How Does Testosterone Affect Blood Pressure?

Testosterone’s relationship with blood pressure is not a simple up-or-down story. In men, naturally low testosterone levels are consistently linked to higher blood pressure, while in women, testosterone excess pushes blood pressure in the opposite direction. To complicate things further, supraphysiological doses of testosterone, like those seen with anabolic steroid abuse, raise blood pressure regardless of sex. The hormone works through multiple competing mechanisms at once, and whether it ultimately raises or lowers your blood pressure depends on the dose, your sex, and the rest of your metabolic health.

Low Testosterone and High Blood Pressure in Men

One of the most replicated findings in this area is that men with lower testosterone levels tend to have higher blood pressure. A study of over 1,100 men aged 30 to 79 found that those with hypertension had significantly lower testosterone than men with normal blood pressure, and both systolic and diastolic readings dropped in a stepwise fashion as testosterone levels rose through each quartile.¹ A more recent analysis of middle-aged and elderly men confirmed this pattern, finding that total testosterone, free testosterone, and sex hormone-binding globulin were all inversely associated with the prevalence of hypertension.²

The relationship holds even after accounting for age, which matters because testosterone naturally declines as men get older while blood pressure tends to climb. A study comparing hypertensive and normotensive men found about a 12% reduction in testosterone levels among those with high blood pressure, and a significant inverse correlation between testosterone and systolic blood pressure persisted in regression analysis.³ This doesn’t prove that low testosterone causes high blood pressure, but the consistency across studies and age groups suggests testosterone is at least a reliable marker of cardiovascular risk in men, and possibly a contributor.

Why the Pattern Reverses in Women

In women, the story is nearly opposite. Women with polycystic ovary syndrome (PCOS) who have elevated androgen levels show a clear positive link between testosterone and blood pressure. In one study of young women with PCOS, those with high bioavailable testosterone had roughly four times the odds of elevated blood pressure compared to those with lower levels, even after adjusting for obesity, insulin resistance, and other metabolic factors.⁴

Research into the mechanism behind this has pointed to testosterone’s effect on the renin-angiotensin system and baroreflex control. Women with the androgen-excess form of PCOS show higher levels of aldosterone and angiotensin-converting enzyme compared to controls, along with decreased baroreflex sensitivity. Importantly, these effects appear to be direct consequences of excess testosterone acting on the vascular system, independent of body weight and insulin resistance.⁵ So while normal male-range testosterone in men seems to be protective, female bodies exposed to excess testosterone appear to respond with higher blood pressure through mechanisms involving how the kidneys handle salt and how the body regulates moment-to-moment blood pressure.

Two Competing Mechanisms Inside the Blood Vessels

Part of the reason this topic is confusing is that testosterone acts on the cardiovascular system through at least two opposing pathways at the same time.

The first is direct vasodilation. In laboratory experiments, testosterone relaxes the smooth muscle of coronary arteries, and it does this even when the inner lining of the blood vessel has been stripped away. That rules out the standard explanation for vasodilation, which involves nitric oxide released from the endothelium. Instead, testosterone appears to act directly on the muscle layer of the artery wall, and higher concentrations produce more relaxation.⁶ In men with coronary heart disease, testosterone infused directly into coronary arteries increased both artery diameter and blood flow at every tested concentration.⁷ If this were the whole story, testosterone would clearly lower blood pressure.

The second pathway works through the kidneys. In animal models, testosterone activates the renin-angiotensin system, the hormonal cascade that tells kidneys to hold onto sodium and water. In salt-loaded rats, testosterone increased blood pressure and caused kidney injury through this mechanism.⁸ Reviews of experimental evidence conclude that exogenous testosterone can trigger production of endothelin and inflammatory cytokines involved in hypertension and kidney damage.⁹ These renal effects push blood pressure up. Whether blood pressure ultimately rises or falls under testosterone’s influence depends on which pathway dominates in a given individual, at a given dose, in a given metabolic context.

Testosterone Replacement Therapy and Blood Pressure

Given the opposing mechanisms, it’s not surprising that clinical trials of testosterone replacement in men with low levels have produced mixed results.

A registry study of hypogonadal men treated with long-acting testosterone undecanoate found meaningful blood pressure reductions over time. Men who were not taking any blood pressure medications saw median drops of about 12.5 mmHg in systolic and 8 mmHg in diastolic pressure. Untreated men in the same registry saw their blood pressure go up.¹⁰ That sounds dramatic, but registry studies have limitations. Patients who stick with long-term treatment may differ from those who drop out in ways that flatter the treatment group.

