What Causes High Blood Pressure During Pregnancy?

High blood pressure during pregnancy most often stems from problems with how the placenta develops and connects to the mother’s blood supply, though the full picture involves the immune system, genetics, metabolic health, and environmental exposures all interacting at once. The condition is not a single disease but a spectrum, and the causes differ depending on which type of hypertensive disorder develops. What researchers have pieced together over the past two decades points to a chain of events that begins surprisingly early, sometimes before a woman even knows she is pregnant.

How Pregnancy Normally Reshapes the Cardiovascular System

To understand why blood pressure can go wrong during pregnancy, it helps to know what is supposed to happen. The cardiovascular system begins changing within weeks of conception. Blood vessels relax and widen, driven largely by nitric oxide and hormonal signals from rising estrogen. This widening causes a drop of roughly a quarter to a third in overall vascular resistance. To compensate, the heart increases its output by about 40 percent, peaking somewhere around 20 to 28 weeks of gestation.¹ Blood pressure actually dips in the first and second trimesters in a healthy pregnancy, then gradually climbs back toward pre-pregnancy levels near term. When that carefully orchestrated relaxation fails or gets overwhelmed, blood pressure rises.

Not One Condition but Several

Doctors classify pregnancy-related high blood pressure into distinct categories, and the causes behind each are not identical. Chronic hypertension means a woman already had high blood pressure before conceiving or before 20 weeks of gestation. Gestational hypertension appears after 20 weeks without other organ involvement. Preeclampsia involves high blood pressure plus signs that organs are being affected, such as protein in the urine, liver inflammation, low platelets, or kidney problems.² These conditions exist on a continuum, and a woman with gestational hypertension can progress to preeclampsia.

Blood pressure patterns differ between these groups even early on. Women who go on to develop gestational hypertension or preeclampsia tend to have higher readings as early as eight weeks, and their blood pressure fails to drop as much during the mid-pregnancy dip that healthy pregnancies show. From about 18 weeks onward, blood pressure rises more steeply, and in preeclampsia the acceleration becomes particularly sharp after 30 weeks.³ These early differences suggest the underlying cause is already in motion well before symptoms appear.

When Spiral Arteries Fail to Remodel

The single most studied cause of preeclampsia, the most dangerous hypertensive disorder of pregnancy, is a failure in how the uterine blood supply adapts to the placenta. In a normal pregnancy, specialized cells from the placenta invade the walls of the mother’s spiral arteries, the small blood vessels that feed the uterine lining. These cells strip away the muscular walls of the arteries, transforming them from narrow, high-resistance tubes into wide, floppy conduits that can deliver large volumes of blood to the growing placenta at low pressure.

In preeclampsia, this remodeling goes wrong. The placental cells fail to invade deeply enough, particularly into the muscular layer of the uterine wall. The spiral arteries stay narrow, thick-walled, and tortuous instead of opening up.⁴ Studies comparing spiral arteries from preeclamptic pregnancies with healthy ones find significantly less muscle disruption and fewer invading placental cells in the deeper segments of the vessel wall.⁵ Recent research has also identified disrupted calcium handling in the smooth muscle cells of these arteries as a contributor to the remodeling failure.⁶

The result is a placenta that does not get enough blood. It becomes stressed, oxygen-deprived, and begins releasing substances into the mother’s bloodstream that cause widespread damage to blood vessel linings throughout her body.

The Protein That Poisons Blood Vessels

One of the key substances the stressed placenta releases is a protein called sFlt1. In normal amounts, sFlt1 helps regulate blood vessel growth. But a poorly perfused placenta dumps excess sFlt1 into the mother’s circulation, where it acts like a sponge, soaking up two growth factors (VEGF and PlGF) that blood vessel linings need to stay healthy.⁷ Without those growth factors available, the endothelium, the thin lining of blood vessels everywhere in the body, starts to malfunction.

