Hypertension Opens the Flood Gates to the Gut Microbiota

Should we get around this problem by a young gut bacteria transplant? Ask your doctor how they would do that. How young are we talking about? 1 month? 1 year? 5 years? 15 years?

Restoring gut bacteria to youthful age linked to improved stroke recovery in mice

http://circres.ahajournals.org/content/120/2/249?etoc=

W. Robert Taylor, Kiyoko Takemiya

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https://doi.org/10.1161/CIRCRESAHA.116.310339

Circulation Research. 2017;120:249-251

Originally published January 19, 2017

There continues to be a rapidly evolving interest in the role of the gut microbiome in cardiovascular disease. It has long been known that the gut microbiome has a fundamentally mutualistic, symbiotic relationship with the human host. However, from earlier observations using mice grown in germ-free environments to more recent advances in identifying unique metabolic products of the gut microbiome,¹ the data have led to a compelling story linking cardiovascular disease to the trillions of prokaryotic organisms that live in the human gut.

Article, see p 312

In this issue of Circulation Research, Santisteban et al² have provided provocative data demonstrating very definitively that, in 2 different animal models of hypertension, there is decreased expression of several tight junction proteins in the gut and a concomitant increase in intestinal permeability. Furthermore, their data show that in the spontaneously hypertensive rat model, the increase in permeability is a result of increased sympathetic nerve activity before the development of hypertension. They therefore conclude that there is a direct, causal link between the sympathetic nerve activity derived from the central nervous system and increased gut permeability (Figure). They further hypothesize that the changes in gut permeability result in hypertension and cause a shift in the types of bacteria that are present in the gut. Finally, they have shown that the changes in sympathetic activity resulting in increased gut permeability are also associated with an increase in inflammatory cells within the intestinal wall thus potentially bringing the contributions of the immune system to hypertension into this pathophysiological mechanism.