Fig. 6. (A) Schematic drawing showing the possible mechanism of regulation of vessel diameter of the main head artery in Xenopus laevis tadpoles before functional innervation of the peripheral vascular system. Endothelin (ET-1) is known to be a potent and long-lasting endothelium-derived vasoconstrictor. Nitric oxide (NO) can also be produced by the endothelium and has a dilatory effect. NO is known to be released in response to shear stress induction. Recent studies (see text, for references) provide evidence for a functional coordination and cooperation between NO and ET-1. The time course is indicated on the axis in B. The numbers in circles indicate the corresponding points in B. (1) Endothelin, possibly released by the endothelium, provokes a strong vasoconstriction, which in turn indirectly induces the release of NO (3) by increasing shear stress (2). NO acts directly on the vascular smooth muscle (vsm) to dilate the vessel (5). In addition, it acts as a ‘physiological brake’ on endothelin function by decreasing the affinity of ET-1 for its receptor (4), which enhances the vasodilation (5). L-NAME is a competitive inhibitor of the endothelial nitric oxide synthase. (6) The effect of preincubation with L-NAME. (B) Typical pharmacological experiments demonstrating the possible coordination and cooperation between NO and ET-1. SNP, sodium nitroprusside.
