Mirabegron-mediated vasodilation in resistance-sized arteries

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β3-adrenergic receptors (β3-ARs) are the most recently established member of the beta-adrenergic sub-family of receptors, however, it’s apparent that β3-ARs contribute to the regulation of the cardiovascular system, including metabolism, vasodilation, and cardiac contractility. β3-ARs have been identified in the cardiac tissue of multiple species, including canine, rodent, and human, where observations suggest that its expression is upregulated in pathological conditions, such as heart failure. Less is understood about the function of β3-ARs in resistance-sized arteries, with most studies utilizing first-generation β3-AR agonists BRL37344, CL316243, and SR58611, which between them have been shown to cause vasodilation in coronary microarteries and thoracic arteries in rodents and dogs. Preliminary Simple Western and immunofluorescence data indicate that β3-ARs are expressed in resistance-sized mesenteric artery endothelial and vascular smooth muscle cells. Mirabegron, an agonist of the more recently established β3-AR subtype, and recently FDA-approved for the treatment of overactive bladder (OAB), causes vasodilation of mesenteric arteries through a cGMP-mediated β3-AR-dependent mechanism at low concentrations, and a β3-AR-independent mechanism at higher concentrations. These data suggest that β3-AR regulates arterial tone in systemic resistance-sized arteries and that Mirabegron causes vasodilation through additional, unknown mechanisms at higher concentrations. American Heart Association This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

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