TY - JOUR
T1 - Functional evidence for sympathetic nerve activity in conscious cervical spinal rats
AU - Trostel, K. A.
AU - Katz, S. A.
AU - Osborn, J. W.
N1 - Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 1991
Y1 - 1991
N2 - Experiments in anesthetized animals have demonstrated sympathetic nerve activity after cervical spinal cord transection (CST), yet little evidence exists for sympathetic nerve activity in conscious spinal animals. We determined the effect of CST on mean arterial pressure (MAP), heart rate (HR), and plasma renin activity (PRA) in conscious rats. Next, we tested for the presence of functionally significant sympathetic nerve activity 24 h after CST by measuring MAP, HR, urine flow, urinary sodium excretion (U(Na)V), urinary potassium excretion (U(K)V), and PRA before and for 2 h during administration of adrenergic antagonists (propranolol + phentolamine) or vehicle. CST resulted in significant decreases in MAP (100.0 ± 1.6 to 75.0 ± 1.4 mmHg), HR (353 ± 7.5 to 315 ± 6.6 beats/min), and PRA (2.2 ± 0.3 to 1.2 ± 0.2 ng angiotensin I · ml-1 · h-1). Subsequent adrenergic blockade resulted in a further drop in HR (-52 ± 21 beats/min), as well as two- to threefold increases in U(Na)V and U(K)V. We conclude that CST causes an overall decrease in sympathetic drive. However, sympathetic nerve activity to the heart and kidney remains after CST and is responsible for support of HR and retention of sodium and potassium.
AB - Experiments in anesthetized animals have demonstrated sympathetic nerve activity after cervical spinal cord transection (CST), yet little evidence exists for sympathetic nerve activity in conscious spinal animals. We determined the effect of CST on mean arterial pressure (MAP), heart rate (HR), and plasma renin activity (PRA) in conscious rats. Next, we tested for the presence of functionally significant sympathetic nerve activity 24 h after CST by measuring MAP, HR, urine flow, urinary sodium excretion (U(Na)V), urinary potassium excretion (U(K)V), and PRA before and for 2 h during administration of adrenergic antagonists (propranolol + phentolamine) or vehicle. CST resulted in significant decreases in MAP (100.0 ± 1.6 to 75.0 ± 1.4 mmHg), HR (353 ± 7.5 to 315 ± 6.6 beats/min), and PRA (2.2 ± 0.3 to 1.2 ± 0.2 ng angiotensin I · ml-1 · h-1). Subsequent adrenergic blockade resulted in a further drop in HR (-52 ± 21 beats/min), as well as two- to threefold increases in U(Na)V and U(K)V. We conclude that CST causes an overall decrease in sympathetic drive. However, sympathetic nerve activity to the heart and kidney remains after CST and is responsible for support of HR and retention of sodium and potassium.
KW - Adrenergic antagonists
KW - Plasma renin activity
KW - Sodium excretion
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U2 - 10.1152/ajpregu.1991.261.2.r434
DO - 10.1152/ajpregu.1991.261.2.r434
M3 - Article
C2 - 1877700
AN - SCOPUS:0026063351
SN - 0002-9513
VL - 261
SP - R434-R441
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
IS - 2 30-2
ER -