Regulation of the Brain’s Vascular Responses to Oxygen

Author:

Demchenko Ivan T.1,Oury Tim D.1,Crapo James D.1,Piantadosi Claude A.1

Affiliation:

1. From Duke University Medical Center (I.T.D., C.A.P.), Durham NC; the University of Pittsburgh Medical Center (T.D.O.), Pittsburgh, Pa; and the National Jewish Medical Center (J.D.C.), Denver, Colo.

Abstract

The mechanism of oxygen-induced cerebral vasoconstriction has been sought for more than a century. Using genetically altered mice to enhance or disrupt extracellular superoxide dismutase (EC-SOD, SOD3), we tested the hypothesis that this enzyme plays a critical role in the physiological response to oxygen in the brain by regulating nitric oxide (NO · ) availability. Cerebral blood flow responses in these genetically altered mice to changes in P o 2 demonstrate that SOD3 regulates equilibrium between superoxide (·O 2 ) and NO · , thereby controlling vascular tone and reactivity in the brain. That SOD3 opposes inactivation of NO · is shown by absence of vasoconstriction in response to P o 2 in the hyperbaric range in SOD3 +/+ mice, whereas NO-dependent relaxation is attenuated in SOD3 −/− mutants. Thus, EC-SOD promotes NO · vasodilation by scavenging ·O 2 while hyperoxia opposes NO · and promotes constriction by enhancing endogenous ·O 2 generation and decreasing basal vasodilator effects of NO · .

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine,Physiology

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