Parasympathetic inhibition of sympathetic neural activity to the pancreas

The present study tested the hypothesis that activation of the parasympathe tic nervous system could attenuate sympathetic activation to the pancreas. To test this hypothesis, we measured pancreatic norepinephrine (NE) spillov er (PNESO) in anesthetized dogs during bilateral thoracic sympathetic nerve stimulation (SNS; 8 Hz, 1 ms, 10 mA, 10 min) with and without (randomized design) simultaneous bilateral cervical vagal nerve stimulation (VNS; 8 Hz, 1 ms, 10 mA, 10 min). During SNS alone, PNESO increased from the baseline of 431 +/- 88 pg/ min to an average of 5,137 +/- 1,075 pg/ min (P < 0.05) o ver the stimulation period. Simultaneous SNS and VNS resulted in a signific antly (P < 0.01) decreased PNESO response [from 411 +/- 61 to an average of 2,760 +/- 1,005 pg/min (P < 0.05) over the stimulation period], compared w ith SNS alone. Arterial NE levels increased during SNS alone from 130 +/- 1 1 to <similar to>600 pg/ml (P < 0.05); simultaneous SNS and VNS produced a significantly (P < 0.05) smaller response (142 +/- 17 to 330 pg/ ml). Musca rinic blockade could not prevent the effect of VNS from reducing the increa se in PNESO or arterial NE in response to SNS. It is concluded that parasym pathetic neural activity opposes sympathetic neural activity not only at th e level of the islet but also at the level of the nerves. This neural inhib ition is not mediated via muscarinic mechanisms.