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High blood pressure takes big toll on small filtering units of the kidney
Date:9/19/2008

as an energy source but also gaining acceptance as an extracellular messenger, he theorizes. "It's an action-reaction kind of event."

When he puts ATP on the vessel it rapidly constricts; when he blocks the ATP receptor it won't. Unfortunately ATP works best in the face of normal pressures: constricting pressure about 25 percent as opposed to 2-3 percent when it's high. Still there are plenty of questions. Whether ATP is really released by the initial stretching is a critical one, he says. Whether ATP really comes from smooth muscle cells is another.

University of Southern California researcher Dr. Janos Peti-Peterdi thinks high pressures tugging the tethers connecting smooth muscle cells to others in the blood vessel wall may really be what releases ATP, a theory Dr. Inscho presented during the Sept. 19 meeting. It may be that hypertension changes the attachment of those tethers so they don't respond and the blood vessel can't either.

"We are trying to figure out how all this fits together," says Dr. Inscho. Figuring out the critical steps of this "amazingly elegant, amazingly precise and very complicated" process will lead to better understanding of what gets corrupted by diseases such as hypertension and diabetes and maybe how to stop kidney destruction.

As scientists are finding with many diseases, Dr. Inscho says inflammation likely plays a big role. "We know we can make these animals hypertensive, treat them with anti-inflammatories and prevent this whole process from occurring," he says of glomeruli destruction. "I think that's pretty exciting, but we don't know exactly how we are doing that." Blood pressure is not affected, just the negative impact on the kidneys. Inflammation, he notes, is likely well-intended but ultimately ends up thickening blood vessel walls and hampering flexibility.


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Contact: Toni Baker
tbaker@mcg.edu
706-721-4421
Medical College of Georgia
Source:Eurekalert  

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