We have investigated the effects of hypothyroidism on the ventilatory control. Adult male rats were made hypothyroid by adding 0.05% PTU (n-propylthiouracil) to the drinking water during 4-6 weeks. Ventilatory responses to hypoxic and hypercapnic atmosphere were studied by whole-body plethysmography in awake animals. Sensitivity of isolated carotid body (CB) to hypoxia (10% or 2% O₂-equilibrated media) and/or hypercapnia (20% CO₂-equilibrated media, pH 6,6) was studied in "in vitro" preparations by: a) recording the electrical activity in the carotid sinus nerve (CSN) and b) measuring the 3H-catecholamine release from CBs previously incubated in the presence of 3H-tyrosine.

In control rats, ten minutes breathing of air containing 12% or 7% O₂ increased pulmonary ventilation by 70% and 172% respectively; these responses were almost halved in PTU-treated animals. Similarly, hypothyroidism reduced by 30% the ventilatory response to hypercapnia (10% CO₂ / 20% O₂ / 70% N2 atmosphere). In CBs isolated from PTU-treated rats, both the increase of action potential frequency in the CSN and the evoked release of 3H-CAs induced by superfusion with low PO₂ were significantly reduced (80% and 52% decrease, respectively). The CSN responses to high extracellular K⁺ and to hypercapnic acidosis were not modified by PTU treatment. The above data suggest that hypothyroid status provokes a decrease in the hypoxic ventilatory drive mediated by a reduction in the chemosensitivity of the CB to hypoxia. Supported by PI052561 and PI042462 grants from the ISCIII.