Peripheral chemoreceptors may play an important role in the, neuroendocrine-mediated, control of glucose homeostasis (Koyama et al. 2000) through a hypoglycaemia-induced stimulation of carotid body glomus cells (Pardal & Lopez-Barneo, 2002). We postulated that carotid body stimulation by hypoglycaemia should therefore, like hypoxia, also induce hyperventilation.

Adult Wistar rats (300-370 g) were anaesthetised with pentobarbitone sodium (60 mg kg^-1, I.P.). Spontaneous ventilation (Î{special}_E) was measured as integrated tracheal airflow and blood pressure monitored from an indwelling arterial catheter. All animals were humanely killed at the end of the experiment. Data are expressed as means ± S.E.M. and significance (P < 0.05) tested with regression analysis and ANOVA.

Basal blood glucose was similar in both sham-operated, control (sham; n = 7) and carotid sinus nerve sectioned (CSNX; n = 7) animals (6.0 ± 0.1 and 6.3 ± 0.1 mmol l^-1 respectively; P > 0.05). Insulin infusion (0.4 U min^-1 kg^-1) lowered blood glucose concentration in both groups (P < 0.0001) to 3.3 ± 0.1 mmol l^-1 in sham and to 3.6 ± 0.1 mmol l^-1 in CSNX animals, values that were not different from each other (P > 0.07). Hypoglycaemia increased Î{special}_E in sham animals from 512.40 ± 7.58 to 613.33 ± 11.28 ml min^-1 kg^-1 (P < 0.001) but without any significant change in the arterial partial pressure of CO₂ (P_a,CJ{special}) or pH. In contrast, Î{special}_E did not increase in CSNX animals during hypoglycaemia and P_a,CJ{special} increased from 44.4 ± 0.7 to 48.7 ± 0.9 mmHg and pH decreased from 7.375 ± 0.007 to 7.348 ± 0.007 (P < 0.003 for both). In a separate group of sham and CSNX animals (n = 4 in each group), oxygen consumption (Î{special}J{special}) was measured using spirometry. Basal levels of Î{special}J{special} (28.22 ± 2.72 and 34.39 ± 3.16 ml min^-1 kg^-1 STPD; P > 0.1) and Î{special}_E/Î{special}J{special} ratios (16.69 ± 2.24 and 12.42 ± 1.55; P > 0.1) were not significantly different in sham and CSNX animals. During hypoglycaemia, Î{special}J{special} in both groups was significantly and similarly increased from the basal levels by 2.36 ± 0.3-fold in sham and 2.22 ± 0.2-fold in CSNX. The Î{special}_E/Î{special}J{special} ratio during hypoglycaemia was decreased significantly in CSNX animals to around half its basal value (P < 0.01) but remained unchanged in sham animals (P > 0.05).

These results demonstrate that hypoglycaemia can induce, as predicted, a carotid body-dependent increase in ventilation and in addition, we show that, in vivo, this response is directly proportional to the increased metabolism induced. Whether the stimulus is hypoglycaemia per se or some other factors related to the increased metabolism is not known.

We acknowledge the financial support of King Khalid University, Saudi Arabia and the British Heart Foundation.