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Is blood pressure control in humans mediated by the peripheral chemoreceptors?
Author(s) -
Werhwein Erica A,
Mohamed E A,
Curry T B,
Basu A,
Rizza R A,
Basu R,
Joyner M J
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1076.3
Subject(s) - hyperoxia , baroreflex , chemoreceptor , blood pressure , medicine , microneurography , peripheral chemoreceptors , epinephrine , norepinephrine , hypoglycemia , endocrinology , hypoxia (environmental) , central chemoreceptors , sympathetic nervous system , anesthesia , baroreceptor , heart rate , chemistry , lung , insulin , receptor , oxygen , organic chemistry , dopamine
Peripheral chemoreceptors in the carotid bodies (CB) mediate sympathetic outflow to hypoxia and hypoglycemic counterregulation. With the developing understanding of the CB as multi‐modal sensors, we tested the hypothesis that the CB also play a role in the sympathetic control of blood pressure. Five young healthy subjects (3M/2F) were exposed to normoxia or hyperoxia to blunt cellular activation in the CB glomus cells during a hyperinsulinemic‐hypoglycemic clamp (60 mg/dl). Mean blood pressure during hypoglycemia was significantly lower with hyperoxia than with normoxia (delta reduction from baseline: −5.4 ± 3.4 mmHg normoxia vs. −13.8 ± 1.9 mmHg hyperoxia). Paradoxically, even though blood pressure was low, hypoglycemia with hyperoxia resulted in a significant reduction in plasma levels of norepinephrine (50.7% normoxia) and epinephrine (62.3% normoxia). The typical baroreflex‐mediated rise in sympathetic activity with lower blood pressure did not occur when the CB were silenced. These findings support the concept that peripheral chemoreceptors may modulate sympathetic control of blood pressure though interactions with the arterial baroreflexes. T32 DK07352, F32 DK84624‐01A1, CTSA 1 UL1 RR024150 , DK 29953