Hypertension during chronic exposure to cold: comparison between Sprague–Dawley and Long–Evans strains

1992 ◽  
Vol 70 (5) ◽  
pp. 701-708 ◽  
Author(s):  
Anne Riesselmann ◽  
Andreas Baron ◽  
Melvin J. Fregly ◽  
Patricia van Bergen

It is now well established that chronic exposure of rats to cold (5–6 °C) induces an elevation of systolic, diastolic, and mean blood pressures and cardiac hypertrophy within 3 weeks. Since rats of the Long–Evans (LE) strain are known to be resistant to the induction of deoxycorticosterone salt induced hypertension, their cardiovascular responses to chronic exposure to cold were compared with those of rats of the Sprague–Dawley (SD) strain. The results of these studies revealed clear differences between the LE and SD strains of rats. Thus, rats of the SD strain had a significant elevation in their blood pressure; a significantly increased urinary output of norepinephrine and epinephrine; a significantly greater dipsogenic responsiveness to acute administration of angiotensin II, and significant increases in weights of the heart, kidneys, adrenals, and brown adipose tissue compared with their warm-adapted controls. All of these changes are characteristic of rats acclimated to cold. In contrast, rats of the LE strain appear to be less responsive to cold in that blood pressure failed to rise as sharply and to attain as high a level. Furthermore, urinary outputs of norepinephrine and epinephrine were significantly lower in cold-treated rats of the LE strain compared with cold-treated rats of the SD strain, but dipsogenic responsiveness to angiotensin II was unchanged. Although increases in the weight of the previously mentioned organs were also observed in cold-treated rats of the LE strain compared with their warm-adapted controls, weights of the heart and interscapular brown adipose tissue of both groups were significantly less than those of counterparts of the SD strain. Thus, the results show striking differences between the two strains and suggest that a reduced secretion of catecholamines by the LE strain may be a factor in the failure of the blood pressure of these rats to reach the level of cold-exposed rats of the SD strain. Additional studies will be required to verify this suggestion.Key words: strains of rats, Long–Evans, Sprague–Dawley, cold, cold-induced hypertension, blood pressure, angiotensin II induced drinking.

1992 ◽  
Vol 263 (1) ◽  
pp. R59-R69
Author(s):  
J. Thornhill ◽  
I. Halvorson

Temperature experiments of 4- and 21 degrees C-acclimated conscious and anesthetized Sprague-Dawley (SD) and Long-Evans (LE) rats revealed that the LE groups or SD rats acclimated to 4 degrees C had significant increases in intracapsular brown adipose tissue (IBAT) temperature above core after ventromedial hypothalamic nucleus (VMH) electrical stimulation or after norepinephrine (NE) infusion (50 micrograms/kg total dose), whereas IBAT temperatures of SD rats (acclimated to 21 degrees C) rose only after intravenous NE. Another study of 21- or 4 degrees C-acclimated SD rats revealed that only the 4 degrees C-acclimated group showed graded increases in IBAT temperature after VMH electrical stimulation as current amplitude or total current duration (not pulse frequency) of the electrical stimulus was increased. In vitro analysis of isolated IBAT tissues of age-matched anesthetized LE or SD rats acclimated to 21 degrees C showed that many indicators of thermogenic capacity including mitochondrial uncoupling protein were significantly lower in the SD group. The results demonstrate that lean male SD rats acclimated to 21 degrees C have suppressed IBAT temperature responses to VMH electrical stimulation compared with lean LE rats due to a reduced thermogenic capacity of that tissue.


2020 ◽  
Author(s):  
Xuemei Liu ◽  
Xiyu Feng ◽  
Chao Deng ◽  
Lu Liu ◽  
Yanping Zeng ◽  
...  

