Formylpeptide Receptor Activation Attenuates Renovascular Remodeling in Neurogenic Hypertension (Kidney)

Inflammation and sympathetic overactivity contribute to end-organ injury associated with hypertension. We previously demonstrated that targeting formylpeptide receptors (FPRs), which regulate and resolve inflammation, prevents cardiovascular damage in preclinical hypertension. Here, we investigated whether the FPR agonist Cmpd17b can reverse renovascular remodeling in established essential hypertension. Cmpd17b selectively reduced blood pressure in BPH/2J mice and improved aortic distensibility without altering cardiac function. Cmpd17b reduced collagen deposition across organs, most prominently in the kidney. RNA sequencing revealed kidney-specific upregulation of Serpina1e and Igfbp2, normalized by Cmpd17b. These findings identify FPR agonism as a promising therapeutic strategy for lowering blood pressure and reversing renovascular fibrosis.