Mirabegron, often known by its brand name Myrbetriq, is a prescription medication used to manage the symptoms of overactive bladder (OAB) in adults. These symptoms typically include urinary urgency, increased frequency of urination, and urge incontinence, which is the involuntary leakage of urine. Understanding a drug’s mechanism of action means learning how it interacts with the body at a biological level to produce its desired effects.
The Physiology of an Overactive Bladder
The urinary bladder is a muscular organ designed to store urine and then release it in a controlled manner. Its wall contains a specialized smooth muscle called the detrusor, which plays a central role in both urine storage and emptying. Normally, as the bladder fills with urine, the detrusor muscle relaxes to allow for increasing volume without a significant rise in pressure. When the bladder is adequately full, nerve signals prompt the detrusor to contract, leading to urination.
In individuals with overactive bladder, this finely tuned process is disrupted, often due to abnormal nerve signaling to and from the bladder muscle. The detrusor muscle contracts involuntarily or too frequently, even when the bladder is not completely full. The core issue involves inappropriate detrusor activity during the bladder’s filling phase.
Mirabegron’s Selective Agonism of Beta-3 Receptors
Mirabegron works by interacting with specific sites on cell surfaces known as receptors. The detrusor muscle, like other tissues in the body, possesses various types of receptors, including beta-adrenergic receptors. Among these, the beta-3 adrenergic receptors are particularly abundant and significant in the human bladder.
When activated, beta-3 adrenergic receptors on the detrusor muscle send a signal that promotes muscle relaxation. Mirabegron is classified as a “selective beta-3 adrenergic agonist,” meaning it specifically targets and activates these beta-3 receptors. This selectivity is important because it allows the drug to primarily influence bladder function without broadly affecting other systems in the body where different beta-adrenergic receptor subtypes might be found.
The drug binds to the beta-3 receptors on the detrusor muscle cells, initiating a signaling pathway that involves an increase in cyclic adenosine monophosphate (cAMP) levels within these cells. Elevated cAMP levels then lead to the relaxation of the detrusor smooth muscle. This process primarily occurs during the bladder’s storage phase, allowing the muscle to remain relaxed even as urine volume increases.
Pharmacological Effects on Bladder Function
The direct consequence of Mirabegron’s action—relaxing the detrusor muscle during the filling phase—is a significant improvement in the bladder’s ability to store urine. This relaxation allows the bladder to comfortably hold a larger volume of urine, increasing its storage capacity.
This enhanced storage capacity directly translates into a reduction of OAB symptoms. Patients typically experience fewer episodes of urinary urgency, meaning the sudden, intense need to urinate becomes less frequent. Additionally, the number of daily urination episodes (frequency) decreases, providing more time between bathroom visits. Ultimately, this leads to a decrease in urge incontinence episodes, as the bladder can hold urine more effectively and provide more warning before a leak occurs.
Distinctions from Antimuscarinic Therapy
Mirabegron represents a different approach to treating overactive bladder compared to another common class of medications, antimuscarinics (also known as anticholinergics). While both drug types aim to improve OAB symptoms, they achieve this through distinct mechanisms. Antimuscarinic drugs work by blocking muscarinic receptors on the detrusor muscle, which are primarily responsible for bladder contraction. By blocking these receptors, antimuscarinics inhibit the involuntary contractions that cause OAB symptoms.
In contrast, Mirabegron does not block these muscarinic receptors; instead, it actively promotes detrusor muscle relaxation by stimulating beta-3 adrenergic receptors. This difference in receptor targeting results in varying side effect profiles between the two drug classes. Antimuscarinic drugs can cause systemic side effects like dry mouth, constipation, and blurred vision because muscarinic receptors are present throughout the body.
Mirabegron’s selective action on beta-3 receptors means it typically has a lower incidence of these common antimuscarinic side effects. While Mirabegron can cause some side effects such as increased blood pressure or headache, its mechanism avoids the widespread muscarinic receptor blockade.