The role of gamma-aminobutyric acid (GABA) in central nervous system (CNS) control of arterial blood pressure has been studied by testing the effects of drugs that either counteract or enhance CNS GABAergic mechanisms while monitoring the arterial pressure of normotensive and hypertensive animals. Drugs that antagonize the effects of GABA (either directly by blocking GABA-mediated responses or indirectly by inhibiting GABA synthesis) cause an increase in arterial pressure. This effect occurs in the forebrain and leads to an increase in sympathetic outflow to the vasculature, including the coronary vessels. GABA and drugs that stimulate GABA receptors (either directly or indirectly by inhibiting GABA metabolism, competing with an endogenous inhibitor of GABA, or activating a GABA chloride ionophore) cause a decrease in arterial pressure. This effect is, in some cases, associated with respiratory depression, and it occurs in the hindbrain, especially at the intermediate area on the ventral surface of the medulla. Hypertensive animals appear to be more sensitive to the hypotensive action of these agents. These results suggest that CNS GABA may have an important role in controlling blood pressure.
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