Parasympathetic Nerves Provide Tonic Vasodilator Influences to Cerebral Blood Vessels

Abstract

Stimulation of parasympathetic nerves from the pterygopalatine ganglia (PPG) to cerebral blood vessels leads to vasodilatation. Transection of the nerves reduces vasodilatation with acute hypertension, but the physiological role of the nerves under basal conditions is not known. We hypothesized that they mediate tonic cerebral vasodilatation and tested that hypothesis in freely breathing anesthetized rats instrumented for recording cerebral blood flow (CBF) with laser flowmetry and arterial blood pressure through an arterial cannula. Ipsilateral to the flow probe we exposed the PPG; and, after recording basal arterial pressure, arterial pCO2, and CBF, we quickly resected the PPG. Manipulating the PPG led to increased CBF, but removal of the PPG caused a gradual 28% decrease in cerebral blood flow (decrease of 13.5 ± 6.5 laser units) without changing mean arterial pressure. Cerebrovascular resistance increased after removal of the ganglion from 1.8 ± 0.3 units to 2.9 ± 0.5 units (p<0.01). After removal of the PPG, arterial pCO2 increased from 26.7 ± 3.2 Torr to 40.1 ± 3.7 Torr (p<0.01). Therefore, removal of parasympathetic input to cerebral blood vessels causes cerebral vasoconstriction. The study supports a tonic vasodilatory input to cerebral vessels from parasympathetic nerves. With hypercarbia the tonic effect is underestimated in these studies. Support: VA Merit Review and NIH R01 HL59593.