Studies on the distribution of exogenous norepinephrine in the sympathetic neurotransmitter store.
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Measurements of the specific activity of norepinephrine in coronary sinus blood were made in intact dogs from 20 minutes to 48 hours after the endogenous norepinephrine pool had been labeled with tritiated norepinephrine. The specific activity in blood was observed to decline sharply during augmented release of norepinephrine into the blood either by tyramine administration or nerve stimulation in all experiments up to 5 hours after labeling the neurotransmitter pool. Although the values in blood more nearly approximated the specific activity measured simultaneously in the heart during augmented release, they were still consistently greater than tissue values. At 24 and 48 hours after labeling the pool, no change in specific activity in blood was observed after administration of tyramine or nerve stimulation and the values in blood and tissue showed no differences. These findings are interpreted to indicate that exogenous norepinephrine initially mixes with a portion of the neurotransmitter store which is in more rapid exchange with the blood and only slowly equilibrates with the entire store. This is presented as further evidence for considering the neurotransmitter pool to be nonhomogeneous.Keywords:
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We assessed the effects of age on cholinergic regulation of the hypothalamic-pituitary-adrenal axis and other neuroendocrine systems by measuring the plasma cortisol and β-endorphin responses to an infusion of the centrally active cholinesterase inhibitor physostigmine (0.0125 mg/kg) in 12 healthy older men (68 ± 1.7 yr) and 9 healthy young men (25 ± 1.4 yr). We also measured the responses to physostigmine of plasma GH, arginine vasopressin, epinephrine, and norepinephrine (NE). As estimated by comparing calculated areas under the curve, older subjects had greater cortisol (P = 0.02) and β-endorphin (P < 0.01) secretory responses, but a reduced GH (P < 0.01) secretory response. The arginine vasopressin response did not differ between groups. By analysis of variance, older subjects also had a greater epinephrine response (P = 0.01). Older subjects had higher basal NE concentrations (P < 0.05), but NE responses to physostigmine did not differ between groups. These findings suggest age-related enhancement of the cholinergic stimulatory regulation of the hypothalamic-pituitary-adrenal axis and adrenal medulla. They also confirm previous reports of reduced GH secretory response with aging in normal men.
Physostigmine
Basal (medicine)
Hypothalamic–pituitary–adrenal axis
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The disposition of norepinephrine (NE) in hypophysectomized rats has been investigated by labeling the neurotransmitter stores in sympathetic nerve endings with tracer doses of 3H-NE. The specific activity of cardiac NE was markedly decreased 24 hr after labeling in hypophysectomized rats. This was not the result of either decreased delivery or impaired uptake of 3H-NE since no defect in accumulationaccumulation was found 5 min after labeling. Similar but less marked changes were noted in the spleens of hypophysectomized rats, but not in the salivary glands. Since the endogenous NE concentration was elevated in the hypophysectomized animals, the increased release of tracer 3H-NE over 24 hr suggests more rapid turnover and synthesis of NE following hypophysectomy. (Endocrinology82: 175, 1968)
Hypophysectomy
Free nerve ending
Normetanephrine
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Reserpine
Tyramine
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The effects of electrical and chemical stimulations of the hypothalamus on the plasma levels of glucagon, insulin, and glucose were studied in undisturbed and free-moving rabbits. Electrical stimulation of the ventromedial hypothalamic nucleus (VMH) caused a marked increase in the circulating level of glucagon coincident with a rapid rise in the glucose level. The level of insulin did not increase during VMH stimulation, but increased after cessation of stimulation. Electrical stimulation of the lateral hypothalamic nucleus (LHN), on the other hand, did not alter the plasma level of either hormone. Microinjection of a minute amount of acetylcholine into the VMH led to a rapid increase in plasma glucagon, with a gradual rise in plasma glucose, but no significant change in the insulin level. The responses of glucagon and glucose to acetylcholine were almost completely blocked by previous treatment of the VMH with hexamethonium, but not with atropine. Microinjections of epinephrine and norepinephrine into the VMH also caused rises in the levels of both glucagon and insulin, although the effects of norepinephrine were much less than those of epinephrine. Injections of dopamine, serotonin, and γ-aminobutyric acid had no effect. Chemical stimulation of the LHN only with epinephrine induced a preferential rise in the insulin level without any significant change in the levels of glucagon and glucose. It is concluded that the actions of acetylcholine in the VMH, probably through activation of nicotinic receptor, and of epinephrine in the LHN are important for hypothalamic modulation of the selective releases of glucagon and insulin, respectively.
