Blood pressure control in arterial‐ and cardiopulmonary receptor denervated dogs

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Abstract
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 < 0.05), and heart rate rose from 85 ± 6 to 124 ± 5 beats min‐l (P < 0.001). The variability of mean arterial blood pressure, but not that of heart rate increased (from 6 ± 1 to 22 ± 2 mmHg (P < 0.001)). The administration of the a‐adrenergic blocker prazosin reduced both mean arterial blood pressure (‐33 ± 8 mmHg, P < 0.01) and its variability (‐ 12 ± 1 mmHg, P < 0.01), thus suggesting an α‐adrenergic mediated hypertension. β‐blockade by propranolol blunted the heart rate increase (‐ 24 ± 5 beats min‐1 P < 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 α and β‐adrenergic component of car diovascular control in a different fashion. While the α‐adrenergic component induces fluctuations around an elevated arterial blood pressure level, the β‐adrenergic tone to the heart increases without any significant increase in variability.