Abstract BackgroundPrescription of second-generation antipsychotic drugs (SGAs) to childhood/adolescent has exponentially increased in recent years, which was associated with the greater risk of significant sedation, weight gain, and dyslipidemia. Statin is considered a potential preventive and treatment approach for reducing SGA-induced weight gain and dyslipidemia in schizophrenia patients. However, the effect of statin treatment in children and adolescents with SGA-induced dyslipidemia is not clearly demonstrated.MethodsTo investigate the efficacy of interventions of statin aimed at reversing SGA-induced dyslipidemia, young Sprague Dawley (SD) rats were treated orally with either olanzapine (1.0 mg/kg, t.i.d.), simvastatin (3.0 mg/kg, t.i.d.), olanzapine plus simvastatin (O+S), or vehicle (control) for 5 weeks.ResultsOlanzapine treatment increased weight gain, food intake and feeding efficiency compared to the control, while O+S co-treatment significantly reversed body weight gain but had no significant effect on food intake. Moreover, olanzapine treatment induced a slight but significant reduction in body temperature, with a decrease in locomotor activity. Fasting plasma glucose, triglycerides (TG), and total cholesterol (TC) levels were markedly elevated in the olanzapine-only group, whereas O+S co-treatment significantly ameliorated these changes. A down-regulating of uncoupling protein-1 (UCP1) and peroxisome-proliferator-activated receptor-γ co-activator-1α (PGC-1α) expression was observed in brown adipose tissue (BAT) in the olanzapine-only group, following a significant decrease in the ratio of phosphorylated PKA (p-PKA)/PKA. Interestingly, these protein changes could be reversed by co-treatment with O+B. Our results demonstrated simvastatin to be effective in ameliorating TC and TG elevated by olanzapine.ConclusionsModulation of BAT activity could be a partial mechanism in reducing metabolic side effects caused by SGAs in child and adolescent patients.


2020 ◽  
Author(s):  
Xuemei Liu ◽  
Xiyu Feng ◽  
Chao Deng ◽  
Lu Liu ◽  
Yanping Zeng ◽  
...  

Abstract Background Prescription of second-generation antipsychotic drugs (SGAs) to childhood/adolescent has exponentially increased in recent years, which was associated with the greater risk of significant weight gain and dyslipidemia. Statin is considered a potential preventive and treatment approach for reducing SGA-induced weight gain and dyslipidemia in schizophrenia patients. However, the effect of statin treatment in children and adolescents with SGA-induced dyslipidemia is not clearly demonstrated.Methods To investigate the efficacy of statin interventions for reversing SGA-induced dyslipidemia, young Sprague Dawley rats were treated orally with either olanzapine (1.0 mg/kg, t.i.d.), simvastatin (3.0 mg/kg, t.i.d.), olanzapine plus simvastatin (O+S), or vehicle (control) for 5 weeks. Results Olanzapine treatment increased weight gain, food intake and feeding efficiency compared to the control, while O+S co-treatment significantly reversed body weight gain but without significant effects on food intake. Moreover, olanzapine treatment induced a slight but significant reduction in body temperature, with a decrease in locomotor activity. Fasting plasma glucose, triglycerides (TG), and total cholesterol (TC) levels were markedly elevated in the olanzapine-only group, whereas O+S co-treatment significantly ameliorated these changes. Pronounced activation of lipogenic gene expression in the liver and down-regulated expression of uncoupling protein-1 (UCP1) and peroxisome-proliferator-activated receptor-γ co-activator-1α (PGC-1α) in brown adipose tissue (BAT) was observed in the olanzapine-only group. Interestingly, these protein changes could be reversed by co-treatment with O+B. Conclusions Simvastatin is effective in ameliorating TC and TG elevated by olanzapine. Modulation of BAT activity by statins could be a partial mechanism in reducing metabolic side effects caused by SGAs in child and adolescent patients.


2021 ◽  
Vol 266 ◽  
pp. 113413 ◽  
Author(s):  
Xiang Li ◽  
Hong-Yuan Lu ◽  
Xiao-Wen Jiang ◽  
Yue Yang ◽  
Bo Xing ◽  
...  

1991 ◽  
Vol 277 (3) ◽  
pp. 665-669 ◽  
Author(s):  
J R D Mitchell ◽  
E D Saggerson

