Delta-9-tetrahydrocannabinol (THC), the primary psychoactive component of cannabis, is responsible for most of the substance’s effects on the heart and blood vessels. The relationship between smoking cannabis and blood pressure is complex, involving immediate physiological reactions and potential long-term adaptations within the cardiovascular system. The body’s response to inhaled cannabis is often described as biphasic, meaning it has two distinct phases that affect blood pressure differently depending on the dosage and the user’s existing health status. Understanding these immediate and sustained effects is important for anyone considering cannabis use.
Immediate Changes to Blood Pressure
Immediately following the inhalation of cannabis, the body typically experiences a rapid change in cardiovascular function. This acute response is biphasic, characterized first by a transient period of low blood pressure, followed by an increase in heart rate. The initial drop, known as orthostatic hypotension, is particularly noticeable when a person stands up quickly. This temporary lowering of blood pressure is caused by the relaxation of blood vessel walls, which reduces vascular resistance.
Within minutes of use, the most consistently observed effect is tachycardia, or an increased heart rate. The heart rate can accelerate significantly, sometimes increasing by 20 to 50 beats per minute above the baseline resting rate. This increased heart rate often coincides with a rise in supine blood pressure, especially systolic pressure.
These immediate changes are dose-dependent; higher concentrations of THC generally lead to more pronounced increases in heart rate and blood pressure. The effects typically begin within 10 minutes of inhalation and can last for two to three hours. This acute rise in cardiac workload increases the heart’s demand for oxygen.
How Cannabinoids Interact with the Circulatory System
The physiological changes observed after smoking cannabis are rooted in the interaction of cannabinoids with the body’s endocannabinoid system (ECS). THC primarily exerts its influence by binding to and activating Cannabinoid Receptor 1 (CB1) receptors, which are distributed throughout the central nervous system, heart, and vascular tissue.
Activation of CB1 receptors on vascular smooth muscle cells is responsible for the initial vasodilation, which contributes to the temporary drop in blood pressure. This action causes blood vessels to relax, lowering the resistance to blood flow.
The subsequent increase in heart rate and blood pressure is driven by the activation of the sympathetic nervous system, often called the “fight or flight” response. THC signaling leads to enhanced sympathetic tone and increased levels of catecholamines, which are stress hormones that accelerate the heart.
This shift in autonomic balance increases cardiac output and the heart’s workload, resulting in the characteristic tachycardia and elevated blood pressure.
Long-Term Cardiovascular Adaptations from Regular Use
When cannabis use is sustained over a long period, the body often develops tolerance to the acute cardiovascular effects. Chronic users may no longer experience the same pronounced immediate swings in heart rate and blood pressure as new users. Despite this tolerance, the long-term impact on baseline blood pressure remains complex and subject to conflicting data. Some large population studies have found no significant association between regular cannabis use and sustained high blood pressure or the incidence of hypertension.
Other research has suggested a modest association between recent, active cannabis use and a slight increase in systolic blood pressure, particularly in younger adults. However, this increase is statistically small and its clinical significance is not always clear. A more concerning long-term consequence is the potential for vascular inflammation and endothelial dysfunction, which can contribute to the hardening of the arteries over time.
Smoking cannabis introduces combustive toxins similar to tobacco smoke, which are associated with increased arterial stiffness and damage to the inner lining of blood vessels. Chronic use has been linked to an increased risk of serious cardiovascular events, including stroke and myocardial infarction (heart attack).
The mechanism is thought to involve chronic inflammation, oxidative stress in the artery walls, and the potential for vasospasm, where arteries suddenly narrow. Regular exposure appears to increase the hazard ratio for these severe cardiac events, indicating that the vascular system is still under strain.
Specific Risks for Individuals with Pre-Existing Conditions
Individuals with pre-existing cardiovascular conditions face a substantially higher risk from the acute effects of smoked cannabis. The temporary increase in heart rate and blood pressure places strain on a compromised heart. For those with coronary artery disease, the increased oxygen demand caused by tachycardia can lower the angina threshold, potentially triggering chest pain or an ischemic event.
Cannabis use has also been associated with a higher occurrence of arrhythmias, or irregular heart rhythms. There are concerns regarding drug interactions, particularly for patients taking medications to manage blood pressure or heart function.
Cannabinoids can interfere with certain liver enzymes responsible for processing many common heart medications, including beta-blockers, statins, and blood thinners.
This interference can alter the concentration of the medication in the bloodstream, making it less effective or dangerously potentiating its effects. For those taking anti-hypertensive drugs, the combination with cannabis-induced vasodilation can lead to severe orthostatic hypotension, increasing the risk of fainting or falls.