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Am J Physiol Heart Circ Physiol 274: H411-H415, 1998;
0363-6135/98 $5.00
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Vol. 274, Issue 2, H411-H415, February 1998

Neuronal NOS-cGMP-dependent ACh-induced relaxation in pial arterioles of endothelial NOS knockout mice

Wei Meng1, Cenk Ayata1, Christian Waeber1, Paul L. Huang2, and Michael A. Moskowitz1

1 Stroke and Neurovascular Regulation Laboratory, Departments of Neurosurgery and Neurology and 2 Cardiovascular Research Center, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129

We evaluated the effects of superfusing 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), eNOS null (B)an inhibitor of soluble guanylyl cyclase, and 7-nitroindazole sodium (7-NI), a selective neuronal nitric oxide synthase (nNOS) inhibitor, on the acetylcholine (ACh) response in endothelial NOS (eNOS) null mice. Pial arteriolar diameter was measured by intravital microscopy through a closed cranial window under alpha -chloralose anesthesia. NOS activity was measured by [3H]arginine-to-[3H]citrulline conversion in subjacent cortex in vitro. The density and distribution of muscarinic receptors in the brain were determined by quantitative [3H]quinuclidinyl benzilate autoradiography and did not differ between the eNOS mutants and wild-type mice. ACh superfusion (1 and 10 µM) dose dependently dilated pial arterioles in eNOS null and wild-type mice. ODQ (10 µM) attenuated ACh-induced dilation in both eNOS mutants (41% decrease at 10 µM ACh, P < 0.01, n = 6) and wild-type strains (n = 5 per group). By contrast, topical superfusion of 7-NI (100 µM) attenuated the ACh response in eNOS mutants only (66%, P < 0.05, and 25% decrease, P < 0.05, at 1 and 10 µM ACh, respectively). Our findings suggest that nNOS-guanosine 3',5'-cyclic monophosphate (cGMP)-dependent pathways dilate pial arterioles by compensatory mechanisms after eNOS gene disruption.

endothelial nitric oxide synthase; neuronal nitric oxide synthase; soluble guanylyl cyclase; mutant mice; acetylcholine; cerebral circulation; closed cranial window


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