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

Hypoxic (HVR) and hypercapnic ventilatory responses (HCVR) are known t o be influenced by the administration of testosterone, but whether the hormone acts centrally or peripherally is unknown. To determine wheth er testosterone alters HVR, HCVR, and carotid sinus nerve (CSN) respon siveness to hypoxia, we compared the ventilatory and CSN responses of neutered male cats treated with testosterone with those of placebo-tre ated cats. Testosterone treatment increased resting ventilation and CO , production but did not change end-tidal or arterial PCO2, implying t hat alveolar ventilation per unit CO2 production was unaltered. Testos terone treatment raised the HVR shape parameter A value 63% in the awa ke animals (from 16.9 +/- 4.2 to 28 +/- 4, p < 0.05) and 69% in the an esthetized cats (from 22.4 +/- 0.9 to 37.8 +/- 3.7, p < 0.05). Testost erone also augmented the HCVR slope S in awake cats (from 0.17 +/- 0.0 2 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-tre ated 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 m easured CSN activity and ventilation during progressive hypoxia showed that the central nervous system translation of CSN output into ventil ation was similar in the hormone- and placebo-treated groups. Unilater al, proximal sectioning of the CSN decreased the ventilatory and the C SN responses to hypoxia in the testosterone-treated animals but not in the placebo group. These results indicated that testosterone increase d hypoxic and hypercapnic ventilatory responsiveness and increased hyp oxic sensitivity of the carotid body. The latter of feet seemed to dep end on descending central neural activity.