Plasma Adrenaline and Noradrenaline After Phenoxybenzamine Administration, and During Haemorrhagic Hypotension, in Normal and Adrenalectomized Dogs

Millar, R.A.; Keener, E. B.; Benfey, B. G.

doi:10.1111/j.1476-5381.1959.tb00921.x

Cited by 33 publications

(20 citation statements)

References 5 publications

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“…We also obtained an inhibitory effect of adrenaline and noradrenaline on stress-induced ulceration (unpublished data). However, phentolamine and tolazoline, which prolong the biologic half-life of catecholamines in blood and urine (14)(15)(16), aggravated the stress-induced ulceration. Thus it was considered that the effect of adrenergic blocking agents on the gastric ulceration did not relate to the biologic half-life of catecholamines.…”

Section: Discussionmentioning

confidence: 99%

Effects of Adrenergic Blocking Agents on Gastric Secretion and Stress-Induced Gastric Ulcer in Rats

Okabe

Saziki

Takagi

1970

Japanese Journal of Pharmacology

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Recently interest in investigations of adrenergic agents (stimulants and inhibitors) on gastric secretion, motility, and ulceration in experimental animals has increased (1-7). Pradhan and Wingate (6) have demonstrated that phentolamine and tolazoline enhanced the spontaneous gastric secretion in dogs while phenoxybenzamine and dichloroisopro terenol showed inhibitory effects on spontaneous as well as induced secretion by food, bethanechol, and histamine. Bass and Patterson (3) have shown that both adrenergic and adrenergic blocking agents (including phentolamine and tolazoline) possessed anti secretory properties on rat gastric secretion. Hence, if gastric acid is a primary element in experimental ulcer, adrenergic and adrenergic blocking aegnts which have antisecretory effect should inhibit gastric ulceration. However, phentolamine, MJ 1999, and isopro terenol did not affect the incidence of histamine-induced ulcer in guinea pigs (6). More over, propranolol and phenoxybenzamine increased the incidence of ulceration in fasted rats immobilized for 8 hours (7). In this study, therefore, an attempt was made to in vestigate the effect of several adrenergic blocking agents on gastric secretion and stress induced ulcer in rats and to clarify a part of the mechanism of gastric ulceration by stress. METHODSGastric secretion studies: Male Donryu strain rats (200-230 g) were used in the follow ing experiments. The animals were deprived of food for 24 hours in individual cages prior to the experiment but were allowed free access to water. Under ether anesthesia, the abdomen was incised and the junction between the pylorus and duodenum was ligated, as described by Shay et al. (8). Four hours later, the animals were killed by a blow on the head and the stomach was removed. Gastric juice was collected in a graduated test tube and the total acidity was determined by titration with 0.1 N NaOH using phenol phthalein as an indicator. The pH was determined with a glass electrode.Stress ulcer studies: As described previously by Takagi and Okabe (9), animals (235 255 g) were placed in a stress cage and immersed into a water bath (23°C) for 7 hours to the level of xiphoid process. At the end of the stress, the animals were killed by a blow * Present address:

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Section: Discussionmentioning

confidence: 99%

Effects of Adrenergic Blocking Agents on Gastric Secretion and Stress-Induced Gastric Ulcer in Rats

Okabe

Saziki

Takagi

1970

Japanese Journal of Pharmacology

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“…For example, arterial NE increased during hemorrhagic hypotension, whereas pancreatic NE output did not. Because the increase of arterial NE observed during hypotension was unaffected by adrenal denervation, this increase of NE likely reflects neuronal NE release rather than the release of NE from the adrenal medulla (9,10). Nonpancreatic noradrenergic nerves thus were activated by hypotension, despite its failure to increase pancreatic noradrenergic activity.…”

Section: Discussionmentioning

confidence: 97%

“…To determine if the rise of NE measured in arterial plasma during stress was of neuronal origin, or derived from the adrenal medulla, as has been suggested by some reports (9,10), other dogs were adrenal deprived; they either had both adrenals surgically removed or completely isolated by ligation.…”

Section: Introductionmentioning

confidence: 99%

Pancreatic noradrenergic nerves are activated by neuroglucopenia but not by hypotension or hypoxia in the dog. Evidence for stress-specific and regionally selective activation of the sympathetic nervous system.