Shorter and more controlled studies have been less reassuring. A single-arm study of testosterone gel in 169 men found a small average increase in 24-hour systolic blood pressure of about 2 mmHg after 16 weeks, and the study could not rule out a clinically relevant drug effect on blood pressure, particularly in men who already had hypertension or diabetes.¹¹ A randomized trial in middle-aged and older men found that testosterone treatment increased 24-hour systolic blood pressure, with the combination of testosterone plus exercise producing the largest rise.¹²

The bottom line for men considering testosterone therapy is that it doesn’t guarantee a blood pressure improvement and may modestly raise it, especially in people with existing cardiovascular risk factors. Monitoring blood pressure during treatment is sensible.

Anabolic Steroids at Supraphysiological Doses

The ambiguity around therapeutic doses vanishes when testosterone is used at the much higher levels typical of anabolic steroid abuse. In bodybuilders using anabolic-androgenic steroids, systolic and diastolic blood pressure were significantly elevated, and the increase tracked with duration of use.¹³ A controlled study comparing current steroid users to non-users found that 24-hour systolic blood pressure averaged about 8 mmHg higher in the user group, and systolic hypertension was three times more common. Perhaps more worrisome, aortic stiffness was increased in both current and former users, suggesting lasting structural damage to the arteries.¹⁴

Reviews of the cardiovascular effects of steroid abuse confirm the association with elevated blood pressure and left ventricular thickening, changes that may persist after stopping.¹⁵ At supraphysiological levels, the kidney-mediated sodium retention pathway clearly overwhelms the direct vasodilatory effects, and the result is straightforward hypertension.

When Testosterone Is Removed Entirely

If high doses raise blood pressure, you might expect that eliminating testosterone would lower it. The opposite tends to happen. Androgen deprivation therapy (ADT), used to suppress testosterone in men with prostate cancer, is linked to increased hypertension risk. A nationwide cohort study found that men who received ADT were about 78% more likely to develop new-onset hypertension than matched controls, and those on combined androgen blockade faced nearly double the risk.¹⁶

The specific type of ADT matters. GnRH agonists and maximal androgen blockade are both associated with increased cardiovascular disease, while GnRH antagonists have not shown the same association in available data.¹⁷ The reasons likely include the metabolic consequences of testosterone elimination: weight gain, increased insulin resistance, and loss of the hormone’s direct vasodilatory effects. Testosterone sits in a metabolic web, and yanking it out has ripple effects that don’t all go in the same direction.

Arterial Stiffness as a Separate Channel

Blood pressure readings capture one snapshot of cardiovascular health, but arterial stiffness, how well your blood vessels flex with each heartbeat, is an independent predictor of heart disease. Testosterone appears to protect against stiffness. In older men without cardiovascular disease, higher free testosterone was strongly associated with greater arterial compliance and lower pulse-wave velocity, a standard measure of stiffness. The relationship held after adjusting for age, blood pressure, cholesterol, and body composition.¹⁸

On the flip side, men undergoing testosterone suppression for prostate cancer showed significantly stiffer aortas compared to age-matched controls, even after accounting for blood pressure differences.¹⁹ When hypogonadal men received testosterone treatment, their pulse-wave velocity dropped within 48 hours and stayed lower at three months.²⁰ This suggests that even when testosterone replacement doesn’t dramatically change blood pressure numbers, it may still benefit the cardiovascular system by keeping arteries more supple.

Testosterone, Insulin Resistance, and the Metabolic Connection

Testosterone doesn’t operate in a vacuum. In men, low testosterone is intertwined with abdominal obesity, insulin resistance, unfavorable blood lipids, and high blood pressure, the cluster known as metabolic syndrome. Testosterone deficiency may contribute to developing this syndrome, while the resulting states of high insulin and obesity further suppress testosterone production, creating a self-reinforcing cycle.²¹ This feedback loop means it’s often hard to tease apart whether low testosterone is raising blood pressure directly or whether both are consequences of the same underlying metabolic deterioration. In practice, both are probably true simultaneously.

Gender-Affirming Testosterone Therapy

Transgender men receiving testosterone as part of gender-affirming care represent another important population for understanding these effects. A systematic review of studies involving various testosterone formulations found that the majority did not show a significant change in systolic or diastolic blood pressure. Three studies reported systolic increases ranging from about 4 to 13 mmHg, while one reported a decrease of about 5 mmHg.²² The variability across studies likely reflects differences in formulation, dose, duration, and the baseline health of participants.