Landmark laboratory work showed this mechanism in action. Serum from women with preeclampsia blocked the normal formation of blood vessel structures in lab dishes, and adding sFlt1 to healthy serum reproduced the same effect. When researchers added back VEGF and PlGF, normal vessel formation resumed. In pregnant rats, injecting sFlt1 caused high blood pressure and kidney damage that closely resembled preeclampsia, while control animals remained healthy.⁸ The ratio of sFlt1 to PlGF in a woman’s blood correlates with how severe her disease is, and clinicians increasingly use this ratio to help diagnose and monitor preeclampsia.⁹

The endothelial damage goes beyond just sFlt1. The stressed placenta also releases inflammatory signals, reactive oxygen species, and autoantibodies that further reduce the availability of nitric oxide and other natural vasodilators while boosting vasoconstrictors. The net effect is blood vessels that clamp down rather than relax, pushing blood pressure up.¹⁰ Oxidative stress in the placenta itself further reduces nitric oxide, creating a vicious cycle.¹¹

The Immune System and the Foreign Fetus

Pregnancy requires the immune system to tolerate tissue that is genetically half foreign. When that tolerance breaks down, it can contribute to poor placental development and hypertension. Women with preeclampsia show increased numbers of circulating natural killer cells with heightened killing activity compared to women with normal blood pressure. In animal models, natural killer cells from the placentas of preeclamptic rats had roughly five times the killing activity of those from controls, and transferring these cells into healthy pregnant rats caused high blood pressure, fetal growth restriction, and the same kind of anti-angiogenic protein imbalance seen in human preeclampsia.¹² This suggests the immune system is not just a bystander but an active participant in the disease process.

Autoimmune conditions can also raise the risk. Antiphospholipid syndrome, a disorder in which the immune system mistakenly attacks certain blood proteins, is associated with placental thrombosis and preeclampsia. Women with severe preeclampsia are often screened for antiphospholipid antibodies because the two conditions overlap frequently enough to warrant attention.¹³

Genetics and the Father’s Contribution

Preeclampsia runs in families, but the inheritance pattern is unusual because genes from both parents contribute. A large population-based study found that both men and women who were themselves born from a preeclamptic pregnancy were more likely to have a child affected by preeclampsia.¹⁴ This makes sense when you remember that the placenta carries the father’s genes too. A man born from a preeclamptic pregnancy may carry fetal genes that make the placenta more likely to develop poorly, and he passes those to his offspring. A woman born from a preeclamptic pregnancy may inherit both fetal risk genes and maternal susceptibility genes that affect how her body responds to pregnancy.¹⁵

This dual contribution helps explain a long-observed pattern: preeclampsia is more common in first pregnancies, and changing partners resets part of the risk. The immune system’s exposure to the father’s genetic material through the placenta appears to play a role in whether subsequent pregnancies go smoothly.

Obesity, Metabolism, and Inflammation

Pre-existing metabolic health has a substantial influence. Obesity increases the risk of all hypertensive disorders of pregnancy through several overlapping pathways. Excess fat tissue produces abnormal levels of signaling molecules called adipokines, particularly too little adiponectin and too much leptin. These imbalances promote insulin resistance and chronic low-grade inflammation, both of which damage blood vessel linings in ways that mirror the endothelial dysfunction seen in preeclampsia.¹⁶ A woman who enters pregnancy already in a state of metabolic stress has less cardiovascular reserve to absorb the additional demands pregnancy places on the system.

Dysregulation of the renin-angiotensin-aldosterone system, the hormonal cascade that controls blood pressure and fluid balance, also plays a role. In normal pregnancy this system ramps up substantially, but in preeclampsia it responds abnormally, contributing to both the acute hypertension and longer-term cardiovascular risk for the mother and even the offspring.¹⁷

Twin Pregnancies and Donor Egg Conception

Carrying twins roughly doubles the circulating levels of sFlt1 compared to a singleton pregnancy, and the increase tracks closely with placental mass. Twin placentas are about 75 percent heavier on average, and the larger the placenta, the more anti-angiogenic protein it produces. The sFlt1-to-PlGF ratio in twin pregnancies is about twice that of singletons, which likely explains much of the higher preeclampsia rate in multiples.¹⁸

Pregnancies conceived with donor eggs carry an even more striking risk. Because the embryo shares no genetic material with the mother, the immune challenge is greater. A systematic review and meta-analysis found that preeclampsia occurred in roughly 11 to 15 percent of donor-egg pregnancies, compared to about 3 percent in naturally conceived pregnancies. Even after adjusting for confounders, the odds were more than three times higher with donor eggs than with natural conception, and about three times higher compared to standard IVF using the woman’s own eggs.¹⁹ Severe preeclampsia risk was elevated even further, by roughly seven-fold compared to natural conception.²⁰ This finding reinforces how central immune tolerance of the placenta is to keeping blood pressure in check.

