Infections can push your blood pressure in either direction, and which way it moves depends on the type of infection, how severe it is, and how long it has been present. A mild cold might barely register on a blood pressure cuff, while a bloodstream infection can send pressure plummeting to life-threatening lows within hours. On the other end, certain chronic infections that linger for years have been linked to a gradual, sustained rise in blood pressure. The relationship between infection and blood pressure is not one story but several, each with a different mechanism and a different set of risks.
Why Acute Infections Tend to Lower Blood Pressure
When your body first detects an invading pathogen, it launches an inflammatory response. Part of that response involves widening blood vessels so immune cells can reach the site of infection more easily. This vasodilation, driven partly by the release of nitric oxide into the bloodstream, naturally lowers the resistance inside your arteries. For a mild infection like a urinary tract infection or a bout of the flu, the dip in blood pressure is usually modest and temporary. You might feel lightheaded when you stand up, or your readings at a pharmacy cuff might run a few points lower than usual.
Fever itself also plays a role. As your core temperature rises, blood vessels near the skin dilate to release heat, which redistributes blood flow away from your core. Dehydration from sweating, vomiting, or reduced fluid intake compounds the effect. Together, these can lower your blood pressure enough to cause dizziness or fatigue even in otherwise healthy people.
Sepsis and the Collapse of Vascular Tone
Sepsis represents what happens when the body’s response to infection spirals out of control. Rather than a contained local response, the immune system floods the entire bloodstream with inflammatory signals, causing blood vessels throughout the body to relax all at once. The result is a dramatic, dangerous drop in blood pressure that can starve organs of oxygen.
Several mechanisms converge to make this happen. One is a massive overproduction of nitric oxide. Research comparing septic patients with healthy controls found that the ability of blood vessels to dilate in a controlled way was severely impaired in sepsis, with flow-mediated dilation dropping to about 1% in septic patients compared to nearly 7% in healthy individuals, and blood flow responses to leg movement falling to a fraction of normal values.1Europe PMC. Nitric oxide-mediated vascular function in sepsis using passive leg movement as a novel assessment: a cross-sectional study That might sound counterintuitive: if nitric oxide is a vasodilator, why is dilation impaired? The answer is that in sepsis, nitric oxide is produced in such enormous quantities by inflammatory enzymes that it overwhelms normal vascular regulation. Blood vessels lose their ability to fine-tune their tone, leading to an uncontrolled, generalized relaxation.
Another piece of the puzzle is the endothelial glycocalyx, a protective gel-like layer lining the inside of blood vessels. In sepsis, this layer gets stripped away. A study of patients with community-acquired pneumonia found that those with elevated levels of syndecan-1, a marker of glycocalyx destruction, had significantly reduced 30-day survival.2PubMed Central / BioMed Central (Crit Care). Endothelial glycocalyx degradation and its association with clinical outcomes and host response aberrations in community-acquired pneumonia across different care settings When the glycocalyx breaks down, fluid leaks out of blood vessels into surrounding tissue, reducing the volume of blood available to maintain pressure. This is why septic patients often develop puffy, swollen tissue while simultaneously having dangerously low blood pressure.
Layered on top of all this is the cytokine storm: a runaway release of inflammatory molecules that acts as the primary driver of organ failure in severe infections.3Europe PMC. The “cytokine storm” in infection and sepsis: win the battle but lose the war The heart itself can be weakened by this inflammatory bombardment, reducing its pumping ability at the very moment the body needs it most. In the most severe form, septic shock, blood pressure drops so low that even aggressive fluid replacement is not enough. Clinicians turn to vasopressors, drugs that artificially constrict blood vessels to raise pressure. Norepinephrine is the standard first choice, since the core problem is a collapse of vascular tone.4PubMed Central. Early norepinephrine use in septic shock Even with vasopressors and fluid resuscitation, restoring adequate organ perfusion remains the central challenge of treating septic shock.5PubMed Central. Vasopressors in septic shock: which, when, and how much?
Chronic Infections That Quietly Raise Blood Pressure
While acute infections tend to push pressure down, some long-term infections do the opposite. The most studied example is cytomegalovirus, or CMV, a member of the herpesvirus family that infects a large portion of the adult population. Most people never know they carry it because it causes few or no symptoms in people with healthy immune systems. But the virus persists in the body indefinitely, and its presence appears to quietly nudge blood pressure upward.
