Adrenaline Release Evokes Hyperpnoea and an Increase in Ventilatory COsub2/sub Sensitivity during Hypoglycemia: a role for the carotid body

Hypoglycaemia in vivo induces a counter-regulatory response that involves the release of hormones to restore blood glucose levels. Concomitantly, hypoglycaemia evokes a carotid body-mediated hyperpnoea that maintains arterial CO ₂ levels and prevents respiratory acidosis in the face of increased metabolism. It is unclear whether the carotid body is directly stimulated by low glucose or by a counter-regulatory hormone such as adrenaline. Minute ventilation was recorded during infusion of insulin-induced hypoglycaemia (8–17 mIU kg ⁻¹ min ⁻¹ ) in Alfaxan-anaesthetised male Wistar rats. Hypoglycaemia significantly augmented minute ventilation (123 ± 4 to 143 ± 7 ml min ⁻¹ ) and CO ₂ sensitivity (3.3 ± 0.3 to 4.4 ± 0.4 ml min ⁻¹ mmHg ⁻¹ ). These effects were abolished by either β-adrenoreceptor blockade with propranolol or adrenalectomy. In this hypermetabolic, hypoglycaemic state, propranolol stimulated a rise in , suggestive of a ventilation–metabolism mismatch. Infusion of adrenaline (1 μg kg ⁻¹ min ⁻¹ ) increased minute ventilation (145 ± 4 to 173 ± 5 ml min ⁻¹ ) without altering or pH and enhanced ventilatory CO ₂ sensitivity (3.4 ± 0.4 to 5.1 ± 0.8 ml min ⁻¹ mmHg ⁻¹ ). These effects were attenuated by either resection of the carotid sinus nerve or propranolol. Physiological concentrations of adrenaline increased the CO ₂ sensitivity of freshly dissociated carotid body type I cells in vitro . These findings suggest that adrenaline release can account for the ventilatory hyperpnoea observed during hypoglycaemia by an augmented carotid body and whole body ventilatory CO ₂ sensitivity.