Contribution of adrenal norepinephrine output to increase aortic norepinephrine during carotid sinus reflex activation in anesthetized dogs

Yamaguchi, Nobuharu; Brassard, Martine; Briand, Richard

doi:10.1016/0024-3205(88)90566-8

Cited by 7 publications

(1 citation statement)

References 12 publications

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“…Therefore, the replaced saline volume was exactly the same as the bypassed adrenal venous blood volume, and the perfusion rate was still under the control of adrenal venous outflow. Adrenal venous blood, thus replaced, was drained continuously into another reservoir, and not returned to the dog (Yamaguchi et al 1988). …”

Section: Functional Adrenalcctomymentioning

confidence: 99%

Direct evidence that an increase in aortic norepinephrine level in response to insulin-induced hypoglycemia is due to increased adrenal norepinephrine output

Yamaguchi¹,

Briand²,

Brassard³

1989

Can. J. Physiol. Pharmacol.

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This study reports on the major source of circulating norepinephrine that is known to increase, progressively, during sustained hypoglycemia induced by intravenous insulin administration. Plasma concentrations of epinephrine, norepinephrine, and dopamine were simultaneously determined for adrenal venous and aortic blood in dogs anesthetized with sodium pentobarbital. The model used allowed us to perform a functional adrenalectomy (ADRX), while continuously monitoring the adrenal medullary secretory function. Under basal conditions, the net output (micrograms/min) of adrenal epinephrine, norepinephrine, and dopamine were 0.169 +/- 0.074, 0.067 +/- 0.023, and 0.011 +/- 0.003, respectively. Plasma concentrations (ng/mL) of aortic epinephrine, norepinephrine, and dopamine were 0.132 +/- 0.047, 0.268 +/- 0.034, and 0.034 +/- 0.009. Following insulin injection (0.15 IU/kg, i.v.), the net output (micrograms/min) of adrenal epinephrine, norepinephrine, and dopamine increased gradually (p less than 0.05), reaching the values of 0.918 +/- 0.200, 0.365 +/- 0.058, and 0.034 +/- 0.007 30 min after insulin administration. Similarly, aortic epinephrine, norepinephrine, and dopamine concentrations (ng/mL) increased significantly (p less than 0.05) to 0.702 +/- 0.144, 0.526 +/- 0.093, and 0.066 +/- 0.024. The aortic glucose concentration (mg/dL) was diminished from 81.8 +/- 4.1 to 36.9 +/- 3.4 (p less than 0.01). After taking the blood sample at 30 min following insulin administration, ADRX was immediately performed. Five minutes after the onset of ADRX, the net output (micrograms/min) of adrenal epinephrine, norepinephrine, and dopamine increased further to 1.707 +/- 0.374 (p less than 0.05), 0.668 +/- 0.139 (p less than 0.05), and 0.052 +/- 0.017.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Functional Adrenalcctomymentioning

confidence: 99%

Direct evidence that an increase in aortic norepinephrine level in response to insulin-induced hypoglycemia is due to increased adrenal norepinephrine output

Yamaguchi¹,

Briand²,

Brassard³

1989

Can. J. Physiol. Pharmacol.

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Simultaneous determination of plasma noradrenaline and adrenaline kinetics

Медведев

Esler

Angus

et al. 1990

Naunyn-Schmiedeberg's Arch Pharmacol

119

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Liquid chromatographic fractionation and detection of exogenous radiolabelled and endogenous catechols was used to examine simultaneously the plasma kinetics of noradrenaline and adrenaline in the conscious rabbit. Plasma clearances and release of noradrenaline and adrenaline into plasma were compared before and during nitroprusside-induced hypotension and 2-deoxyglucose-induced glucopenia, stimuli purported to differentially affect catecholamine release from sympathetic neurons and the adrenal medulla. Plasma concentrations of dihydroxyphenylglycol (DHPG) were also measured to assess presynaptic sympathetic function. Plasma clearances of adrenaline correlated with, but were significantly less than those of noradrenaline. Plasma clearances of both catecholamines showed significant decreases during nitroprusside-induced hypotension and 2-deoxyglucose-induced glucopenia. Glucopenia and hypotension increased the release into plasma of noradrenaline and adrenaline, but the adrenaline response relative to the noradrenaline response was greater during glucopenia than during hypotension. Plasma DHPG concentrations increased during glucopenia and hypotension, consistent with increased neuronal reuptake of noradrenaline and therefore a neuronal source--as opposed to an adrenal source--of most of the noradrenaline appearing in plasma during the stimuli. The increase in plasma DHPG relative to that of noradrenaline was greater after 2-deoxyglucose than after nitroprusside suggesting that the presynaptic handling of noradrenaline during glucopenia was different from that during hypotension or that the two stimuli released DHPG from regionally distinct sources.

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A differential effect of yohimbine on adrenal and neuronal catecholamine release during bilateral carotid occlusion in the dog

Yamaguchi

Brassard

1988

Journal of the Autonomic Nervous System

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Contribution of adrenal norepinephrine output to increase aortic norepinephrine during carotid sinus reflex activation in anesthetized dogs

Cited by 7 publications

References 12 publications

Direct evidence that an increase in aortic norepinephrine level in response to insulin-induced hypoglycemia is due to increased adrenal norepinephrine output

Direct evidence that an increase in aortic norepinephrine level in response to insulin-induced hypoglycemia is due to increased adrenal norepinephrine output

Simultaneous determination of plasma noradrenaline and adrenaline kinetics

A differential effect of yohimbine on adrenal and neuronal catecholamine release during bilateral carotid occlusion in the dog

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