| First Author | Meng W | Year | 1998 |
| Journal | Am J Physiol | Volume | 274 |
| Issue | 2 Pt 2 | Pages | H411-5 |
| PubMed ID | 9486242 | Mgi Jnum | J:45785 |
| Mgi Id | MGI:1196115 | Doi | 10.1152/ajpheart.1998.274.2.H411 |
| Citation | Meng W, et al. (1998) Neuronal NOS-cGMP-dependent ACh-induced relaxation in pial arterioles of endothelial NOS knockout mice. Am J Physiol 274(2 Pt 2):H411-5 |
| abstractText | 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 microM) dose dependently dilated pial arterioles in eNOS null and wild-type mice. ODQ (10 microM) attenuated ACh-induced dilation in both eNOS mutants (41% decrease at 10 microM ACh, P < 0.01, n = 6) and wild-type strains (n = 5 per group). By contrast, topical superfusion of 7-NI (100 microM) attenuated the ACh response in eNOS mutants only (66%, P < 0.05, and 25% decrease, P < 0.05, at 1 and 10 microM 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. |
