High AngII levels put stress on the ER and cause hypertension

Published on December 18, 2012 at 4:18 AM · No Comments

When the heart works too hard, the brain may be to blame, says new Cornell University research that is changing how scientists look at high blood pressure (hypertension). The study, published in the Journal of Clinical Investigation in November, traces hypertension to a newfound cellular source in the brain and shows that treatments targeting this area can reverse the disease.

In what peer reviewers are calling "a new paradigm" for tackling the worldwide hypertension epidemic, this insight into its roots could give hope to the billion people it currently afflicts. Hypertension occurs when the force of blood against vessel walls grows strong enough to potentially cause such problems as heart attack, stroke and heart or kidney disease. The heart pumps harder, and often the hormone angiotensin-II (AngII) gets the pressure cooking by triggering nerve cells that constrict blood vessels.

"We knew the central nervous system orchestrates this process, and now we've found the conductor," said Robin Davisson, a professor of molecular physiology with a joint appointment at Cornell's College of Veterinary Medicine and Weill Cornell Medical College.

Two-thirds of Americans have hypertension, which is the leading cause of North America's No. 1 killer: heart disease, according to the Centers for Disease Control and Prevention.

Davisson's lab traced neurochemical signals back to endoplasmic reticulum (ER), the protein factory and stress-management control center in every cell. If something goes wrong in a cell, the ER activates processes to adapt to the stress. Long-term ER stress can cause chronic disease, and several stressors that ER responds to have been connected to hypertension. Davisson's lab found that high levels of AngII put stress on the ER, which responds by triggering the cascade of neural and hormonal signals that start hypertension.

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