Hypertension Following Adrenal Enucleation and Its Absence During Desoxycorticosterone Treatment in Long—Evans Rats1

Hall, Charles A.; Ayachi, S; Hall, O.

doi:10.1210/endo-92-4-1175

Cited by 17 publications

(6 citation statements)

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“…The BN rat, however, is not unique in being unresponsive. Systolic blood pressures of three other rat strains are relatively low after several weeks of DOCA-salt treatment: Wistar Furth, 123Ϯ5 mmHg at 5 wk and only 136Ϯ2 mmHg at 10 wk (32); Dahl salt resistant, 131Ϯ6 mmHg at 4 wk (33); and Long Evans, 133Ϯ3 mmHg at 4 wk (34). Interestingly, of these strains that are resistant to DOCA-salt, the Dahl salt resistant rat also is resistant to twokidney one-clip Goldblatt hypertension (33), whereas the Wistar Furth is susceptible (32).…”

Section: Discussionmentioning

confidence: 99%

Genetic susceptibility to hypertension-induced renal damage in the rat. Evidence based on kidney-specific genome transfer.

Churchill

Churchill²,

Bidani³

et al. 1997

J. Clin. Invest.

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To test the hypothesis that genetic factors can determine susceptibility to hypertension-induced renal damage, we derived an experimental animal model in which two genetically different yet histocompatible kidneys are chronically and simultaneously exposed to the same blood pressure profile and metabolic environment within the same host. Kidneys from normotensive Brown Norway rats were transplanted into unilaterally nephrectomized spontaneously hypertensive rats (SHR-RT1.N strain) that harbor the major histocompatibility complex of the Brown Norway strain. 25 d after the induction of severe hypertension with deoxycorticosterone acetate and salt, proteinuria, impaired glomerular filtration rate, and extensive vascular and glomerular injury were observed in the Brown Norway donor kidneys, but not in the SHR-RT1.N kidneys. Control experiments demonstrated that the strain differences in kidney damage could not be attributed to effects of transplantation-induced renal injury, immunologic rejection phenomena, or preexisting strain differences in blood pressure. These studies ( a ) demonstrate that the kidney of the normotensive Brown Norway rat is inherently much more susceptible to hypertension-induced damage than is the kidney of the spontaneously hypertensive rat, and ( b ) establish the feasibility of using organ-specific genome transplants to map genes expressed in the kidney that determine susceptibility to hypertensioninduced renal injury in the rat. ( J. Clin. Invest. 1997. 100: 1373-1382.)

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Section: Discussionmentioning

confidence: 99%

Genetic susceptibility to hypertension-induced renal damage in the rat. Evidence based on kidney-specific genome transfer.

Churchill

Churchill²,

Bidani³

et al. 1997

J. Clin. Invest.

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“…Compared with SD rats, LE rats exhibit 1) greater anorexia and body weight reduction in response to immobilization stress (13), 2) greater reductions in HR and body temperature following neurotoxicant exposure (16), 3) reduced drinking and greater sodium excretion in response to a number of dipsogenic agents (14), 4) diminished blood pressure and sympathetic responses to several weeks of cold exposure (36), and 5) resistance to DOCA hypertension (19). This list is neither comprehensive nor particularly revealing concerning fundamental underlying differences in physiology between these outbred rat strains.…”

Section: Strain Differences and Similaritiesmentioning

confidence: 99%

Long-Evans and Sprague-Dawley rats exhibit divergent responses to refeeding after caloric restriction

