The sensation of lightheadedness or dizziness experienced when standing up after using marijuana is common. This temporary feeling of faintness is a medical condition known as orthostatic hypotension (OH), or postural hypotension. It occurs because the body’s normal mechanisms for maintaining blood pressure are temporarily impaired. The physiological interaction between cannabis compounds and the body’s regulatory systems explains this sudden drop in blood pressure. This article explores the underlying biological mechanisms linking marijuana use to OH.
Defining Orthostatic Hypotension
Orthostatic hypotension is defined as a sustained drop in systolic blood pressure of at least 20 mm Hg or diastolic blood pressure of at least 10 mm Hg within three minutes of standing or sitting up. When a person moves to a standing posture, gravity causes blood (roughly 300 to 800 milliliters) to pool in the lower extremities. This pooling reduces the blood returning to the heart, subsequently lowering the heart’s output and arterial pressure.
The body uses a rapid compensatory mechanism, called the baroreceptor reflex, to counteract this shift. Specialized receptors sense the pressure drop and immediately signal the sympathetic nervous system to increase activity. This reflex causes blood vessels to constrict and the heart rate to increase, quickly raising peripheral vascular resistance to maintain adequate blood flow to the brain. OH occurs when this reflex fails or is too slow, leading to temporary insufficient blood flow to the brain, which causes symptoms like dizziness or blurred vision.
The Endocannabinoid System and THC
The active compound in marijuana responsible for its psychoactive and physiological effects is delta-9-tetrahydrocannabinol (THC). This compound exerts its influence by interacting with the body’s native regulatory network, the Endocannabinoid System (ECS). The ECS is a complex signaling system that regulates numerous bodily functions, including mood, appetite, pain sensation, and cardiovascular function.
The ECS operates through receptors, primarily the cannabinoid receptor type 1 (CB1). THC acts as an agonist, meaning it mimics the body’s natural cannabinoids and binds directly to and activates these CB1 receptors. CB1 receptors are widely distributed throughout the body, including the central and peripheral nervous systems, as well as in the smooth muscle lining of blood vessels.
Activation of these receptors in the central nervous system, particularly in areas like the brainstem, plays a role in regulating blood pressure and sympathetic tone. The presence of CB1 receptors on the walls of arteries and veins allows THC to directly influence vascular function. By activating these receptors, THC essentially hijacks this regulatory system, leading to unintended cardiovascular consequences and initiating the drop in blood pressure.
Cardiovascular Effects Leading to Low Blood Pressure
The activation of CB1 receptors by THC leads to orthostatic hypotension through two primary, interconnected cardiovascular mechanisms. The first is peripheral vasodilation, which is the relaxation and widening of blood vessels throughout the body. When THC activates CB1 receptors on the smooth muscle cells of the arterial walls, it triggers events that cause the vessels to relax.
This widespread vasodilation increases the overall capacity of the circulatory system. With the same volume of blood distributed across a larger space, the systemic vascular resistance significantly decreases. This reduction in resistance leads to a measurable fall in overall blood pressure, even when the person is lying down.
The second mechanism involves the inhibition of the sympathetic nervous system’s function. The sympathetic nervous system is responsible for the rapid “fight or flight” response, including the reflex that constricts blood vessels upon standing. THC interferes with the release of neurotransmitters that normally signal the heart to speed up and the vessels to constrict, dampening this regulatory response.
By inhibiting this sympathetic tone, the body loses its ability to quickly compensate for the gravitational pooling of blood when standing. The combination of widespread vessel widening (vasodilation) and the inability to reflexively constrict those vessels and increase heart rate results in a failure of the baroreceptor reflex. This failure prevents blood pressure from being maintained against gravity, leading to temporary cerebral hypoperfusion and the symptoms of orthostatic hypotension.