Invited Symposium
Cerebral vasospasm and the hemoglobin-NO hypothesis
NO and tyrosine kinase signalling
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Macdonald, R.L. (Section of Neurosurgery, University of Chicago, USA)
Kowalczuk, A. (Section of Neurosurgery, University of Chicago, USA)
Zhang, Z-D. (Section of Neurosurgery, University of Chicago, USA)
Weir, B. (Section of Neurosurgery, University of Chicago, USA)
Abstract
Nitric oxide (NO) is a potent vasodilator with antiproliferative effects in smooth muscle. NO binds to heme groups and free -SH residues in proteins which can have positive or negative modulatory effects on enzymatic activity. NO has been shown to contribute to decreased tyrosine phosphorylation in a number of cell types including vascular smooth muscle. The in vitro application of hemoglobin solutions to arterial preparations causes vasoconstriction which may be mediated by binding or destruction of NO by hemoglobin. This contraction to hemoglobin is much greater in cerebral arteries than peripheral arteries and is not dependent upon an intact endothelium. The mechanism of action of hemoglobin in cerebral artries is consistent with NO binding for a nitric oxide synthase inhibitor induced a similar greater contraction of cerebral vs. peripheral arteries. We propose that an endogenously active nitric oxide synthase maintains tone in cerebral artery smooth muscle through the modulation of tyrosine kinase signalling pathways.
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Presentation Number SAmarton0628
Keywords: nitric oxide, hemoglobin, tyrosine, smooth muscle, cerebral artery
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