Cardiopulmonary receptors with vagal afferents tonically inhibit ADH release in the dog

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Abstract
The effect of cardiopulmonary (CP) receptors with vagal afferents on tonic inhibition of secretion of vasopressin (ADH) was studied. The independent influence of these CP receptors on ADH secretion was not studied previously. The CP receptor role was assessed by measuring changes in plasma ADH (immunoassay), arterial pressure (AP), and heart rate (HR) in response to serial section of aortic (A), carotid sinus (CS) and vagal afferents in 6 anesthetized dogs. With vagal nerves intact, section of the A and of the CS afferents (in 6 dogs) caused minimal ADH changes, although AP and HR increased with each nerve pair section. Following sinoaortic denervation (SAD), vagotomy produced significant (P < 0.05) increases in ADH (11 .+-. 2 to 96 .+-. 38 .mu.U[micro units]/ml), AP (138 .+-. 9 to 210 .+-. 14 mmHg), and HR (182 .+-. 17 to 216 .+-. 20 beats/min). In 7 dogs simultaneous aortic and vagal nerve section produced significant increases in AP, HR and ADH (46 .+-. 20 to 81 .+-. 16 .mu.U/ml). Carotid baroreceptor denervation in these 7 dogs and in 2 others with prior vagotomy resulted in large increases in AP and ADH (36 .+-. 8 to 91 .+-. 17 .mu.U/ml), and a modest heart rate increase. CP receptors with vagal afferents prevented vasopressin increases following section of the sinoaortic baroreceptor afferents. After SAD, a pronounced inhibitory influence on ADH secretion was terminated by vagotomy.