engleski

Natriuretic peptides and bradykinin in mouse ischemic brain injury

Cessation of glucose and oxygen supply after ischemic brain injury leads to apoptotic and nectotic processes, which results in breakdown of the blood-brain barrier and consequent cerebral edema formation. Bradykinin is involved in the formation of cerebral edema increasing the size of brain damage. The aim of our research was clarifying the possible mechanisms of action of natriuretic peptides on bradykinin signaling, and their interaction after ischemic brain injury, since natriuretic peptides decrease brain edema via still unknown mechanisms. The results of this research indicate the existence of an endogenous antagonist of the bradykinin type 2 receptor and the possible protective role of natriuretic peptides in treatment of stroke.

natriuretic peptides; bradykinin; ischemic brain injury

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