Depletion of the gut microbiota enhances the blood pressure-lowering effect of captopril: implication of the gut microbiota in resistant hypertension.

The role of the gut microbiota in the initiation and progression of hypertension has been newly identified, suggesting that targeting the gut microbiota may provide a new treatment strategy. This entails a complicated interaction between the gut microbiota and different host systems (e.g., immune system) or organs (e.g., gut, spleen) that contribute to blood pressure control. The significance of the gut microbiota in treatment-resistant hypertension is still unknown, owing to a lack of appropriate animal models. Given that the gut microbiota has a variety of enzymatic activities, we hypothesized that the gut microbiota may be involved in the metabolism of antihypertensive medications, causing treatment-resistant hypertension. We investigated this hypothesis in a simple, new hypertension paradigm and found that hypertensive rats pretreated with antibiotics to reduce the gut microbiota had a better response to the angiotensin-converting enzyme inhibitor captopril. This is a simple rodent model for testing the effectiveness of antihypertensive medications. Further mechanistic research may shed light on the pathogenic function of the gut microbiota in resistant hypertension. Our method presents a novel model that has the potential to be employed in the research of resistant hypertension.