Blood pressure control in arterial- and cardiopulmonary receptor denervated dogs

The mechanisms influencing arterial blood pressure and heart rate were studied in conscious foxhounds after chronic sino-aortic and cardiopulmonary denervation (N = 6). In previous investigations it was shown, that this denervation produces hypertension and tachycardia, which is confirmed by the present study: Mean arterial blood pressure increased from 101 +/- 3 to 123 +/- 6 mmHg (P less than 0.05), and heart rate rose from 85 +/- 6 to 124 +/- 5 beats min-1 (P less than 0.001). The variability of mean arterial blood pressure, but not that of heart rate increased (from 6 +/- 1 to 22 +/- 2 mmHg (P less than 0.001). The administration of the alpha-adrenergic blocker prazosin reduced both mean arterial blood pressure (-33 +/- 8 mmHg, P less than 0.01) and its variability (-12 +/- 1 mmHg, P less than 0.01), thus suggesting an alpha-adrenergic mediated hypertension. beta-blockade by propranolol blunted the heart rate increase (-24 +/- 5 beats min-1, P less than 0.05). Although plasma renin activity increased in the denervated dogs, converting enzyme inhibition had little effect on mean arterial blood pressure and heart rate. In conclusion, chronic sino-aortic and cardiopulmonary denervation enhances the alpha and beta-adrenergic component of cardiovascular control in a different fashion. While the alpha-adrenergic component induces fluctuations around an elevated arterial blood pressure level, the beta-adrenergic tone to the heart increases without any significant increase in variability.