Reductions in carotid chemoreceptor activity with low‐dose dopamine improves baroreflex control of heart rate during hypoxia in humans

• Published in: Physiological reports Vol. 4; no. 13; pp. np - n/a
• Main Authors: Mozer, Michael T., Holbein, Walter W., Joyner, Michael J., Curry, Timothy B., Limberg, Jacqueline K.
• Format: Journal Article
• Language: English
• Published: United States John Wiley & Sons, Inc 01.07.2016; John Wiley and Sons Inc
• Subjects: Adult; Baroreceptors; Baroreflex; Baroreflex - drug effects; Blood Pressure; Blood Pressure - drug effects; Carotid body; Carotid Body - drug effects; Carotid Body - physiopathology; Catheters; Chemoreceptors (internal); chemoreflex; Chronic illnesses; Dopamine; Dopamine - administration & dosage; Dopamine Agents - administration & dosage; Dose-Response Relationship, Drug; EKG; Female; Heart; Heart - innervation; Heart failure; Heart rate; Heart Rate - drug effects; Humans; Hyperoxia; Hypertension; Hypoxemia; Hypoxia; Hypoxia - drug therapy; Hypoxia - physiopathology; Infusions, Intravenous; Intravenous administration; Male; Nitrogen; Original Research; Physiology; Receptors, Dopamine - drug effects; Reflexes; tidal volume; Time Factors; Young Adult; blood pressure; heart rate; tidal volume; chemoreflex; dopamine; Baroreflex
• ISSN: 2051-817X; 2051-817X
• DOI: 10.14814/phy2.12859

The purpose of the present investigation was to examine the contribution of the carotid body chemoreceptors to changes in baroreflex control of heart rate with exposure to hypoxia. We hypothesized spontaneous cardiac baroreflex sensitivity (scBRS) would be reduced with hypoxia and this effect would be blunted when carotid chemoreceptor activity was reduced with low‐dose dopamine. Fifteen healthy adults (11 M/4 F) completed two visits randomized to intravenous dopamine or placebo (saline). On each visit, subjects were exposed to 5‐min normoxia (~99% SpO2), followed by 5‐min hypoxia (~84% SpO2). Blood pressure (intra‐arterial catheter) and heart rate (ECG) were measured continuously and scBRS was assessed by spectrum and sequence methodologies. scBRS was reduced with hypoxia (P < 0.01). Using the spectrum analysis approach, the fall in scBRS with hypoxia was attenuated with infusion of low‐dose dopamine (P < 0.01). The decrease in baroreflex sensitivity to rising pressures (scBRS “up‐up”) was also attenuated with low‐dose dopamine (P < 0.05). However, dopamine did not attenuate the decrease in baroreflex sensitivity to falling pressures (scBRS “down‐down”; P > 0.05). Present findings are consistent with a reduction in scBRS with systemic hypoxia. Furthermore, we show this effect is partially mediated by the carotid body chemoreceptors, given the fall in scBRS is attenuated when activity of the chemoreceptors is reduced with low‐dose dopamine. However, the improvement in scBRS with dopamine appears to be specific to rising blood pressures. These results may have important implications for impairments in baroreflex function common in disease states of acute and/or chronic hypoxemia, as well as the experimental use of dopamine to assess such changes. We hypothesized spontaneous cardiac baroreflex sensitivity (scBRS) would be reduced with hypoxia and this effect would be blunted when the carotid chemoreceptors were desensitized with low‐dose dopamine. Present findings are consistent with a reduction in scBRS with systemic hypoxia and we show this effect is partially mediated by the carotid body chemoreceptors, given the fall in scBRS is attenuated when the chemoreceptors are desensitized with low‐dose dopamine.However, the improvement in scBRS with dopamine appears to be specific to rising blood pressures.