A study of older adults found that those who were CMV-seropositive had a mean systolic blood pressure about 3 mmHg higher than those who were seronegative, and this difference held even after adjusting for a wide range of biological and socioeconomic factors.6PubMed Central. Cytomegalovirus infection is associated with an increase in systolic blood pressure in older individuals Three points might not sound like much for an individual, but across a population, even small average shifts in blood pressure translate into meaningful differences in heart attack and stroke rates. In younger men, the association showed up too: higher CMV antibody levels were independently linked to elevated systolic and diastolic blood pressure, as well as impaired blood vessel function measured by flow-mediated dilation.7PubMed Central. Relation of high cytomegalovirus antibody titres to blood pressure and brachial artery flow-mediated dilation in young men: the Cardiovascular Risk in Young Finns Study
Animal research helps explain why. In mice, CMV infection alone caused a significant increase in arterial blood pressure, independent of any atherosclerotic plaque formation. The virus boosted levels of inflammatory cytokines like IL-6 and TNF-α, and it stimulated the expression of renin, a key enzyme in the system that regulates blood pressure, in a dose-dependent manner.8PLoS Pathogens. Cytomegalovirus Infection Causes an Increase of Arterial Blood Pressure In other words, CMV appears to hijack the body’s own blood pressure regulation system, turning up the dial on the renin-angiotensin pathway that normally controls how tightly arteries constrict.
Gum Disease and Blood Pressure
Periodontitis, the advanced form of gum disease, is another chronic infection with a surprisingly well-documented connection to elevated blood pressure. The bacteria responsible for periodontitis do not stay confined to your gums. They and their inflammatory byproducts enter the bloodstream, triggering a low-grade systemic inflammatory process. This chronic inflammation directly affects the lining of blood vessels, impairing their ability to relax and dilate properly.
Research has shown that the immune response to one particularly common periodontal pathogen, Porphyromonas gingivalis, can lead directly to increased blood pressure, blood vessel inflammation, and impaired vascular function. Periodontitis has also been linked to increased arterial stiffness.9PubMed Central. Periodontitis, Blood Pressure, and the Risk and Control of Arterial Hypertension: Epidemiological, Clinical, and Pathophysiological Aspects—Review of the Literature and Clinical Trials What makes this connection especially interesting from a practical standpoint is that treating periodontal disease has been shown to improve endothelial function in both people with diabetes and people without it. That suggests the vascular damage is at least partly reversible when the infection is controlled.
COVID-19 and the Blood Pressure System It Exploits
SARS-CoV-2, the virus behind COVID-19, has a unique relationship with blood pressure because of how it enters cells. The virus uses a receptor called ACE2 as its doorway into human tissue. ACE2 is also a critical component of the renin-angiotensin system, where it normally works to lower blood pressure by breaking down a molecule called angiotensin II. When the virus binds to and effectively disables ACE2, angiotensin II can accumulate, promoting vasoconstriction and fluid retention.
This helps explain why people with pre-existing hypertension faced worse outcomes during COVID. In one study of 201 COVID-19 patients, hypertension carried a hazard ratio of 1.70 for death and 1.82 for developing acute respiratory distress syndrome. A separate study of 191 patients found an even starker association, with a hazard ratio of 3.05 for in-hospital mortality among those with hypertension.10Molecular Therapy. Methods & Clinical Development. The Two Faces of ACE2: The Role of ACE2 Receptor and Its Polymorphisms in Hypertension and COVID-19 The same review noted that patients taking ACE inhibitors or angiotensin receptor blockers, both of which affect the renin-angiotensin system, had a mortality rate of about 4% compared to roughly 10% in those not on such medications.
When Blood Pressure Stays Unstable After the Infection Clears
For some people, the effects of an infection on blood pressure do not end when the pathogen is gone. Post-infectious autonomic dysfunction, where the nervous system that regulates heart rate and blood pressure stops working properly, has become especially visible in the wake of COVID-19. About 30% of people with post-acute COVID syndrome show features of cardiovascular autonomic dysfunction.11PubMed Central. Autonomic dysfunction and postural orthostatic tachycardia syndrome in post-acute COVID-19 syndrome
The most recognized form is postural orthostatic tachycardia syndrome, or POTS. People with POTS experience an exaggerated heart rate increase when they stand up, along with symptoms like dizziness, fatigue, brain fog, sweating, and exercise intolerance.12PubMed Central. Autonomic Dysfunction Related to Postacute SARS-CoV-2 Syndrome While POTS is defined by its heart rate abnormality, blood pressure is not spared. Patients with post-COVID POTS have been found to have higher nighttime systolic blood pressure than healthy controls, disrupted circadian blood pressure rhythms, and more frequent daytime episodes of low blood pressure.13PubMed Central. Blood Pressure Regulation in Post-COVID POTS: Beyond Sinus Tachycardia The combination of hypotensive episodes during the day and elevated pressure at night is the opposite of what healthy blood pressure regulation looks like, and it can leave patients feeling constantly off-balance.
POTS was recognized well before COVID, typically triggered by viral infections, surgery, or pregnancy. But the sheer scale of the pandemic created an enormous new population of people dealing with it. The mechanism likely involves autoimmune damage to small nerve fibers that control blood vessel constriction, though researchers are still working out the details.