An interesting finding from adolescent transgender males is that puberty suppression with GnRH analogs (which lower both estrogen and testosterone) appeared to raise diastolic blood pressure, and adding testosterone restored it to previous levels.²³ This small pilot study hints that the complete absence of sex hormones may be worse for blood pressure than having testosterone present, echoing the pattern seen in androgen deprivation therapy for prostate cancer.

The Role of Aromatization

Some of testosterone’s cardiovascular benefits may not come from testosterone itself, but from estrogen. The body converts a portion of testosterone into estradiol through an enzyme called aromatase, and estradiol has well-established protective effects on blood vessels. In female rats, blocking aromatase raised blood pressure and caused markers of kidney injury, suggesting that the conversion of testosterone to estrogen plays a protective cardiovascular role.²⁴ This adds another layer of complexity: part of what looks like a “testosterone effect” on blood pressure may actually be an estrogen effect, and anything that disrupts aromatization, whether medications, aging, or genetic variation, could shift the balance toward higher blood pressure.

Genetics and the Androgen Receptor

Not everyone’s body responds to testosterone identically, and one reason is genetic variation in the androgen receptor itself. The androgen receptor gene contains a stretch of repeating DNA, the CAG repeat, and its length affects how sensitive tissues are to testosterone. Shorter repeats mean a more sensitive receptor. In a study of Chinese middle-aged and elderly men, those with fewer than 22 CAG repeats had higher blood pressure and a greater prevalence of hypertension than those with longer repeats.²⁵

This pattern also appears early in life. Adolescent boys with short CAG repeats, meaning more androgen-sensitive receptors, had more intra-abdominal fat, higher blood pressure, and greater sympathetic nervous system activity compared to peers with longer repeats. The blood pressure differences were most pronounced during mental stress, with gaps of 8 to 9 mmHg.²⁶ These findings suggest that two men with identical testosterone levels could have meaningfully different blood pressure responses to that hormone, based purely on the genetic sensitivity of their receptors. It also offers one possible explanation for the link between androgen signaling, abdominal fat, and hypertension: heightened sympathetic nervous system activation may be the thread connecting all three.

Testosterone and Blood Pressure During Pregnancy

Pregnancy adds yet another clinical context where testosterone and blood pressure intersect. Women who develop preeclampsia, a dangerous hypertensive disorder of pregnancy, tend to have elevated testosterone levels. Animal studies that replicate the pattern and magnitude of testosterone increase seen in preeclamptic pregnancies have reproduced key features of the condition, including gestational hypertension, impaired blood vessel remodeling in the uterus, placental oxygen deprivation, and restricted fetal growth.²⁷

The mechanism appears to involve both blunted nitric oxide signaling and heightened responsiveness to angiotensin II. In pregnant rats given testosterone at levels matching those seen in human preeclampsia, blood pressure climbed significantly in the final days of pregnancy, driven by reduced nitric oxide-mediated vasodilation.²⁸ Additional work showed that this gestational hypertension is mediated specifically through angiotensin II type 1 receptor signaling, providing a molecular link between elevated maternal testosterone and the blood pressure dysregulation characteristic of preeclampsia.²⁹ While this research is still largely in animal models, it raises the possibility that testosterone-lowering strategies could eventually play a role in managing preeclampsia.

Sleep Apnea as a Mediating Factor

Obstructive sleep apnea is strongly linked to both low testosterone and high blood pressure, and testosterone therapy can change the picture in unexpected ways. In a trial of obese men with severe sleep apnea, testosterone treatment mildly worsened sleep-disordered breathing at seven weeks, increasing the oxygen desaturation index by about 10 events per hour. By 18 weeks, however, there was no significant difference from placebo.³⁰ Sleep apnea causes repeated drops in oxygen throughout the night, which drives up sympathetic nervous system activity and blood pressure. If testosterone temporarily worsens sleep apnea, it could indirectly raise blood pressure through this route even while having neutral or beneficial direct vascular effects. For men with untreated sleep apnea who start testosterone therapy, this temporary worsening is worth being aware of.

Circadian Blood Pressure Rhythm

Healthy blood pressure follows a circadian pattern, dipping at night and rising in the morning. Loss of this nocturnal dip is itself a cardiovascular risk factor. Animal research on cross-sex hormone therapy found that castration combined with estrogen treatment disrupted this circadian rhythm, even when average 24-hour blood pressure remained unchanged.³¹ This finding, though limited to rats, raises an intriguing question: could some of the cardiovascular risk associated with hormonal manipulation come not from changes in average blood pressure but from disruption of its daily rhythm? Standard blood pressure measurements at a clinic would miss this entirely, which is one reason 24-hour ambulatory monitoring is increasingly recommended for people on long-term hormone therapy.