Havel¹,

Veith²,

Dunning³

et al. 1988

J. Clin. Invest.

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To determine if acute stress activates pancreatic noradrenergic nerves, pancreatic norepinephrine (NE) output (spillover) was measured in halothane-anesthetized dogs. Central neuroglucopenia, induced by intravenous 2-deoxy-D-glucose (12-DGJ 600 mg/kg + 13.5 mg/kg-' per min') increased pancreatic NE output from a baseline of 380±100 to 1,490±340 pg/min (A = +1,110±290 pg/min, P < 0.01). Surgical denervation of the pancreas reduced this response by 90% (A = +120±50 pg/ min, P < 0.01 vs. intact innervation), suggesting that 2-DG activated pancreatic nerves by increasing the central sympathetic outflow to the pancreas rather than by acting directly on nerves within the pancreas itself. These experiments provide the first direct evidence of stress-induced activation of pancreatic noradrenergic nerves in vivo. In contrast, neither hemorrhagic hypotension (50 mmHg) nor hypoxia (6-8% 02) increased pancreatic NE output (A = +80±110 and -20±60 pg/min, respectively, P < 0.01 vs. neuroglucopenia) despite both producing increases of arterial plasma NE and epinephrine similar to glucopenia. The activation of pancreatic noradrenergic nerves is thus stress specific. Furthermore, because both glucopenia and hypotension increased arterial NE, yet only glucopenia activated pancreatic nerves, it is suggested that a regionally selective pattern of sympathetic activation can be elicited by acute stress, a condition in which sympathetic activation has traditionally been thought to be generalized and nondiscrete.

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“…It may in part be due to a direct cardiac stimulant effect. Millar, Keener & Benfey (1959) have shown that intravenous injection of phenoxybenzamine raises the plasma levels of adrenaline and noradrenaline in dogs and the plasma level of noradrenaline in adrenalectomized dogs, and Benfey, Ledoux & Melville (1959) proved that increased plasma levels of adrenaline and noradrenaline result in an increased urinary excretion of catechol amines. These effects they attributed largely to nervous stimulation, reflex or direct, of adrenal medullary secretion because administration of hexamethonium prevented them.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Reserpine on the Pressor Response to Injection of 2‐halogenoethylamine

Graham

1961

British Journal of Pharmacology and Chemotherapy

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Dibenamine-like compounds sometimes caused an increase in blood pressure when injected intravenously in mammals. This response varied with species, with the preparation, and with the structure of the compound. The response became smaller after repeated injections. In spinal atropinized rats injected with hexamethonium 5 mg/kg this pressor effect produced by injection of the adrenaline antagonist, compound AT3 [ethylfluoren-9-yl(2-iodoethyl)amine hydriodide], was reduced by prior treatment for five days with 1 mg/kg reserpine. Acute adrenalectomy also reduced this effect of the adrenaline antagonist; reserpine plus adrenalectomy abolished it. Subsequent injection of adrenaline and noradrenaline restored it.It is well known that compounds like phenoxybenzamine [benzyl-(2-chlorethylXlmethyl-2-phenoxyethyl)amine] antagonize the pressor response to injected catechol amines and lower the blood pressure for prolonged periods. Less attention has been paid to the acute pressor response which may be caused by intravenous injection of the 2-halogenoethylamine itself. A study of this phenomenon may reveal an aspect of the activity of these compounds which is an essential preliminary to their antagonistic effect. METHODSDemonstration of the pressor action. Carotid blood pressure was recorded manometrically from the following preparations: (a) dogs anaesthetized with 40 mg/kg pentobarbitone sodium intravenously and injected with 5 mg of atropine sulphate subcutaneously,

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Plasma Adrenaline and Noradrenaline After Phenoxybenzamine Administration, and During Haemorrhagic Hypotension, in Normal and Adrenalectomized Dogs

Cited by 33 publications

References 5 publications

Effects of Adrenergic Blocking Agents on Gastric Secretion and Stress-Induced Gastric Ulcer in Rats

Effects of Adrenergic Blocking Agents on Gastric Secretion and Stress-Induced Gastric Ulcer in Rats

Pancreatic noradrenergic nerves are activated by neuroglucopenia but not by hypotension or hypoxia in the dog. Evidence for stress-specific and regionally selective activation of the sympathetic nervous system.

The Effect of Reserpine on the Pressor Response to Injection of 2‐halogenoethylamine

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