Effects of inhibition of nitric oxide synthesis and of hypercapnia on blood pressure and brain blood flow in the turtle

In the mammalian brain, nitric oxide (NO) is responsible for a vasodilatory tonus as well as the elevation of cerebral blood flow (CBF) induced by hypercapnia, There have been few comparative studies of cerebral vasoregulation in lower vertebrates, Using epi-illumination microscopy in vivo to observe CBF velocity on the brain surface (cerebral cortex), we show that turtles (Trachemys scripta) exposed to hypercapnia (inspired P-CO2=4.9 kPa) displayed a 62 % increase in CBF velocity, while systemic blood pressure remains constant, Exposing turtles to a P-CO2 of 14.9 kPa caused an additional increase in CBF velocity, to 104 % above control values, as well as a 30 % increase in systemic blood pressure. The elevated CBF velocity during hypercapnia could not be blocked by a systemic injection of the NO synthase (NOS) inhibitor NG-nitro-L-arginine (L-NA), However, L-NA injection caused a temporary stop in CBF as well as a persistent increase in systemic blood pressure, suggesting that there is a NO tonus that is attenuated by the NOS-inhibitor and that CBF is strongly dependent on this tonus, although compensatory mechanisms exist, Thus, although the cerebrovascular reaction to hypercapnia appeared to be NO-independent, the results suggest that there is a NO-dependent vasodilatory tonus affecting both cerebral and systemic blood circulation in this species.