Blood pressure is not usually the first thing people associate with a bile acid, but TUDCA turns up in a surprising number of hypertension studies. The reason is that researchers use it as a tool: it is one of the standard chemical chaperones for relieving endoplasmic reticulum (ER) stress, and several labs wanted to know whether ER stress helps keep blood pressure high. In spontaneously hypertensive rats, two weeks of TUDCA lowered systolic pressure and normalized how small arteries responded to pressure [1]. Similar results came from salt-and-hormone models and from angiotensin II models in rats and mice. The human picture is much thinner. No randomized trial has measured blood pressure as an outcome in people taking TUDCA, and the two small human studies of blood vessel function point in different directions [2] [3]. This page sets out what was tested, how the compound was given, and why none of it is a reason to change blood pressure treatment.
Key Takeaways
- In spontaneously hypertensive rats, TUDCA at 100 mg/kg/day for two weeks lowered systolic blood pressure and reduced ER stress markers in the arteries [1].
- In angiotensin II-infused rats, TUDCA given by injection lowered blood pressure by about 20 mm Hg compared with angiotensin II alone [4].
- One mouse study found angiotensin II hypertension was abolished when TUDCA was infused directly into the brain’s fluid spaces, which points to the brain as one site of action, not the gut [5].
- In 12 healthy young adults, a single 1500 mg oral dose prevented the drop in artery dilation that a glucose drink normally causes [2], but a second 12-person study found no protection against a different vascular injury [3].
- No randomized controlled trial has tested TUDCA for hypertension or measured blood pressure as an outcome in people.
Why Hypertension Researchers Reach for TUDCA
The endoplasmic reticulum is where cells fold the proteins they make. When folding falls behind demand, the cell switches on a set of alarm signals called the unfolded protein response. Markers such as GRP78, CHOP, PERK and IRE1 rise when that happens, and researchers measure them as a readout of ER stress. TUDCA is a hydrophilic bile acid that acts as a chemical chaperone and reduces those signals in many tissues.
That makes it a convenient probe. If a lab suspects ER stress is helping drive a disease, giving TUDCA and watching what happens is one of the quickest tests. In the hypertension literature, TUDCA often appears beside a second chaperone, 4-phenylbutyric acid, and sometimes in place of it. The point of most of these studies was to ask whether ER stress matters in high blood pressure, not to develop TUDCA as a blood pressure drug. That framing is worth keeping in mind when a result is quoted as evidence that TUDCA lowers blood pressure.
The Rat and Mouse Studies, Model by Model
Spontaneously hypertensive rats. This is a genetic strain that develops high blood pressure on its own. Male rats were treated with TUDCA at 100 mg/kg/day for two weeks and compared with untreated hypertensive rats and normal Wistar Kyoto rats [1]. Systolic pressure fell in the treated group. Arteries from untreated hypertensive rats showed more pressure-induced tone and weaker endothelium-dependent relaxation, and TUDCA normalized both. ER stress markers including Bip, ATF6, CHOP, IRE1, XBP1, PERK and eIF2α were raised in the hypertensive rats and reduced by treatment [1].
DOCA-salt rats. In this model, rats lose one kidney and receive a mineralocorticoid hormone plus salt water, which drives blood pressure up over 12 weeks. One research group gave TUDCA at 150 mg/kg/day by intraperitoneal injection for the final four weeks [6]. Systolic pressure fell, endothelial function improved, plasma nitric oxide rose, and ER stress proteins in the vessels moved back toward normal [6]. The same group reported from the same model that TUDCA reversed the rise in systolic pressure and ventricular contractions and reduced cardiac inflammation and fibrosis [7], and that it lowered systolic pressure and improved liver inflammation and fibrosis [8]. These three papers come from one research program using one model, so they are best read as one line of evidence measured in different organs, not three independent replications.
Angiotensin II models. Angiotensin II is a hormone that raises blood pressure, and infusing it is a standard way to produce hypertension in animals. In rats given angiotensin II for 28 days, injected TUDCA at 100 mg/kg/day lowered blood pressure by about 20 mm Hg compared with angiotensin II alone, and reduced apoptosis, collagen and fibrosis in the aorta [4]. A mouse study reported that TUDCA lowered blood pressure in angiotensin II-infused mice and in mice lacking the energy-sensing enzyme AMPK-α2, whose arteries constrict abnormally [9].