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It is unknown whether plasma catecholamines have direct physiologic effects on pituitary-adrenocortical secretion in man. Therefore we investigated the effects of epinephrine and norepinephrine on plasma concentrations of adrenocorticotropin (ACIH), β-endorphin and cortisol. Nineteen healthy male volunteers received infusions of either NaCl, epinephrine (0.10 µg/kg/min) or norepinephrine (0.15 µg/kg/min) for 20 minutes. 30 min before to 120 min after the infusion blood was continuously drawn to determine plasma levels of epinephrine, norepinephrine, and cortisol. In addition, ACIH and β-endorphin plasma concentrations were analyzed at 6 time points before, during and after infusion. Infusion of catecholamines increased epinephrine and norepinephrine concentrations in physiological ranges as observed during intense psychological stress or exhausting physical exercise. However, these increases in catecholamine plasma levels neither affected concentrations of POMC-derived hormones nor plasma levels of cortisol. We conclude that in man, physiologic increases in circulating catecholamines have no influence on pituitary-adrenal hormone concentrations.
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The iv injection of Asp1Val1-angiotensin II (All) was followed by increases in arterial plasma norepinephrine (NE) and epinephrine (E) concentrations and elevation of arterial blood pressure in the anesthetized Pekin duck. AII injection did not affect the concentration of unconjugated dopamine in arterial plasma. Adrenalectomy inhibited the increases in plasma NE and E concentrations elicited by AII. Pressor responses to AII also were diminished after adrenalectomy, whereas pressor responses to exogenous NE and tyramine were not measurably affected. The α-adrenergic blocking drug phenoxybenzamine diminished the pressor effect of AII in both shamoperated and adrenalectomized ducks. The blockade of α-adrenergic receptors by phenoxybenzamine was incomplete, since pressor responses to exogenous NE were lessened but not abolished. We concluded from these experiments that AII increases arterial blood pressure in the Pekin duck by mobilizing NE and E from both adrenal and extraadrenal stores. It remains unknown whether the residual pressor response to AII in phenoxybenzamine-treated, adrenalectomized ducks involves an α-adrenergic mechanism.
Phenoxybenzamine
Normetanephrine
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Measurements of the specific activity of norepinephrine in coronary sinus blood were made in intact dogs from 20 minutes to 48 hours after the endogenous norepinephrine pool had been labeled with tritiated norepinephrine. The specific activity in blood was observed to decline sharply during augmented release of norepinephrine into the blood either by tyramine administration or nerve stimulation in all experiments up to 5 hours after labeling the neurotransmitter pool. Although the values in blood more nearly approximated the specific activity measured simultaneously in the heart during augmented release, they were still consistently greater than tissue values. At 24 and 48 hours after labeling the pool, no change in specific activity in blood was observed after administration of tyramine or nerve stimulation and the values in blood and tissue showed no differences. These findings are interpreted to indicate that exogenous norepinephrine initially mixes with a portion of the neurotransmitter store which is in more rapid exchange with the blood and only slowly equilibrates with the entire store. This is presented as further evidence for considering the neurotransmitter pool to be nonhomogeneous.
Tyramine
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Norepinephrine (NE) is a neurotransmitter of the sympathetic nervous system which is important in GH secretion. It also is a counterregulatory hormone which is released in response to insulin hypoglycemia. We measured the plasma NE, epinephrine, GH, and cortisol responses to insulininduced hypoglycemia in 29 short healthy children. The 8 patients (5 males and 3 females) which had isolated GH deficiency had no plasma NE response to insulin hypoglycemia, whereas mean plasma NE increased 2-fold in the 21 GH-sufficient children. Plasma epinephrine concentrations increased in both groups, but were lower in the GH-deficient patients. While these findings do not permit us to determine whether the reduced plasma catecholamine responses to acute hypoglycemia are the cause, the consequence, or unrelated to the GH deficiency, we speculate that there is a relationship between the NE and GH deficiencies.
Sympathetic nervous system
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