1. Measurements were made, relative to tissue DNA, of the activities of enzymes of glycerolipid synthesis in homogenates of interscapular brown adipose tissue. These were: mitochondrial and microsomal forms of glycerolphosphate acyltransferase (GPAT), Mg(2+)-dependent phosphatidate phosphohydrolase (PPH) and fatty acyl-CoA synthetase (FAS). 2. In normal animals, 3 days of cold-exposure (4 degrees C) increased all activities. The increase in mitochondrial GPAT activity was particularly pronounced (5-fold). Administration of the beta-adrenergic agonist BRL 26830A mimicked the effect of cold on microsomal GPAT activity. Mitochondrial GPAT, PPH and FAS activities were unresponsive to BRL 26830A. The alpha-adrenergic agonist phenylephrine significantly decreased activities of GPAT and PPH. 3. Streptozotocin-diabetes decreased mitochondrial GPAT activity, but did not abolish the effect of cold to increase this activity or the activity of microsomal GPAT. Diabetes abolished the effect of cold on PPH and FAS activities. 4. The findings are relevant to signals that drive early events in mitochondriogenesis and cell proliferation in brown adipose tissue on exposure to cold.


1981 ◽  
Vol 91 (3) ◽  
pp. 515-524 ◽  
Author(s):  
GERARD MORY ◽  
DANIEL RICQUIER ◽  
PIERRE PESQUIÉS ◽  
PHILIPPE HÉMON

Hypothyroidism was induced in adult rats by oral absorption of methimazole and its effects on brown adipose tissue (BAT) were studied. Hypothyroidism partially mimicked the effects of chronic exposure to cold: BAT weight and its DNA content were increased and the mitochondrial components (proteins, phospholipids) of the tissue were greatly enhanced when expressed per unit of fresh tissue weight. Moreover, hypothyroidism had the same effects as adaptation to cold on the fatty-acid composition of both total and mitochondrial phospholipids. Basal respiratory rate and total cytochrome C oxidase activity of the tissue were also increased. However, the increase in the concentration of the '32 000 mol. wt protein', a polypeptide which regulates the dissipation of heat by BAT, was smaller and non-selective in hypothyroid rats. The amount of this protein was increased per mg tissue, but not per mg mitochondrial proteins, as in rats adapted to cold. Furthermore, in contrast with the large mobilization of the lipid stores in BAT of euthyroid animals, the BAT lipid stores of hypothyroid rats were not mobilized during the first hours of exposure to cold. It may be concluded that (a) hypothyroidism induces several alterations in BAT which are characteristic of an active thermogenic state (this may be because of the response of the organism to the deficiency of thermogenesis induced by hypothyroidism), (b) this potential increase in thermogenic capacity in the BAT of hypothyroid rats has probably a limited physiological role, since thyroid hormones are necessary for the mobilization of the tissue lipids which are the fuel for production of heat and (c) these data provide evidence for a limited role of thyroid hormones in the trophic response of BAT during adaptation to cold.


2014 ◽  
Vol 306 (6) ◽  
pp. R394-R400 ◽  
Author(s):  
Mazher Mohammed ◽  
Youichirou Ootsuka ◽  
William Blessing

Body temperature increases when individuals experience salient, emotionally significant events. There is controversy concerning the contribution of nonshivering thermogenesis in brown adipose tissue (BAT) to emotional hyperthermia. In the present study we compared BAT, core body, and brain temperature, and tail blood flow, simultaneously measured, to determine whether BAT thermogenesis contributes to emotional hyperthermia in a resident Sprague-Dawley rat when an intruder rat, either freely-moving or confined to a small cage, is suddenly introduced into the cage of the resident rat for 30 min. Introduction of the intruder rat promptly increased BAT, body, and brain temperatures in the resident rat. For the caged intruder these temperature increases were 1.4 ± 0.2, 0.8 ± 0.1, 1.0 ± 0.1°C, respectively, with the increase in BAT temperature being significantly greater ( P < 0.01) than the increases in body and brain. The initial 5-min slope of the BAT temperature record (0.18 ± 0.02°C/min) was significantly greater ( P < 0.01) than the corresponding value for body (0.10 ± 0.01°C/min) and brain (0.09 ± 0.02°C/min). Tail artery pulse amplitude fell acutely when the intruder rat was introduced, possibly contributing to the increases in body and brain temperature. Prior blockade of β3 adrenoceptors (SR59230A 10 mg/kg ip) significantly reduced the amplitude of each temperature increase. Intruder-evoked increases in BAT temperature were similar in resident rats maintained at 11°C for 3 days. In the caged intruder situation there is no bodily contact between the rats, so the stimulus is psychological rather than physical. Our study thus demonstrates that BAT thermogenesis contributes to increases in body and brain temperature occurring during emotional hyperthermia.


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