Kidney Infections and Pressure Swings
When infections reach the kidneys, blood pressure effects can be particularly pronounced in both directions. The kidneys are the body’s primary long-term blood pressure regulators, controlling how much fluid and sodium you retain. Infections that impair kidney function can activate the renin-angiotensin-aldosterone system, promoting sodium retention and elevated blood pressure. Conversely, severe kidney infections associated with sepsis can cause hypotension through the mechanisms described earlier. A review of renal diseases in acute care settings noted that hypertension tends to predominate in conditions involving chronic kidney damage due to renin-angiotensin activation and sodium retention, while hypotension is more characteristic of septic or shock-associated acute kidney injury.14PubMed Central. Renal diseases and blood pressure dysregulation in acute care: Pathophysiology, clinical patterns
Repeated urinary tract infections that scar kidney tissue can lead to a condition called reflux nephropathy, which is a known cause of secondary hypertension in younger adults. In these cases, the infection itself may have cleared years ago, but the damage it left behind continues to drive elevated blood pressure. This is one of the clearest examples of an infection having lasting blood pressure consequences well beyond the acute illness.
Cold Medications You Should Know About
Here is something most people overlook: when you are fighting an infection, the medication you take for symptoms can affect your blood pressure more than the infection itself. Pseudoephedrine, the decongestant found in many over-the-counter cold and sinus medications, works by constricting blood vessels in the nasal passages to reduce congestion. But that constriction is not limited to the nose. A meta-analysis found that pseudoephedrine causes a small but statistically significant increase in systolic blood pressure and heart rate, with immediate-release formulations raising systolic pressure by about 1.5 mmHg on average.15JAMA Internal Medicine. Effect of Oral Pseudoephedrine on Blood Pressure and Heart Rate: A Meta-analysis Sustained-release versions did not show a significant blood pressure effect in the same analysis.
For most healthy people, a one-to-two-point bump in systolic pressure is clinically meaningless. But if you already have high blood pressure, are on antihypertensive medications, or have heart disease, that small nudge on top of the cardiovascular stress from the infection itself can matter. Nonsteroidal anti-inflammatory drugs like ibuprofen, another common choice for fever and aches during illness, can also raise blood pressure by promoting sodium retention and reducing kidney blood flow. The combination of an infection, dehydration, a decongestant, and an NSAID can produce blood pressure readings that look nothing like your baseline.
How Gut Infections Might Affect Blood Pressure Through the Microbiome
A newer area of research connects the gut microbiome to blood pressure, with potential implications for how gastrointestinal infections or prolonged antibiotic use could have vascular effects. The bacteria in your gut produce short-chain fatty acids like acetate, propionate, and butyrate when they ferment dietary fiber. These molecules have been shown to cause dose-dependent relaxation of blood vessels, lowering blood pressure both acutely and with chronic exposure.16PubMed Central. Short Chain Fatty Acid Receptors and Blood Pressure Regulation When delivered intravenously in animal studies, short-chain fatty acids cause blood pressure to drop within seconds and recover over minutes. Sustained oral intake also lowers pressure over time.
The relevance to infection is indirect but potentially significant. Gut infections, severe diarrheal illnesses, and broad-spectrum antibiotic courses used to treat infections can all disrupt the gut microbiome, reducing the populations of bacteria that produce these blood-pressure-lowering compounds. Whether this disruption meaningfully contributes to blood pressure changes during or after illness is still being investigated, but the pathway is biologically plausible and increasingly supported by animal data. For anyone who has noticed that their blood pressure seems “off” for weeks after a course of antibiotics, this could be part of the explanation.
Why Your Blood Pressure Readings During Illness Can Be Misleading
If you monitor your blood pressure at home, readings taken during an active infection need context. Fever, dehydration, pain, anxiety, poor sleep, and medications can all independently move your numbers in ways that have nothing to do with your underlying cardiovascular health. A systolic reading that looks 10 or 15 points higher than usual during a stressful bout of illness does not mean you have developed hypertension. Likewise, a reading that dips lower than normal during a fever is usually a temporary effect of vasodilation and fluid loss, not a sign of a new cardiac problem.
The practical advice is straightforward: if you are tracking blood pressure for a chronic condition, note that you were sick and do not adjust medications based on readings taken during an active infection unless a doctor tells you to. Wait until you have been fever-free and feeling recovered for several days before comparing readings to your baseline. If blood pressure remains abnormal weeks after recovery, particularly if you notice symptoms like persistent dizziness, rapid heartbeat on standing, or unexplained fatigue, that is worth a medical conversation. Post-infectious autonomic changes, kidney involvement, or medication effects may need to be sorted out from any pre-existing condition.