Could candesartan counteract adverse intestinal changes induced by hypertension?

Study Objectives

It has recently been shown that hypertension is associated with the disruption of the intestinal barrier. Damage to the intestinal barrier promotes the development of a chronic inflammatory environment that contributes to the pathogenesis of hypertensive organ damage. The presented study examined the pharmacological effect of the angiotensin II AT₁ receptor blocker candesartan on the disrupted intestinal barrier and gut dysbiosis in spontaneously hypertensive rats.

Findings

The results showed that administration of candesartan increases the expression of genes encoding proteins ensuring tight epithelial junctions (cingulin, occludin, and tight junction protein 1) in the intestines of these rats. In the serum of candesartan-treated rats, a higher level of lipopolysaccharide-binding protein was found, supporting the hypothesis that candesartan acts against the disruption of the intestinal barrier.

Administration of candesartan in hypertensive experimental animals also led to an increase in the amounts of short-chain fatty acids (acetic acid, propionic acid, butyric acid) in the stool.

Further, rDNA sequencing in the stool showed that rats treated with candesartan exhibited normalization of the ratio between Firmicutes and Bacteroides strains, which is disrupted in hypertension, as well as an increase in the representation of lactic acid-producing lactobacilli strains.

Conclusion

This study was the first to suggest that candesartan might act against the pathophysiological disturbances in the gut induced by hypertension.

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Source: Wu D., Tang X., Ding L. et al. Candesartan attenuates hypertension-associated pathophysiological alterations in the gut. Biomed Pharmacother 2019 Aug; 116: 109040, doi: 10.1016/j.biopha.2019.109040.