Evans¹,

Messina²,

Knight³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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Mature male Sprague-Dawley (SD) and Long-Evans (LE) rats were instrumented with telemetry transmitters for measurement of heart rate (HR) and housed in room calorimeters for assessment of food intake and oxygen consumption (V O2) at standard laboratory temperatures (23°C) to examine physiological responses to caloric restriction (CR; 60% of baseline ad libitum calories for 2 wk) and refeeding. Ad libitum controls had stable food intake (84 -88 kcal/day) and gained weight at rates of 3-4 g/day. Groups from both strains assigned to CR exhibited similar patterns of weight loss and reductions in V O2 and HR. Upon refeeding, SD rats exhibited a mild, transient hyperphagic response (1 day) accompanied by sustained suppression of V O2 and HR that remained evident 8 days after refeeding. In contrast, LE rats exhibited sustained daily hyperphagia that persisted 8 days after refeeding and was accompanied by a complete restoration of HR and V O2. The lower HR and V O2 observed during refeeding in SD rats were not due to reduced locomotor activity. The results reveal a strain-dependent divergent response to recovery from CR. We conclude that during recovery from CR, homeostatic stimulation of appetite or suppression of energy expenditure may occur selectively to restore body weight. hyperphagia; thermogenesis; indirect calorimetry; energy homeostasis CALORIC RESTRICTION (CR) produces a multifaceted set of adaptations that reduce energy expenditure and increase appetite in an attempt to defend body fat and body weight (29,41,44). Frequently, sexually mature but rapidly growing male rats are used to examine mechanisms of energy homeostasis. These animals are in positive energy balance, consuming excess calories that are used to increase both lean and fat mass at rates of weight gain often exceeding 25 g/wk. Thus growing Sprague-Dawley (SD) rats treated with CR (rats fed 60% of control caloric intake) lose very little weight and reach a fairly stable weight within a week, whereas ad libitum control rats continue to rapidly grow. As a result, the weight differences are due more to growth of controls than weight loss in treated rats. When SD rats are refed, this strain of rats exhibits a sustained reduction in energy expenditure that appears to contribute to restoration of fat mass (3, 7).The primary purpose of this study was to examine physiological responses to CR in another commonly used rat strain.As the results indicate, we observed that outbred Long-Evans (LE) rats and SD rats exhibit similar physiological responses during CR but exhibit unexpectedly divergent strategies for normalization of weight during refeeding. The findings indicate that suppressed thermogenesis is not always observed after CR. METHODSAll experimental procedures and protocols were approved by the Institutional Animal Care and Use Committee at Florida State University. Male LE [(Crl:LE)BR; Charles River, Raleigh, NC] and SD rats [Crl:CD(SD)IGSBR; Charles River Laboratories] were purchased at 5-6 wk of age and individually housed in polycarbonate cages ...

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“…A similar strain difference was observed with daily injections of ACTH, which led to an elevation of blood pressure in WKY, but not in Wistar rats [un published observation]. Chronic ACTH ad ministration is known for its hypertensiog enic action [16,17], Strain differences have also been observed after prolonged treatment with the mineralocorticoid desoxycorticosterone, which induces an increased blood pres sure [19] in Sprague-Dawley but not in LongEvans rats [20].…”

Section: Discussionmentioning

confidence: 61%

Long-Term Effects of Betamethasone on Blood Pressure and Hypothalamo-Pituitary-Adrenocortical Function in Spontaneously Hypertensive and Normotensive Rats

Häusler¹,

Girard

Baumann

et al. 1983

Horm Res

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An enhanced hypothalamo-pituitary-adrenocortical (HPA) activity has been described during onset of elevated blood pressure in spontaneously hypertensive rats (SHR). An instability of the HPA axis could thus contribute to the development of hypertension in these animals. Glucocorticoid effects on blood pressure and HPA function were studied therefore in SHR and normotensive Wistar-Kyoto (WKY) and Wistar rats. Beginning at 4 weeks of age, the rats were treated with 0.1 and 0.5 µg betamethasone per milliliter drinking water for 7 weeks. SHR and WKY responded with a significant elevation in average blood pressure. In SHR, mean blood pressure rose from 181.4 ± 3.9 (mean ± SEM) to 203.1 ± 2.8 mm Hg in response to the lower dose of betamethasone and to 209.2 ± 4.0 mm Hg in response to 0.5 µg betamethasone per milliliter drinking water. In WKY, blood pressure increased from 134.4 ± 3.3 to 148.2 ± 3.0 and 157.9 ± 4.5 mm Hg in response to the lower and higher dose of betamethasone, respectively. No significant effect was seen in Wistar rats, where the mean blood pressure values changed insignificantly from 133.8 ± 2.1 to 136.3 ± 3.2 and 135.6 ± 2.4 mm Hg. Stress-induced secretion of corticosterone was significantly suppressed in a dose-dependent manner in all three strains. Stress-induced secretion of adrenocorticotropin was markedly reduced by 0.5 µg betamethasone per milliliter in SHR and by both doses in WKY. No significant effect, however, was seen in Wistar rats. A predisposition to the hypertensiogenic actions of glucocorticoids was found therefore in SHR and WKY, but not in Wistar rats.

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Hypertension Following Adrenal Enucleation and Its Absence During Desoxycorticosterone Treatment in Long—Evans Rats1

Cited by 17 publications

References 0 publications

Genetic susceptibility to hypertension-induced renal damage in the rat. Evidence based on kidney-specific genome transfer.

Genetic susceptibility to hypertension-induced renal damage in the rat. Evidence based on kidney-specific genome transfer.

Long-Evans and Sprague-Dawley rats exhibit divergent responses to refeeding after caloric restriction

Long-Term Effects of Betamethasone on Blood Pressure and Hypothalamo-Pituitary-Adrenocortical Function in Spontaneously Hypertensive and Normotensive Rats

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