential of flavonoids from Chinese Herbal Medicine: A review. Pharmacol Res (2021). PMID 34601080
These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure, or prevent any disease. Content is for informational purposes only and is not medical advice; consult a qualified healthcare provider before starting any supplement. As an Amazon Associate we earn from qualifying purchases.