EFFECTS OF TESTOSTERONE ON HYPOXIC VENTILATORY AND CAROTID-BODY NEURAL RESPONSIVENESS

Hypoxic (HVR) and hypercapnic ventilatory responses (HCVR) are known to be influenced by the administration of testosterone, but whether the hormone acts centrally or peripherally is unknown. To determine whether testosterone alters HVR, HCVR, and carotid sinus nerve (CSN) responsiveness to hypoxia, we compared the ventilatory and CSN responses of neutered male cats treated with testosterone with those of placebo-treated cats. Testosterone treatment increased resting ventilation and CO, production but did not change end-tidal or arterial PCO2, implying that alveolar ventilation per unit CO2 production was unaltered. Testosterone treatment raised the HVR shape parameter A value 63% in the awake animals (from 16.9 +/- 4.2 to 28 +/- 4, p < 0.05) and 69% in the anesthetized cats (from 22.4 +/- 0.9 to 37.8 +/- 3.7, p < 0.05). Testosterone also augmented the HCVR slope S in awake cats (from 0.17 +/- 0.02 to 0.25 +/- 0.04, p < 0.05). Placebo treatment did not change HVR or HCVR. The CSN response to hypoxia was greater in the testosterone-treated than in the placebo-treated animals(A = 53.6 +/- 7.1 versus 27.1 +/- 5.5 respectively, p < 0.05). The crossplot of the simultaneously measured CSN activity and ventilation during progressive hypoxia showed that the central nervous system translation of CSN output into ventilation was similar in the hormone- and placebo-treated groups. Unilateral, proximal sectioning of the CSN decreased the ventilatory and the CSN responses to hypoxia in the testosterone-treated animals but not in the placebo group. These results indicated that testosterone increased hypoxic and hypercapnic ventilatory responsiveness and increased hypoxic sensitivity of the carotid body. The latter of feet seemed to depend on descending central neural activity.