The Effect of Insulin Hypoglycemia on the Secretion of Adrenaline and Noradrenaline from the Suprarenal of Cat<sup>1</sup>

Dunér, H

doi:10.1111/j.1748-1716.1954.tb01155.x

Cited by 66 publications

(20 citation statements)

References 3 publications

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“…The finding suggests, first, that the central neural representations of the adrenal medulla and the vasomotor systems are in part distinct. This feature of the central organization of the autonomic nervous system is not widely appreciated, but it is implicit in findings that adrenal catecholamines may be released reflexively through activation of receptors within the central nervous system by hypoglycemia induced by insulin or 2-deoxy-D-glucose (26)(27)(28)(29)(30)(31)(32) in the absence of significant hypertension (27). Second, it indicates that pathways originating in or passing through the AH exert control over the adrenal medulla, thereby pointing to a specific area of the brain involved in adrenomedullary control.…”

Section: Discussionmentioning

confidence: 99%

Fulminating arterial hypertension with pulmonary edema from release of adrenomedullary catecholamines after lesions of the anterior hypothalamus in the rat.

Nathan¹,

Reis²

1975

Circulation Research

100

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Bilateral electrolytic lesions of the anterior hypothalamus in unrestrained rats resulted in the development, within 2 hours, of arterial hypertension, tachycardia, hyperthermia, and increased locomotor activity, often leading to pulmonary edema and death. Similar lesions in paralyzed, artificially ventilated rats produced comparable changes in arterial blood pressure and body temperature with a similar time course. The arterial hypertension was a consequence of an increase in total peripheral resistance to 15% of control with a reduction in cardiac output to 49% of control. Arterial hypertension, elevated peripheral resistance, and diminished cardiac output were reversed toward normal by alpha-receptor blockade with phentolamine (1 mg/kg, iv). Bilateral adrenalectomy, adrenal demedullation, or adrenal denervation performed prior to lesion placement prevented the development of arterial hypertension and pulmonary edema as well as the changes in peripheral resistance, cardiac output, and body temperature. We conclude that arterial hypertension following lesions of the anterior hypothalamus is due to a neurally mediated increase in peripheral resistance initiated by the release of adrenal medullary catecholamines and that pulmonary edema is due to myocardial failure secondary to the ensuing ventricular overload. Structures originating in or passing through the anterior hypothalamus may exert selective control over the adrenal medulla independent of vasomotor neurons.• In 1954, Maire and Patton (1) demonstrated that bilateral electrolytic lesions of the anterior hypothalamus (AH) result in the development of a syndrome of hyperactivity, hyperthermia, and fatal pulmonary edema in the rat. Although cardiovascular measurements were not made, Maire and Patton attributed the pulmonary edema to a neurogenically mediated shift of blood from the capacitance vessels into the pulmonary circulation (2). More recently, Doba and Reis (3, 4) have observed that fulminating pulmonary edema can also be produced in the rat by bilateral lesions of the nucleus tractus solitarii (NTS), a brainstem nucleus in the medulla oblongata serving as a site of termination of arterial baroreceptors. In this instance, the pulmonary edema is due to the rapid development of neurogenic arterial hypertension with a marked increase in total peripheral resistance leading to a reduction in cardiac output and myocardial failure. Thus, the possibility exists that the pulmonary edema observed by Maire and This work was supported by Grant NS 03346 from NINDS and Grant NGR-33-010-179 from NASA and by the Harris Foundation.Received September 11, 1974. Accepted for publication May 13, 1975. Patton (1,2) after lesion of the AH was secondary to the development of arterial hypertension.In the present study, we investigated the hemodynamic changes following placement of lesions in the AH in the rat. Such lesions produced pulmonary edema as a consequence of arterial hypertension, and the hypertension was due to a neurally mediated release of adrenomedull...

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Section: Discussionmentioning

confidence: 99%

Fulminating arterial hypertension with pulmonary edema from release of adrenomedullary catecholamines after lesions of the anterior hypothalamus in the rat.

Nathan¹,

Reis²

1975

Circulation Research

100

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“…In certain species, the best documented of which is the cat, the proportions of adrenaline and noradrenaline have been found to vary with the particular type of stimulus employed (von Euler, 1956). Thus, adrenaline is released preferentially in response to hypoglycaemia in cats (Duner, 1954) and sheep (Crone, 1965). In the cat von Euler & Folkow (1953) originally showed that carotid occlusion favours the release of noradrenaline whereas stimulation of either the brachial or sciatic plexus favors the release of noradrenaline.…”

Section: Analytical Proceduresmentioning

confidence: 99%

Adrenal catecholamine output in response to stimulation of the splanchnic nerve in bursts in the conscious calf.

