Deadly Link Between High Salt Intake And Obesity May Be Explained By Abnormal Activation Of A Protein
How Obesity and a High-Salt Diet Team Up
Dr. Fujita's team studied the effects of a high-salt diet in rats bred to have high blood pressure and different levels of blood pressure sensitivity to salt. When obese "salt-sensitive" rats were fed a high-salt diet, the team found that Rac1 activated the mineralocorticoid receptor (MR) on the rats' kidney cells. This receptor is normally activated by the hormone aldosterone. When turned on, MR leads to the expression of a protein called epithelial sodium channel (ENaC) and an enzyme called the sodium pump. Both of these substances promote the reabsorption of salt, which causes the body to retain fluid and results in high blood pressure. This is the first time scientists have seen Rac1 usurp aldosterone's role in activating MR in the regulation of blood pressure. The protein's usual duties entail regulating an array of cellular events such as cell growth.
The team made the discovery when attempting to treat the obese, hypertensive rats with drugs designed to block MR activation and inhibit Rac1. When Rac1 inhibitors were successful in lowering the rats' blood pressure, the team knew they had discovered a mechanism by which obesity and a high-salt diet team up to wreak havoc on blood pressure and the kidneys.
Importance of the Findings
According to Dr. Fujita, the team's findings carry important implications for the treatment of hypertension. "Our data indicate that the Rac1-mediated pathway in the kidneys can be an alternative therapeutic target for salt-sensitive hypertension and salt-mediated kidney injury," he said. "Based upon our results, we can speculate that Rac1 in the kidneys regulates salt susceptibility of blood pressure, and that Rac1 inhibitors, as well as MR antagonists, may be effective in the treatment of salt-sensitive hypertension."
Dr. Fujita is discussing the team's research in his presentation titled, "Aberant Rac1-MR Pathway in Salt-Sensitive Hypertension and Metabolic Syndrome" at the 7th International Symposium on Aldosterone and the ENaC/Degenerin Family of Ion Channels, being held September 18-22 in Pacific Grove, Calif. The conference is sponsored by the American Physiological Society. Additional information about the meeting is posted online at http://www.the-aps.org/press/releases/11/24.htm. Source: EurekAlert!, the online, global news service operated by AAAS, the science society
American Physiological Society
Source: EurekAlert!, the online, global news service operated by AAAS, the science society
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