Diabetes plus hypertension. In type 2 diabetic rats with surgically induced hypertension in one kidney, blood pressure after six weeks averaged 135 mm Hg with TUDCA against 151 mm Hg without it, and TUDCA reduced albumin in the urine, and lessened glomerular injury [10]. A separate study in diabetic db/db mice found that TUDCA at 250 mg/kg/day by injection for four weeks reduced arterial stiffness and improved endothelium-dependent dilation in mesenteric arteries [11]. That study measured stiffness and dilation, not blood pressure.
The Brain Result Changes How to Read the Rest
One of the most cited papers in this area did not deliver TUDCA to the body at all. In mice given a slow, low-dose angiotensin II infusion, hypertension developed over time and was abolished when TUDCA was infused into a lateral cerebral ventricle [5]. The researchers traced the effect to the subfornical organ, a small brain region that sits outside the blood-brain barrier and is rich in angiotensin II receptors, and they could reproduce the protection by raising the ER chaperone GRP78 in that region alone [5].
This matters for anyone thinking about capsules. It shows that at least part of the blood pressure effect in these models runs through the brain, and the brain was reached directly with a cannula. Most of the other rodent studies gave TUDCA by injection into the abdomen. None of the hypertension studies above tested the oral route that a supplement uses, so they do not show how much of a swallowed dose would reach the vessels, the kidney or the brain.
What Has Been Measured in People
Two small human studies used oral TUDCA and looked at blood vessels, not blood pressure. Both measured flow-mediated dilation, an ultrasound test of how well the brachial artery widens when blood flow increases. It is a marker of endothelial health, and a lower value is a bad sign.
In the first, 12 young healthy adults (seven men, five women) took 1500 mg of TUDCA or placebo in a single-blind randomized crossover before drinking a glucose load [2]. On placebo, dilation fell by 32% at 60 minutes and 28% at 120 minutes. On TUDCA, the changes were -4% and +0.3%, which were not significant [2]. Blood glucose and insulin were not altered by TUDCA, and oxidative stress markers did not change in either condition [2].
In the second, 12 young adults took a placebo or 1,500 mg of TUDCA before 20 minutes of arm ischemia followed by reperfusion [3]. Ischemia-reperfusion reduced dilation in both conditions, from 5.0% to 3.5% on placebo and from 5.6% to 3.9% on TUDCA, with no difference between them [3]. The same study measured what reached the blood: TUDCA ingestion raised circulating TUDCA by 145 ng/ml and its unconjugated form, ursodeoxycholic acid, by 560 ng/ml [3]. After the oral dose, UDCA rose further in the blood than intact TUDCA did.
So one study found a protective effect on a short-term glucose challenge and one found nothing on a different type of injury. Neither enrolled people with hypertension, neither lasted more than a single visit per condition, and neither measured blood pressure.
A Finding That Points the Other Way
Bile acid levels in the body are not a simple more-is-better story. In rats made hypertensive with a high-salt diet, levels of four bile acids rose, and tauroursodeoxycholic acid was one of them [12]. Those raised levels correlated positively with the vascular injury markers endothelin-1 and TNF-α [12]. This is a correlation in a different model, not evidence that TUDCA causes harm, and it does not cancel the treatment studies. It is a reminder that a bile acid can rise as part of a disease process, and that the body’s own levels do not tell you what a supplement dose will do.
What This Means in Practice
The animal evidence is consistent enough to say that ER stress takes part in several forms of experimental hypertension, and that blocking it with TUDCA lowers pressure in rats and mice. That is a genuine research finding. It is not the same as showing that a TUDCA supplement lowers blood pressure in people, and there is no trial that tests that.
Blood pressure medicines have outcome data on strokes, heart attacks and deaths behind them. Replacing or reducing them on the strength of rodent results would be a poor trade. If you take TUDCA for another reason and also have high blood pressure, keep measuring it the usual way and tell your prescriber what you take, since TUDCA affects bile acid handling and its interactions with blood pressure drugs have not been studied in trials. Anyone who notices a real change in their readings after starting any supplement should report it rather than adjust medication on their own.
