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Journal ArticleDOI

The human sympathochromaffin system.

TLDR
It is proposed that extra-CNS catecholamine-producing tissues be termed the sympathochromaffin system consisting of two components: 1) the sympathetic nervous system that releases the neurotransmitter norepinephrine from its postganglionic neurons, and 2) the chromaffin tissues that contain cells that secrete epinephrine, norpinephrine, or dopamine.
Abstract
Hypoglycemia stimulates adrenomedullary epinephrine secretion; standing stimulates sympathetic neural norepinephrine release. In five bilaterally adrenalectomized persons plasma epinephrine, measured with a sensitive single-isotope derivative assay, rose from 15 +/- 2 to 35 +/- 7 pg/ml (P less than 0.02) during hypoglycemia but did not increase during standing. In contrast, plasma norepinephrine rose during standing but not during hypoglycemia. Thus, in humans 1) extra-adrenal epinephrine secretion is regulated and derived from innervated cells other than sympathetic postganglionic neurons; 2) because the plasma levels of epinephrine in adrenalectomized individuals even in response to the potent stimulus of hypoglycemia are below physiological thresholds, any biological actions of extra-adrenal epinephrine in adults must be paracrine rather than endocrine in nature; 3) hypoglycemia does not appear to stimulate the sympathetic nervous system. In view of these findings, we propose that extra-CNS catecholamine-producing tissues be termed the sympathochromaffin system consisting of two components: 1) the sympathetic nervous system that releases the neurotransmitter norepinephrine from its postganglionic neurons, and 2) the chromaffin tissues, including the adrenal medullae, that contain cells that secrete epinephrine, norepinephrine, or dopamine. The plasma epinephrine concentration is a valid measure of its chromaffin tissue (predominantly adrenomedullary) secretion, whereas the plasma norepinephrine concentration is an index of sympathetic neuronal activity under some but not all conditions.

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Citations
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Journal ArticleDOI

Hypoglycemia-associated autonomic failure in insulin-dependent diabetes mellitus. Recent antecedent hypoglycemia reduces autonomic responses to, symptoms of, and defense against subsequent hypoglycemia.

TL;DR: Elevated glycemic thresholds for autonomic responses to hypoglycemia are a feature of IDDM per se, not classical diabetic autonomic neuropathy; and a single episode of afternoon hypglycemia results in both elevated glycemic threshold for autonomics and symptomatic responses to Hypoglycemi and impaired physiological defense against hypoglyCEmia the next morning in IDDM.
Journal ArticleDOI

Glycemic thresholds for activation of glucose counterregulatory systems are higher than the threshold for symptoms.

TL;DR: The glycemic thresholds for activation of glucose counterregulatory systems during decrements in plasma glucose lie within or just below the physiologic plasma glucose concentration range, and are substantially higher than the threshold for hypoglycemic symptoms in normal humans.
Journal ArticleDOI

Evolution of concepts of stress

David S. Goldstein, +1 more
- 01 Jun 2007 - 
TL;DR: This essay describes the evolution of stress as a medical scientific idea as a condition characterized by a perceived discrepancy between information about a monitored variable and criteria for eliciting patterned effector responses.
Journal ArticleDOI

Reversal of hypoglycemia unawareness, but not defective glucose counterregulation, in IDDM

TL;DR: It is concluded that several neuroendocrine responses to hypoglycemia (including the adrenomedullary and parasympathetic components of the autonomic response) can be dissociated from symptomatic responses in IDDM patients with hypoglyCEmia awareness and during reversal of hypoglycesmia unawareness in ID DM.
Journal ArticleDOI

Iatrogenic hypoglycemia as a cause of hypoglycemia-associated autonomic failure in IDDM. A vicious cycle.

TL;DR: Hypoglycemia-associated autonomic failure in IDDM, a disorder distinct from classical diabetic autonomic neuropathy, is proposed, with the following hypothesis concerning one potential pathogenetic mechanism.
References
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Journal ArticleDOI

Norepinephrine and Epinephrine Release and Adrenergic Mediation of Smoking-Associated Hemodynamic and Metabolic Events

TL;DR: Since significant smoking-associated increments, in pulse rate, blood pressure and blood lactate/pyruvate ratio, preceded measurable increments in plasma catecholamine concentrations, but were adrenergically mediated, these changes should be attributed to norepinephrine released locally from adrenergic axon terminals within the tissues rather than to increments in circulating catechlamines.
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Control of Enzymatic Synthesis of Adrenaline in the Adrenal Medulla by Adrenal Cortical Steroids

TL;DR: The activity of phenylethanolamine N- methyltransferase, the enzyme that catalyzes the N-methylation of noradrenaline to form adrenaline, falls following hypophysectomy, and can be restored by injections of adrenocorticotropic hormone (ACTH) or of dexamethasone, a potent synthetic glucOCorticoid.
Journal ArticleDOI

Measurements of plasma norepinephrine concentrations in human primary hypertension. A word of caution on their applicability for assessing neurogenic contributions.

TL;DR: It is concluded that NE concentrations in forearm or mixed venous blood are unreliable indicators of sympathetic neural contributions to essential hypertension, tending to underestimate this element, and that regional measurements of NE overflow are needed for a reliable analysis.
Journal ArticleDOI

Measurement of Norepinephrine and Epinephrine in Small Volumes of Human Plasma by a Single Isotope Derivative Method: Response to the Upright Posture

TL;DR: A single-isotope modification of the double- isotope derivative method for the measurement of norepinephrine and epinephrine, employing S-adenosylmethionine (3H-methyl) rather than S-andenosyln-methyl (14C-methyl), was found to be sufficiently sensitive and reproducible for the measurements of these catecholamines in 1.0 ml of human plasma obtained from supine, resting subjects.
Journal ArticleDOI

Isotope-derivative Measurements of Plasma Norepinephrine and Epinephrine in Man

Philip E. Cryer
- 01 Nov 1976 - 
TL;DR: It is concluded that excess of sympathetic drive only partly explains the level of the blood pressure in essential hypertension.
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