TY - JOUR
T1 - Reflex stimulation of renal sympathetic nerve activity and blood pressure in response to apnea
AU - O'Donnell, C. P.
AU - Schwartz, A. R.
AU - Smith, P. L.
AU - Robotham, J. L.
AU - Fitzgerald, R. S.
AU - Shirahata, M.
PY - 1996
Y1 - 1996
N2 - The purpose of this study was to examine the role of afferent input in the reflex modulation of renal sympathetic nerve activity (SNA) in response to apnea. Apneas of 20-, 40-, and 60-s duration were induced in the anesthetized, paralyzed cat (n = 7) ventilated with either room air or 100% oxygen. While receiving room air, there were increases (p < 0.005) in renal SNA of 34.5 ± 4.2%, 53.3 ± 6.4%, and 59.9 ± 7.2% of maximum during the 20-, 40-, and 60-s apneas, respectively. There were corresponding increases (p < 0.025) in mean arterial pressure (P̄ā) of 9 ± 3, 30 ± 9, and 45 ± 12 mm Hg during the 20-, 40-, and 60-s apneas while receiving room air, respectively. The effect of 100% oxygen was to reduce (p < 0.0001) the renal SNA response to apnea, at a matched level of Pa(CO2), by at least 800%, and to eliminate any increase in P̄ā. During the first breath of the postapneic period, there was a partial inhibition of renal SNA. During the second and third breaths of the postapneic period, there was a marked fall in renal SNA that was associated with a precipitous decline in directly recorded carotid chemoreceptor activity (n = 2). The magnitude of the fall in renal SNA after apnea was related to the degree of postapneic hypertension. We conclude that hypoxic chemoreceptor stimulation is the predominant factor generating the renal SNA response to apnea, with modulating inputs from thoracic afferents and arterial baroreceptors likely contributing to the marked inhibition of renal SNA immediately after the apnea.
AB - The purpose of this study was to examine the role of afferent input in the reflex modulation of renal sympathetic nerve activity (SNA) in response to apnea. Apneas of 20-, 40-, and 60-s duration were induced in the anesthetized, paralyzed cat (n = 7) ventilated with either room air or 100% oxygen. While receiving room air, there were increases (p < 0.005) in renal SNA of 34.5 ± 4.2%, 53.3 ± 6.4%, and 59.9 ± 7.2% of maximum during the 20-, 40-, and 60-s apneas, respectively. There were corresponding increases (p < 0.025) in mean arterial pressure (P̄ā) of 9 ± 3, 30 ± 9, and 45 ± 12 mm Hg during the 20-, 40-, and 60-s apneas while receiving room air, respectively. The effect of 100% oxygen was to reduce (p < 0.0001) the renal SNA response to apnea, at a matched level of Pa(CO2), by at least 800%, and to eliminate any increase in P̄ā. During the first breath of the postapneic period, there was a partial inhibition of renal SNA. During the second and third breaths of the postapneic period, there was a marked fall in renal SNA that was associated with a precipitous decline in directly recorded carotid chemoreceptor activity (n = 2). The magnitude of the fall in renal SNA after apnea was related to the degree of postapneic hypertension. We conclude that hypoxic chemoreceptor stimulation is the predominant factor generating the renal SNA response to apnea, with modulating inputs from thoracic afferents and arterial baroreceptors likely contributing to the marked inhibition of renal SNA immediately after the apnea.
UR - http://www.scopus.com/inward/record.url?scp=0030447536&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030447536&partnerID=8YFLogxK
U2 - 10.1164/ajrccm.154.6.8970368
DO - 10.1164/ajrccm.154.6.8970368
M3 - Article
C2 - 8970368
AN - SCOPUS:0030447536
SN - 1073-449X
VL - 154
SP - 1763
EP - 1770
JO - American journal of respiratory and critical care medicine
JF - American journal of respiratory and critical care medicine
IS - 6
ER -