Bottom Line
TUDCA lowered blood pressure in spontaneously hypertensive rats [1], in DOCA-salt rats [6], and by about 20 mm Hg in angiotensin II rats [4], mostly given by injection and once straight into the brain [5]. In people, no study has measured blood pressure. A single 1500 mg dose protected artery dilation during a glucose challenge in 12 healthy adults [2], while a matching study of ischemia-reperfusion injury found no effect [3]. The research supports ER stress as a player in hypertension. It does not support TUDCA as a blood pressure treatment.
Frequently Asked Questions
Does TUDCA lower blood pressure?
In rodents, yes, in several models: TUDCA lowered systolic pressure in spontaneously hypertensive rats [1] and reduced pressure by about 20 mm Hg in angiotensin II rats [4]. No human study has measured blood pressure as an outcome, so whether a supplement dose does the same in people is unknown.
Can I take TUDCA instead of my blood pressure medication?
No. There is no human trial of TUDCA for hypertension, and the animal studies mostly injected it rather than giving it by mouth [6]. Blood pressure drugs have outcome data that TUDCA does not. Any change to your treatment belongs with your prescriber.
Is there any human evidence on TUDCA and blood vessels?
Two small studies. In 12 healthy adults, 1500 mg of TUDCA prevented the fall in artery dilation after a glucose drink [2]. In another 12 adults, the same dose did not protect against ischemia-reperfusion injury, and blood UDCA rose more than intact TUDCA [3].
References
- Choi SK, et al. Inhibition of endoplasmic reticulum stress improves coronary artery function in the spontaneously hypertensive rats. Scientific Reports (2016). PMID 27550383
- Walsh LK, et al. Administration of tauroursodeoxycholic acid prevents endothelial dysfunction caused by an oral glucose load. Clinical Science (2016). PMID 27503949
- Hemingway HW, et al. Effect of endoplasmic reticulum stress on endothelial ischemia-reperfusion injury in humans. American Journal of Physiology: Regulatory, Integrative and Comparative Physiology (2020). PMID 33074709
- Spitler KM, et al. Endoplasmic reticulum stress contributes to aortic stiffening via proapoptotic and fibrotic signaling mechanisms. Hypertension (2014). PMID 24379182
- Young CN, et al. ER stress in the brain subfornical organ mediates angiotensin-dependent hypertension. Journal of Clinical Investigation (2012). PMID 23064361
- Han S, et al. Inhibition of endoplasmic reticulum stress protected DOCA-salt hypertension-induced vascular dysfunction. Vascular Pharmacology (2019). PMID 30458302
- Bal NB, et al. Hypertension-induced cardiac impairment is reversed by the inhibition of endoplasmic reticulum stress. Journal of Pharmacy and Pharmacology (2019). PMID 31579948
- Bal NB, et al. Reversal of deleterious effect of hypertension on the liver by inhibition of endoplasmic reticulum stress. Molecular Biology Reports (2020). PMID 32072406
- Liang B, et al. Aberrant endoplasmic reticulum stress in vascular smooth muscle increases vascular contractility and blood pressure in mice deficient of AMP-activated protein kinase-α2 in vivo. Arteriosclerosis, Thrombosis, and Vascular Biology (2013). PMID 23288166
- Wang Z, et al. Synergistic Interaction of Hypertension and Diabetes in Promoting Kidney Injury and the Role of Endoplasmic Reticulum Stress. Hypertension (2017). PMID 28348018
- Battson ML, et al. Tauroursodeoxycholic Acid Reduces Arterial Stiffness and Improves Endothelial Dysfunction in Type 2 Diabetic Mice. Journal of Vascular Research (2017). PMID 28930750
- Zeng B, et al. Bile Acid Metabolism Analysis Provides Insights into Vascular Endothelial Injury in Salt-Sensitive Hypertensive Rats. Metabolites (2024). PMID 39195548
These statements have not been evaluated by the FDA. This product is not intended to diagnose, treat, cure, or prevent any disease.
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.
