NOS activity in brain and endothelium: relation to hypercapnic rise of cerebral blood flow in rats

The American Journal of Physiology
M FabriciusM Lauritzen

Abstract

We examined whether attenuation of the hypercapnic increase of cerebral blood flow (CBF) associated with nitric oxide synthase (NOS) inhibition is related to local neuronal or aortic endothelial NOS activity or local endothelial/neuronal NOS-dependent vasodilation. Halothane-anesthetized rats were ventilated, and CBF was measured by laser-Doppler flowmetry over the parietal and cerebellar cortex. Intravenous N omega-nitro-L-arginine (L-NNA; 30 mg/kg) inhibited brain and aortic NOS activity by 67-70%. Topical L-NNA (1 mM) inhibited brain NOS activity by 91-94%, whereas aortic NOS activity remained constant. In contrast, intravenous L-NNA attenuated the hypercapnic CBF rise much more efficiently than topical L-NNA. 7-Nitroindazole, another NOS inhibitor, attenuated endothelial and neuronal NOS activity equally well and inhibited the hypercapnic CBF increase as effectively as L-NNA. Topical L-NNA and 7-nitroindazole abolished local endothelial NOS-dependent vasodilation after 15 min, whereas hypercapnic CBF was only slightly reduced. L-NNA injected into the tissue abolished neuronal NOS-dependent vasodilation, whereas hypercapnic CBF was unchanged. The findings suggest that local NOS activity, whether neuronal or endothelial, is u...Continue Reading

Citations

Aug 22, 2001·American Journal of Physiology. Heart and Circulatory Physiology·U LindauerU Dirnagl
Sep 20, 2000·American Journal of Physiology. Heart and Circulatory Physiology·K ThomsenM Lauritzen
Sep 16, 2003·Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism·Stephen C JonesAlejandro D Perez-Trepichio
May 2, 2006·American Journal of Physiology. Heart and Circulatory Physiology·Jonas HinkErik Jansen

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