EFFECTS OF INHIBITION OF NITRIC-OXIDE SYNTHESIS AND OF HYPERCAPNIA ONBLOOD-PRESSURE AND BRAIN BLOOD-FLOW IN THE TURTLE

In the mammalian brain, nitric oxide (NO) is responsible for a vasodil atory tonus as well as the elevation of cerebral blood flow (CBF) indu ced by hypercapnia, There have been few comparative studies of cerebra l vasoregulation in lower vertebrates, Using epi-illumination microsco py in vivo to observe CBF velocity on the brain surface (cerebral cort ex), we show that turtles (Trachemys scripta) exposed to hypercapnia ( inspired P-CO2=4.9 kPa) displayed a 62 % increase in CBF velocity, whi le systemic blood pressure remains constant, Exposing turtles to a P-C O2 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 pr essure. The elevated CBF velocity during hypercapnia could not be bloc ked by a systemic injection of the NO synthase (NOS) inhibitor NG-nitr o-L-arginine (L-NA), However, L-NA injection caused a temporary stop i n CBF as well as a persistent increase in systemic blood pressure, sug gesting that there is a NO tonus that is attenuated by the NOS-inhibit or and that CBF is strongly dependent on this tonus, although compensa tory mechanisms exist, Thus, although the cerebrovascular reaction to hypercapnia appeared to be NO-independent, the results suggest that th ere is a NO-dependent vasodilatory tonus affecting both cerebral and s ystemic blood circulation in this species.