Conditions Determining Adrenal Secretion

Hartman, Frank A.; McCordock, Howard A.; M, Loder

doi:10.1152/ajplegacy.1923.64.1.1

Cited by 30 publications

(5 citation statements)

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“…It is known that A is released in animals subjected to severe cold exposure (Hartman et al 1923, Cannon et al 1927, Saito 1928, Wada, Seo and Abe 1935. However, as shown by later workers (Heroux 1955, Desmarais 1957, Leduc 1961 adrenalectomy does not prevent animals from adapting and surviving cold exposure.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Gold Exposure on the Catecholamine Excretion of Rats Treated with Decaborane

Johnson

1966

Acta Physiologica Scandinavica

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JOHNSON, D. G. The efect of cold exposure on the catecholamine excretion of rats treated with decaborane. Acta physiol. scand. 1966. 68. 129-1 33.Rats treated with decaborane exhibited a marked reduction in the noradrenaline (NA) content of heart. liver, and spleen but no significant fall in adrenal catecholamines. Decaborane-treated animals excreted less NA but more adrenaline (A) than control animals. When exposed to 3" C, control animals survived and showed increased NA excretion in contrast to decaborane-treated rats, which, however, responded with increased excretion of A until death after 4-6 days. Unlike adrenalectomized controls adrenalectomized rats treated with decaborane failed to increase their NA excretion during cold exposure and died in less than 20 hrs. Thesurvival of cold-exposed animals appears to be related to the liberation of NA, with A release serving as an important secondary mechanism of defense against cold. T h e results suggest that decaborane treatment curtails the supply of NA in vivo, presumably owing to inhibition of synthesis.

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Section: Discussionmentioning

confidence: 99%

The Effect of Gold Exposure on the Catecholamine Excretion of Rats Treated with Decaborane

Johnson

1966

Acta Physiologica Scandinavica

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“…The early work of Hartman et al (1923) and of Cannon et al (1927) implicated catecholamine secretion from the adrenal medulla in non-shiver ing thermogenesis, and Heish et al (1957) demonstrated the im portance of the peripheral sympathetic nervous system in the regulation of heat production by showing that sympathetic blockade inhibits the rise in oxygen consumption during cold expsoure. Later studies revealed that cold exposure increases catecholamine excretion (Von Euler, 1960;Leduc, 1961), and more recently Oliverio and Stjdrne (1965) found an increased turnover rate of heart NE in mice exposed to 5°.…”

Section: Evidence For the Importance Of Brain Ne In Thermoregulationmentioning

confidence: 99%

Brain Amines and Temperature Regulation

et al. 1968

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“…Interestingly, cold exposure of equithesin-anaesthetized rats over a period of 60 min resulted in a continuous rise in the plasma levels of noradrenaline and adrenaline, and while the rise in the plasma level of adrenaline was prevented by adrenalectomy, that of noradrenaline was not (Khalilet al 1986). Release of adrenaline from the adrenals in response to cold was first demonstrated in the 1920s Hartman, McCordock & Loder, 1923;Cannon, Querido, Britton & Bright, 1927). Hebb & Stavraky (1936) drew attention to an effect of the adrenal on salivary glands in the cold, both adrenaline and cold being found to increase the glucose concentration of saliva in the cat.…”

Section: Discussionmentioning

confidence: 98%

The role of circulating catecholamines in the depletion of parotid acinar granules in conscious rats in the cold

Asztély¹,

Tobin²,

Ekström³

1996

Experimental Physiology

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SUMMARYThe possibility that circulating catecholamines might affect parotid gland function during feeding (over a period of 80 min) and cold stress (2-4°C) was investigated in rats that had been fasted for 30 h. In the first set of experiments, in which the glands had been sympathectomized by removing both superior cervical ganglia 10-12 days previously, there was a substantial reduction in the density of acinar secretory granules (42 % compared with non-fed animals in the cold) and in the total glandular amylase activity (54 %). However, similar, or even greater, losses were recorded in rats subjected to additional bilateral adrenal medullectomy and pretreatment with atropine and aand ,/-adrenoceptor blockers. The losses were therefore attributed to activation of parasympathetic non-adrenergic, non-cholinergic mechanisms. In a second set of experiments, employing only morphometric assessment, the parasympathetic auriculotemporal nerve was cut on one side in addition to bilateral sympathectomy and, as a further precaution, the animal was atropinized. It was then found that there was a loss of 17 % of granules in the parasympathectomized plus sympathectomized gland, but not the contralateral gland, of non-fed cold-exposed rats compared with non-fed animals kept at room temperature. When rats were fed as well as exposed to cold the number of granules in parasympathectomized plus sympathectomized glands fell by 46 % compared with similar non-fed animals in the cold and by 55 % compared with those at room temperature. After adrenal medullectomy, cold exposure alone had no effect on the granular density of parasympathectomized plus sympathectomized glands but, when combined with feeding, granular loss amounted to 30 %. Pretreatment with a combination of

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Conditions Determining Adrenal Secretion

Abstract: and Card noted that, in rats, a restricted diet delayed pubes¬ cence, shortened the period of sexual activity, and increased sterility.Blood

Cited by 30 publications

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The Effect of Gold Exposure on the Catecholamine Excretion of Rats Treated with Decaborane

The Effect of Gold Exposure on the Catecholamine Excretion of Rats Treated with Decaborane

Brain Amines and Temperature Regulation

The role of circulating catecholamines in the depletion of parotid acinar granules in conscious rats in the cold

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