“…Our own laboratory has suggested that the pathway may contribute to cerebral vasodilatation during hypertension and thus extend cerebrovascular autoregulation (Talman, W. T. et al, 1994), a suggestion that has been echoed by others in the field (Toda, N. and Okamura, T., 1992). We have shown that arterial baroreceptors are critical for cerebral vasodilatation when blood pressure has been raised beyond the autoregulatory range (Talman, W. T. et al, 1994;Talman, W. T. and Nitschke Dragon, D., 1995b;Talman, W. T. and Nitschke Dragon, D., 2002); that the NTS, where arterial baroreceptor fibers terminate in the central nervous system (Blessing, W. W. et al, 1999;Ciriello, J., 1983;Kalia, M. and Sullivan, J. M., 1982;Torrealba, F. and Claps, A., 1988), projects directly to the SSN (Agassandian, K. et al, 2002); that interruption of function at the level of SSN or pterygopalatine ganglia extends the autoregulatory range during hypertension as does baroreflex interruption (Agassandian, K. et al, 2003;Talman, W. T. and Nitschke Dragon, D., 2000), and that non-selective inhibition of synthesis of NO released by those ganglionic fibers had the same effect (Talman, W. T. and Nitschke Dragon, D., 1995a). These studies further suggest that nitroxidergic nerves projecting from the pterygopalatine ganglion to cerebral blood vessels play a roll in the increase in CBF seen in breakthrough (Talman, W. T. and Nitschke Dragon, D., 2000).…”