Ion Channel Protein Linked to Blood Pressure Regulation

This research follows earlier studies on mechanoreceptors in the worm Caenorhabditis elegans.

In the current study, the investigators genetically engineered a line of mice to lack the genes required for synthesis of ASIC2. They reported in the December 24, 2009, issue of the journal Neuron that conscious ASIC2 negative mice developed hypertension, had exaggerated sympathetic and depressed parasympathetic control of the circulation, and a decreased gain of the baroreflex, all indicative of an impaired baroreceptor reflex. This genetic disruption of ASIC2 closely mimicked the pathologic picture seen in heart failure and hypertension and identified a molecular defect that may be relevant to their development.

"The ASIC2 channel allows a current to be generated at the nerve endings in blood vessels,” said senior author Dr. Frank Abboud, professor of internal medicine, molecular physiology, and biophysics at the University of Iowa. "However, when there is no ASIC2, those nerve endings become defective and cannot produce electrical current, and the nervous system loses the ability to get the blood vessels to dilate when necessary. As a result, the vessels remain constricted and the blood pressure stays high even when it should not.”

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