Effect of baroreceptor denervation on vasopressin and cortisol responses to angiotensin II infusion in conscious dogs

Recent studies suggest that the pressor response to exogenous angiotensin II infusion may, through baroreceptor-dependent mechanisms, counteract the stimulatory effect of the peptide on vasopressin and adrenocorticotropic hormone (ACTH) secretion. To test this hypothesis, the effect of combined cardiac and sinoaortic baroreceptor denervation on the increases in plasma concentrations of vasopressin and cortisol (used as an index of ACTH secretion) produced by angiotensin II infusion was studied in conscious dogs. In eight intact dogs, 30-min angiotensin II infusions at 5, 10, and 20 ng · kg^-1 · min^-1 increased mean arterial pressure from 108 ± 5 to 126 ± 5 mmHg, from 101 ± 4 to 130 ± 4 mmHg, and from 99 ± 3 to 138 ± 4 mmHg, respectively (P < 0.001). Plasma cortisol concentration increased from 19 ± 4 to 27 ± 4 ng/ml, from 19 ± 4 to 43 ± 4 ng/ml, and from 19 ± 4 to 71 ± 6 ng/ml (P < 0.01), and plasma vasopressin concentration increased from 2.2 ± 0.3 to 3.1 ± 0.3 pg/ml, from 2.3 ± 0.3 to 3.5 ± 0.4 pg/ml, and from 2.2 ± 0.4 to 5.0 ± 0.5 pg/ml (P < 0.01). In five to six baroreceptor-denervated dogs, angiotensin II infusion produced increases in mean arterial pressure, plasma vasopressin concentration, and plasma cortisol concentration that were not consistently different from those in the intact dogs. These results demonstrate that baroreceptor denervation does not enhance the vasopressin or cortisol responses to angiotensin II infusion in conscious dogs.