Smoking cannabis involves complex physiological responses to the primary psychoactive compound, delta-9-tetrahydrocannabinol (THC). The immediate effect of THC on blood vessels is not simple constriction, but rather a dual action that includes dilation in some areas. This initial response sets off a chain of systemic cardiovascular reactions as the body attempts to maintain balance. Understanding these acute effects is essential for grasping the overall impact of cannabis use on the circulatory system.
Acute Vascular Response: Dilation and Constriction
The most immediate and visible effect of inhaled THC is vasodilation, or the widening of blood vessels, in the periphery. This is famously observed in the eyes, where THC binding causes the capillaries in the conjunctiva to dilate, leading to the characteristic “red-eye” appearance. This peripheral vasodilation causes a temporary lowering of peripheral resistance and, consequently, a slight drop in blood pressure.
However, the vascular response is not uniform throughout the body. Some research suggests a transient increase in central blood pressure and an increase in the tone of cerebral vasculature, which could be interpreted as a form of constriction in the brain’s blood vessels. Furthermore, the act of smoking itself introduces combustion byproducts, similar to those in tobacco smoke, which acutely impair the function of the endothelium (blood vessel lining). This impairment negatively affects the vessels’ ability to regulate blood flow properly.
Systemic Effects on Heart Rate and Blood Pressure
Despite the initial peripheral vasodilation, the acute systemic response to THC involves a notable increase in heart rate, a condition known as tachycardia. This increase can range significantly, sometimes causing a rise of 20% to 100% above the baseline rate within minutes of inhalation. The heart speeds up as a compensatory mechanism to counteract the temporary drop in peripheral blood pressure caused by vasodilation.
This rapid change in hemodynamics increases the workload on the heart. Studies consistently show that THC inhalation, whether smoked or vaporized, acutely increases both heart rate and mean arterial pressure. The acute effects can also lead to orthostatic hypotension, a sudden drop in blood pressure when moving from a sitting or lying position to standing, due to compromised peripheral vascular resistance.
The Endocannabinoid System and Vascular Regulation
The biological mechanism driving these vascular changes involves the body’s native signaling network, the endocannabinoid system (ECS). This system includes cannabinoid receptors, primarily CB1 and CB2, which are found throughout the body, including on the smooth muscle and endothelial cells of blood vessels. THC mimics the body’s natural endocannabinoids and binds to these receptors.
Activation of the CB1 receptors is the main driver of the peripheral vasodilation observed in the eyes and other tissues. CB1 receptors are also present in cardiovascular tissues, and their activation by THC is linked to changes in heart rate. In contrast, the CB2 receptors are mostly associated with immune cells, and their activation may offer a protective, anti-inflammatory effect in the vasculature. The overall effect depends on the specific concentration of THC and the density of CB1 and CB2 receptors in that tissue.
Long-Term Cardiovascular Considerations
While the acute effects of cannabis on blood vessels are transient, chronic and heavy use raises concerns about long-term cardiovascular health. Repeated exposure to combustion byproducts, chemically similar to tobacco smoke, can lead to persistent damage to the endothelial lining of blood vessels. This damage is a precursor to conditions like atherosclerosis, where plaque builds up and hardens arteries, leading to poor vascular function.
Chronic cannabis use has been associated with an increased risk of serious cardiovascular events, including heart attack and stroke. Long-term use of THC, even in non-smoked forms, is independently linked to reduced blood vessel function and may increase arterial stiffness, placing a greater strain on the heart over time.