The general adaptation syndrome and the diseases of adaptation

Selye, Hans

doi:10.1016/0021-8707(46)90159-1

Cited by 41 publications

(22 citation statements)

References 141 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Darrow & Miller (1942) and Selye (1946Selye ( , 1951 produced lesions in the cardiovascular system of rats by repeated injections of DOCA. Though Selye & Hall (1946) found that desoxocortisone administered to hypophysectomized animals causes slight or no morphological lesions in the cardiovascular system, histological examinations will be needed to show whether a qualitative difference exists between the hearts of hypophysectomized rats treated with DOCA or growth hormone.…”

Section: Discussionmentioning

confidence: 99%

The effect of adrenocortical hormones alone and in combination with growth hormone on cardiac hypertrophy and blood pressure of hypophysectomized rats

Beznák¹

1954

The Journal of Physiology

View full text Add to dashboard Cite

There is no cardiac hypertrophy or hypertension in hypophysectomized rats after narrowing of their descending aortae (Hajdu & Beznak, 1943. ACTH, in a dose that completely prevented the atrophy of the adrenals due to hypophysectomy, had no influence on the cardiac weight and blood pressure of such rats (Beznak, 1952b). Treatment with growth hormone, on the other hand, completely restored the cardiac weight and blood pressure of hypophysectomized rats to normal and on aortic narrowing the same degree of cardiac hypertrophy and hypertension resulted as in normal rats (Beznak, 1954 b). For this, however, very large daily doses of growth hormone (4-10 mg in terms of Armour standard 22KR2) were necessary. The question arose whether some other hormones, notably the adrenocortical and thyroid hormones, could potentiate the effect of growth hormone. The thyroids and adrenals are not indispensable for the production of cardiac hypertrophy and hypertension because cardiac hypertrophy and hypertension take place in thyroidectomized (Beznak & Hajdu, 1944 as well as in adrenalectomized rats on aortic narrowing (Beznik, 1952b). Hay (1946) observed that lyophilized anterior pituitary (LAP) caused an increase in the weight of the kidneys and the heart in normal and in thyroidectomized rats. Yet that these hormones may have some effect was shown by the circumstance that both cardiac hypertrophy and hypertension-though present-were somewhat smaller in thyroidectomized and adrenalectomized rats than in normal rats on similar aortic constriction. It is known that the thyroids influence growth hormone secretion and the reaction of the tissues to growth hormone (Schwann,

show abstract

Section: Discussionmentioning

confidence: 99%

The effect of adrenocortical hormones alone and in combination with growth hormone on cardiac hypertrophy and blood pressure of hypophysectomized rats

Beznák¹

1954

The Journal of Physiology

View full text Add to dashboard Cite

show abstract

“…The mammalian stress response evokes a series of neuroendocrine responses that result in activation ofthe hypothalamic-pituitary-adrenal (HPA) l axis and the sympathetic nervous system ( 1,2). Interactions between these stress response systems occur at multiple levels including the brain, pituitary gland, adrenal gland, and peripheral blood vessel (3).…”

Section: Introductionmentioning

confidence: 99%

Vascular heat shock protein expression in response to stress. Endocrine and autonomic regulation of this age-dependent response.

Udelsman¹,

Blake²,

Stagg³

et al. 1993

J. Clin. Invest.

199

View full text Add to dashboard Cite

Adaptation to stress requires coordinated interactions between the vascular and endocrine systems. Previously we demonstrated that restraint stress induces the expression of the major heat shock protein, HSP7O, in the adrenal cortex of the rat. Here we demonstrate that restraint also induces expression of HSP70 in the vasculafure. We further demonstrate that the adrenal and vascular responses are differentially regulated: the adrenal response is adrenocorticotropin dependent, whereas the vascular response is under adrenergic control. In addition, the adrenal response is restricted to members of the HSP70 gene family, whereas in vascular tissue the low molecular weight HSP, HSP27, is also induced by restraint. Further characterization of the vascular response revealed that HSP70 induction occurred in both the thoracic and abdominal aortas as well as in the vena cava. However, no HSP70 induction was apparent in the heart or in a wide variety of other tissues examined. In situ hybridization showed that the vascular expression was localized to the aortic smooth muscle cells with minimal expression in the endothelium. Induction of HSP70 mRNA in both the adrenal cortex and aorta was followed by an elevation in HSP70 protein. Maximum HSP70 protein levels were seen within 3-12 h after restraint, but declined thereafter. Stress induced HSP70 expression was dramatically reduced with age, which may explain, in part, the diminished tolerance to stress seen in elderly individuals. (J. Clin. Invest. 1993.91:465473.)

show abstract

“…Serum (16,18). Conversely, in the hyperglycemic state insulin levels rise and decrease bleod glucose levels by stimulating glucose uptake and glycogen synthesis in liver and muscle and by increasing glucose uptake and lipogenesis in adipose tissue (17,18 (66), it now appears that their physiologic role during stress is to protect the organism from an overstimulated inflammatory response (65,67). Glucocorticoids achieve this by inhibiting the production of, or antagonizing the actions of, inflammatory mediators such as prostaglandins, leukotrienes, interleukins, and atrial natriuretic factor (7,16,65).…”

Section: Hypercorticisman Adaptive Response To Nutrient Stressmentioning

confidence: 99%

Caloric restriction as a mechanism mediating resistance to environmental disease.

Frame

Hart

Leakey

1998

Environ Health Perspect

View full text Add to dashboard Cite

It has been observed that susceptibility to many degenerative diseases increases concurrently with industrialization and rising living standards. Although epidemiologic studies suggest that specific environmental and dietary factors may be important, caloric intake alone (as reflected in body size) may account for much of the differential risk observed among diverse human populations. It has been suggested from animal studies that caloric intake may be the primary effector for many hormonal, metabolic, physiologic, and behavioral responses that coordinate reproductive strategy to apparent availability of food. When caloric intake is excessive, particularly at critical developmental stages, physiologic priorities are set for body growth and fecundity rather than for endurance and longevity. The converse occurs during periods of famine, thus increasing the probability that sufficient individuals survive to restore the population when conditions improve. Calorically restricted rodents have significantly longer reproductive and total life spans than their ad libitum-fed controls and exhibit a spectrum of biochemical and physiologic alterations that characterize their adaptation to reduced caloric intake. These include reduced stature, hypercorticism in the absence of elevated adrenocorticotropic hormone levels, increased metabolic efficiency, decreased mitogenic response coupled with increased rates of apoptosis, reduced inflammatory response, induction of stress proteins and DNA repair enzymes, altered drug-metabolizing enzyme expression, and modified cell-mediated immune function. The overall profile of these changes is one of improved defense against environmental stress. This has been suggested as the mechanistic basis for the protective effects of low body weight on radiationand chemically induced cancers in experimental animals. It may also explain the significantly higher thresholds of acute toxicity observed when calorically restricted rodents are exposed to certain test compounds.

show abstract

The general adaptation syndrome and the diseases of adaptation

Cited by 41 publications

References 141 publications

The effect of adrenocortical hormones alone and in combination with growth hormone on cardiac hypertrophy and blood pressure of hypophysectomized rats

The effect of adrenocortical hormones alone and in combination with growth hormone on cardiac hypertrophy and blood pressure of hypophysectomized rats

Vascular heat shock protein expression in response to stress. Endocrine and autonomic regulation of this age-dependent response.

Caloric restriction as a mechanism mediating resistance to environmental disease.

Contact Info

Product

Resources

About