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Nitric oxide regulation of the central aortae of the toad Bufo marinus occurs independently of the endothelium

Brad R. S. Broughton^* and John A. Donald

School of Biological and Chemical Sciences, Deakin University, Geelong, Victoria, Australia 3217

View larger version (12K): [in a new window]   Fig. 1. (A) Tension recording showing the effect of sodium nitroprusside (SNP) on the lateral aorta. The aorta was exposed to endothelin-1 (ET-1; 10-8 mol l-1) until a maximal constriction was achieved and then SNP (10-4 mol l-1) was added. SNP caused a marked vasodilation. (B) Mean responses (% vasodilation) of pre-constricted lateral and dorsal aortae to SNP (10-4 mol l-1; N=5).

View larger version (12K): [in a new window]   Fig. 2. (A) Tension recording showing the effect of acetylcholine (ACh) on the dorsal aorta. The aorta was exposed to endothelin-1 (ET-1; 10-8 mol l-1) until a maximal constriction was achieved and then ACh (10-5 mol l-1) was added. ACh caused a marked vasodilation. (B) Mean responses (% vasodilation) of pre-constricted lateral and dorsal aortae to acetylcholine (10-5 mol l-1; N=5).

View larger version (10K): [in a new window]   Fig. 3. Tension recordings showing the effect of acetylcholine (ACh) on the dorsal aorta with (A) or without (B) the presence of the soluble guanylyl cyclase inhibitor oxadiazole quinoxalin-1 (ODQ). The vessels were pre-treated with ODQ (10-5 mol l-1) for approximately 10 min before being constricted with endothelin-1 (ET-1; 10-8 mol l-1). At the peak of vasoconstriction, ACh (10-5 mol l-1) was administered. ACh caused a constriction in the preparation incubated with ODQ (A) and a vasodilation in the preparation without ODQ (B) (N=5).

View larger version (9K): [in a new window]   Fig. 4. Tension recordings showing the effect of acetylcholine (ACh) on the lateral aorta with (A) or without (B) the presence of the NOS inhibitor N-nitro-L-arginine (L-NNA). The preparations were pre-treated with L-NNA (10-4 mol l-1) for approximately 10 min before being constricted with endothelin-1 (ET-1; 10-8 mol l-1). At the peak of vasoconstriction, acetylcholine (Ach; 10-5 mol l-1) was administered, which only caused a marked vasodilation in the preparation without L-NNA (B) (N=5).

View larger version (13K): [in a new window]   Fig. 5. Tension recordings showing the vasodilatory effect of acetylcholine (ACh) on the lateral aorta with the endothelium removed (A) and with the endothelium intact (A). The preparations were exposed to endothelin-1 (ET-1; 10-8 mol l-1) until a maximum constriction was achieved and then ACh (10-5 mol l-1) was added. (C) Mean response (% vasodilation) of ACh on pre-constricted lateral and dorsal aortae with the endothelium removed (filled bars) or the endothelium intact (open bars). Note that there is no significant difference in the ACh-mediated dilation (lateral aortae, P=0.26; dorsal aorta, P=0.35; N=5).

View larger version (15K): [in a new window]   Fig. 6. Tension recordings showing the effect of acetylcholine (ACh) on the lateral aorta with (A) or without (B) the nNOS inhibitor vinyl-L-NIO. The preparations were exposed to endothelin-1 (ET-1; 10-8 moll-1) until a maximum constriction was achieved and then vinyl-L-NIO (10-4 moll-1) was added for approximately 10min. Subsequently, ACh (10-5 moll-1) was added. The vasodilatory response was reduced in the presence of vinyl-L-NIO. (C) Mean response (% vasodilation) of ACh on ET-1-constricted lateral and dorsal aortae with (filled bars) or without (open bars) the presence of vinyl-L-NIO. Note that vinyl-L-NIO significantly reduced the ACh-mediated vasodilation (lateral and dorsal aortae, P<0.05, *denotes significant difference; N=5).

View larger version (165K): [in a new window]   Fig. 7. Photomicrographs showing whole-mount preparations of the rat aorta (A,B) and the toad lateral aorta (C,D) following processing for NADPH diaphorase histochemistry (A,C) and endothelial nitric oxide synthase (NOS) immunohistochemistry (B,D). In the rat aorta, punctate NOS-positive staining (arrowheads) occurred around the nuclei (arrows) of the endothelial cells, which was demonstrable with both techniques (A,B). In contrast, no NOS-positive staining was observed around the nuclei of the endothelial cells in the toad lateral aorta (C,D). Scale bars, 10µm.

View larger version (162K): [in a new window]   Fig. 8. Photomicrographs showing whole-mount preparations of the toad lateral (A,B) and dorsal (C,D) aortae following processing for NADPH diaphorase histochemistry (A,C) and neural nitric oxide synthase (NOS) immunohistochemistry (B,D). Using both techniques, a plexus of neural (n)NOS-positive perivascular nerve fibres (arrows) was observed in the outer layers of the wall of both vessels. In addition, some larger nNOS-positive perivascular nerve bundles (A, arrowhead) were observed. Scale bars, 100µm.