New study IDs proteins regulating water retention in salt-sensitive hypertension

Oct 22, 2010

Research conducted by scientists at LSU Health Sciences Center New Orleans has found that two proteins in the brain act as valves to turn the hormone that regulates water retention in the body on and off. Their findings may lead to advances in treatment for diseases like high blood pressure, congestive heart failure, and cirrhosis of the liver. The research is published in the November 1, 2010 issue of Endocrinology.

Daniel Kapusta, PhD, Professor of Pharmacology at LSU Health Sciences Center New Orleans, and Richard Wainford, PhD, LSUHSC Instructor of Pharmacology, report the role of these brain proteins, called Gαq and Gαz, in producing elevated secretion of the hormone, vasopressin, and water retention in salt-sensitive hypertension, a condition in which blood pressure becomes elevated when salt is consumed. It is estimated that salt-sensitive hypertension occurs in about 26% of Americans with normal blood pressure and in 58% of those whose blood pressure is already high.

"Throughout the day, vasopressin, a peptide hormone produced by the hypothalamus, is released into the circulation from the pituitary gland and plays a vital role as the flood-gate keeper to prevent excessive loss of water from the kidneys," notes Dr. Kapusta. "Under most conditions, the water-retaining action of vasopressin is vital for survival. However, it has remained essentially a black box as to why, in susceptible individuals, the regulatory mechanisms that control vasopressin secretion cannot turn off when the body already has elevated water content."

For 21-days, the research team fed groups of male salt-resistant and salt-sensitive rats a diet containing either normal or high salt. Then they measured how the treatments influenced the animal's ability to excrete water and how the salt stress altered levels of vasopressin, Gαq and Gαz.

The consumption of high salt triggered a decrease in Gαq proteins in the brain of salt-resistant, but not salt-sensitive, rats. In salt-sensitive rats, the team demonstrated that reducing brain Gαq proteins returned plasma vasopressin to normal levels, decreased salt-induced , and restored the animal's ability to excrete water.

"Our findings are novel and provide evidence that the Gαq sub-unit proteins in the hypothalamus act as a molecular/cellular switch to control the level of vasopressin secretion," says Dr. Wainford.

The researchers concluded that reducing brain Gαq proteins plays a critical counter-regulatory role in preventing the secretion of too much vasopressin in those with salt-resistance and may represent a new therapeutic target in diseases associated with fluid retention.

Explore further: The impact of bacteria in our guts

Provided by Louisiana State University Health Sciences Center

5 /5 (1 vote)
add to favorites email to friend print save as pdf

Related Stories

Why you are not thirsty while sleeping

Mar 02, 2010

(PhysOrg.com) -- New research suggests the body's internal clock is what prevents you from becoming dehydrated and needing to drink during sleep.

Opening a channel for salt retention

Apr 25, 2008

A research team has developed the first small molecule that can reversibly activate a key protein involved in balancing sodium levels, paving the way for drugs that can treat low blood pressure and related conditions.

Eating less salt could prevent cardiovascular disease

Apr 20, 2007

People who significantly cut back on the amount of salt in their diet could reduce their chances of developing cardiovascular disease by a quarter, according to a report in British Medical Journal today.

Recommended for you

The impact of bacteria in our guts

13 hours ago

The word metabolism gets tossed around a lot, but it means much more than whether you can go back to the buffet for seconds without worrying about your waistline. In fact, metabolism is the set of biochemical ...

Stem cell therapies hold promise, but obstacles remain

13 hours ago

(Medical Xpress)—In an article appearing online today in the journal Science, a group of researchers, including University of Rochester neurologist Steve Goldman, M.D., Ph.D., review the potential and ch ...

New hope in fight against muscular dystrophy

14 hours ago

Research at Stockholm's KTH Royal Institute of Technology offers hope to those who suffer from Duchenne muscular dystrophy, an incurable, debilitating disease that cuts young lives short.

Biologists reprogram skin cells to mimic rare disease

Aug 21, 2014

Johns Hopkins stem cell biologists have found a way to reprogram a patient's skin cells into cells that mimic and display many biological features of a rare genetic disorder called familial dysautonomia. ...

User comments : 0