Edwards¹

1982

The Journal of Physiology

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SUMMARY1. Different patterns of stimulation have been applied to the peripheral end of the right splanchnic nerve, below behavioural threshold, in conscious 2-5-week-old calves.2. The effects of continuous stimulation at 4 Hz for 10 min were compared with those of stimulation at 40 Hz in 1 s bursts at 10 s intervals for the same period. Delivering the same total number of impulses in the form of bursts in this way increased the output of both adrenaline and noradrenaline and this increase was statistically significant in the case of adrenaline (P < 0'02) but not noradrenaline.3. The effects of stimulation in 1 s bursts at 10 s intervals for 2-3 min were investigated over the frequency range 10-150 Hz and compared with the effects of continuous stimulation over the range 1-15 Hz obtained previously in conscious calves of the same age (Edwards, Furness & Halle, 1980). The output of adrenaline but not noradrenaline was found to be significantly greater in response to stimulation in bursts at frequencies of up to 40 Hz than when the equivalent number of impulses were delivered at a constant rate (P < 0 02).4. It is concluded that the release of catecholamines from the adrenal gland is maximal at relatively high frequencies (40-100 Hz) when the impulses are delivered in bursts.

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“…For example, the maintenance of peripheral arterial resistance depends on the continuous transmission of appropriate signals through the lumbar sympathetic chain (but not, for example, the superior cervical ganglia); lipolysis in adipocytes is largely influenced by the coeliac ganglion and adrenal medullae (and less so by the superior cervical ganglia); the acceleration of melatonin synthesis that occurs when a mammal is placed in a dark environment involves signals carried by the superior cervical ganglia (but not by the stellate ganglion or the adrenal medullae) (Wurtman, Axelrod & Fischer, 1964); while that caused by hypoglycemia (Duner, 1954;Lynch, Ho & Wurtman, 1977) or the stress of immobilization (Lynch et al 1977) is mediated by adrenalin secretion from the adrenals.…”

Section: Introductionmentioning

confidence: 99%

Selective response of rat peripheral sympathetic nervous system to various stimuli

Ulus

Wurtman

1979

The Journal of Physiology

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SUMMARY1. We utilized the induction of tyrosine hydroxylase, a catecholamine-synthesizing enzyme, in sympathetic ganglia and adrenal medullae to explore the central and peripheral mechanisms through which choline, various environmental stresses, and drugs that alter blood pressure or central neurotransmission affect various portions of the sympathetic nervous system. Animals received each treatment chronically, and enzyme activity was measured in the superior cervical, stellate, and coeliac ganglia and in the adrenal medullae.2. Choline administration increased tyrosine hydroxylase activity in all four tissues, probably by increasing the release of acetylcholine from preganglionic sympathetic neurones that synapse on catecholamine-producing ganglion and chromaffin cells; carbachol and nicotine had similar effects.3. Insulin enhanced tyrosine hydroxylase activity primarily in the coeliac ganglion and the adrenal medullae, but not in the superior cervical ganglia.4. Reserpine and phenoxybenzamine increased the activity of the enzyme in all four tissues.5. Prolonged exposure to a cold environment increased enzyme activity in all four tissues, but especially in the stellate and coeliac ganglia; forced swimming affected tyrosine hydroxylase only in these two ganglia.6. Several drugs known to modify central neurotransmission were found to increase tyrosine hydroxylase activity in some portions of the sympathetic nervous system but not in others. 5,7-Dihydroxytryptamine, which destroys terminals of serotoninergic neurones, enhanced enzyme activity in all four tissues, but primarily in the coeliac ganglion and adrenal medullae. ET-495 (a dopaminergic agonist), D-amphetamine, and morphine induced tyrosine hydroxylase activity in the adrenal medullae and the coeliac ganglion, but not in the superior cervical ganglia. Oxotremorine, a centrally acting muscarinic agonist, increased tyrosine hydroxylase activity only in the adrenal medullae; its effect was not blocked by methylatropine, a peripheral muscarinic blocker.7. These data indicate that specific neurones in the central nervous system, which

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The Effect of Insulin Hypoglycemia on the Secretion of Adrenaline and Noradrenaline from the Suprarenal of Cat¹

Cited by 66 publications

References 3 publications

Fulminating arterial hypertension with pulmonary edema from release of adrenomedullary catecholamines after lesions of the anterior hypothalamus in the rat.

Fulminating arterial hypertension with pulmonary edema from release of adrenomedullary catecholamines after lesions of the anterior hypothalamus in the rat.

Adrenal catecholamine output in response to stimulation of the splanchnic nerve in bursts in the conscious calf.

Selective response of rat peripheral sympathetic nervous system to various stimuli

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The Effect of Insulin Hypoglycemia on the Secretion of Adrenaline and Noradrenaline from the Suprarenal of Cat1

Cited by 66 publications

References 3 publications

Fulminating arterial hypertension with pulmonary edema from release of adrenomedullary catecholamines after lesions of the anterior hypothalamus in the rat.

Fulminating arterial hypertension with pulmonary edema from release of adrenomedullary catecholamines after lesions of the anterior hypothalamus in the rat.

Adrenal catecholamine output in response to stimulation of the splanchnic nerve in bursts in the conscious calf.

Selective response of rat peripheral sympathetic nervous system to various stimuli

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The Effect of Insulin Hypoglycemia on the Secretion of Adrenaline and Noradrenaline from the Suprarenal of Cat¹