Peripheral chemoreceptor contributions to sympathetic and cardiovascular responses during hypercapnia

Abstract

We tested the hypothesis that integrated sympathetic and cardiovascular reflexes are modulated by systemic CO2 differently in hypoxia than in hyperoxia (n = 7). Subjects performed a CO2 rebreathe protocol that equilibrates CO2 partial pressures between arterial and venous blood and that elevates end tidal CO2 (PETCO2) from ~40 to ~58 mmHg. This test was repeated under conditions where end tidal oxygen levels were clamped at 50 (hypoxia) or 200 (hyperoxia) mmHg. Heart rate (HR; EKG), stroke volume (SV; Doppler ultrasound), blood pressure (MAP; finger plethysmograph), and muscle sympathetic nerve activity (MSNA) were measured continuously during the two protocols. MAP at 40 mmHg PETCO2 (i.e., the first minute of the rebreathe) was greater during hypoxia versus hyperoxia (P < 0.05). However, the increase in MAP during the rebreathe (P < 0.05) was similar in hypoxia (16±3 mmHg) and hyperoxia (17 ± 2 mmHg PETCO2). The increase in cardiac output (Q) at 55 mmHg PETCO2 was greater in hypoxia (2.61 ± 0.7 L/min) versus hyperoxia (1.09 ± 0.44 L/min) (P < 0.05). In both conditions the increase in Q was due to elevations in both HR and SV (P < 0.05). Systemic vascular conductance (SVC) increased to similar absolute levels in both conditions but rose earlier during hypoxia (>50 mmHg PETCO2) than hyperoxia (>55 mmHg). MSNA increased earlier during hypoxic hypercapnia (>45 mmHg) compared with hyperoxic hypercapnia (>55 mmHg). Thus, in these conscious humans, the dose–response effect of PETCO2 on the integrated cardiovascular responses was shifted to the left during hypoxic hypercapnia. The combined data indicate that peripheral chemoreceptors exert important influence over cardiovascular reflex responses to hypercapnia. Key words: blood pressure, cardiac output, muscle sympathetic nerve activity, sympathetic nervous system, end tidal CO2, hypoxia.