Sleep Apnea as a Hidden Driver

Obstructive sleep apnea, which becomes more common during pregnancy as weight increases and airways narrow, can contribute to hypertensive disorders through a separate pathway. Repeated nighttime breathing pauses cause cycles of low oxygen and reoxygenation that ramp up the sympathetic nervous system, the branch of the nervous system responsible for the fight-or-flight response. Women with preeclampsia have been observed to have elevated sympathetic activity, and the intermittent oxygen deprivation from sleep apnea may worsen or even initiate that process.²¹ The repeated oxygen swings also cause endothelial dysfunction and increased production of stress hormones, both of which push blood pressure higher.²² Sleep apnea is worth flagging because it is treatable, and identifying it during pregnancy could reduce an otherwise avoidable risk.

Air Pollution and Environmental Exposures

A growing body of evidence connects air pollution to pregnancy-related hypertension. A systematic review and meta-analysis found that fine particulate matter (PM2.5) exposure was associated with roughly a 57 percent higher risk of hypertensive disorders in pregnancy and about a 31 percent higher risk of preeclampsia specifically, per modest increases in exposure.²³ The first and second trimesters appear to be the most vulnerable windows.²⁴

One particularly interesting finding is that the effect of air pollution on gestational hypertension may be amplified by prenatal depression. In a large study, women with prenatal depression showed significantly stronger associations between pollutant exposure around the time of conception and later gestational hypertension, while the associations were essentially absent in women without depression.²⁵ The mechanism is not fully clear, but stress and depression can alter inflammation and vascular function in ways that may make the body more susceptible to environmental insults.

Calcium and Low-Dose Aspirin for Prevention

Two interventions have enough evidence behind them to be used in clinical practice. Low-dose aspirin works by suppressing thromboxane, a substance that promotes blood clotting and constriction, while relatively preserving prostacyclin, which opens blood vessels.²⁶ For women identified as high-risk, starting low-dose aspirin before 16 weeks of gestation is now standard guidance in many countries.

Calcium supplementation is recommended for pregnant women in populations with low dietary calcium intake. Abnormal calcium metabolism has been observed in women with pregnancy-related hypertension, including lower levels of active vitamin D and reduced calcium in the urine.²⁷ The World Health Organization recommends 1,500 to 2,000 milligrams daily for at-risk populations, but two large trials involving 11,000 women each found that a 500-milligram dose was just as effective as a 1,500-milligram dose in reducing preeclampsia, with incidence rates around 3 percent in both groups.²⁸ That is a practical finding: a smaller, easier-to-take dose appears to work just as well.

What Pregnancy Hypertension Means for Long-Term Health

The consequences of high blood pressure during pregnancy do not end at delivery. Women who have had preeclampsia face roughly a fourfold increase in future heart failure, about double the risk of coronary heart disease and stroke, and double the risk of dying from cardiovascular causes, even after adjusting for other risk factors.²⁹ A large Korean cohort study with over 20 years of follow-up confirmed elevated risks of ischemic heart disease and stroke in women with a preeclampsia history.³⁰

This is not simply because preeclampsia unmasks women who were already at risk. The endothelial dysfunction, inflammation, and metabolic changes that drive preeclampsia share roots with the processes behind heart disease, and the pregnancy itself may accelerate them. Women with severe or recurrent preeclampsia, or those who delivered preterm, face the highest long-term risk and are significantly more likely to develop chronic hypertension within a decade of the pregnancy.³¹ Awareness of this connection is still surprisingly low, and many women are never told that a complicated pregnancy should prompt closer cardiovascular monitoring for years afterward.

An Evolutionary Tug-of-War

One way to understand why pregnancy hypertension exists at all is through the lens of evolutionary conflict. The fetus benefits from extracting as many resources as possible from the mother, while the mother’s body benefits from holding some resources back for her own survival and future pregnancies. The placenta, built from fetal genes, aggressively remodels maternal blood vessels to maximize blood flow. When that process overshoots or meets resistance, the result can be a dangerous imbalance. Preeclampsia has been described as what happens when the conflict over resource allocation goes too far, depriving maternal tissues of adequate blood flow and triggering organ damage.³² Human pregnancy is unusually invasive compared to that of most mammals, with the placenta burrowing deeply into the uterine wall. That deep invasion is what allows human babies to grow large brains, but it also creates more opportunities for things to go wrong at the maternal-fetal interface.