scholarly journals A G-protein-biased S1P1 agonist, SAR247799, improved LVH and diastolic function in a rat model of metabolic syndrome

2021 ◽  
Author(s):  
Maria Francesca Evaristi ◽  
Bruno Poirier ◽  
Xavier Chénedé ◽  
Anne-Marie Lefebvre ◽  
Alain Roccon ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Cardiac Hypertrophy ◽  
Diastolic Dysfunction ◽  
Diastolic Function ◽  
G Protein ◽  
Rat Model ◽  
Left Ventricular ◽  
Heart Weight ◽  
Functional Components

Aim: Heart failure with preserved ejection fraction (HFpEF) is a major cause of death worldwide with no approved treatment. Left ventricular hypertrophy (LVH) and diastolic dysfunction represent the structural and functional components of HFpEF, respectively . Endothelial dysfunction is prevalent in HFpEF and predicts cardiovascular events. We investigated if SAR247799, a G-protein-biased sphingosine-1-phosphate receptor 1 (S1P 1 ) agonist with endothelial-protective properties, could improve cardiac and renal functions in a rat model of metabolic syndrome LVH and diastolic function. Methods: 31- and 65-week-old obese ZSF1 (Ob-ZSF1) rats, representing young and old animals with LVH and diastolic dysfunction, were randomized to a chow diet containing 0.025% (w/w) of SAR247799, or control (CTRL) chow for 4 weeks. Age-matched lean ZSF1 (Le-ZSF1) rats were fed control chow. Echocardiography, telemetry, biochemical and histological analysis were performed to evaluate the effect of SAR247799. Results: Echocardiography revealed that Ob-ZSF1 rats, in contrast to Le-ZSF1 rats, developed progressive diastolic dysfunction and cardiac hypertrophy with age. SAR247799 blunted the progression of diastolic dysfunction in young and old animals: in young animals E/e’ was evaluated at 21.8 ± 1.4 for Ob-ZSF1-CTRL, 19.5 ± 1.2 for Ob-ZSF1-SAR247799 p<0.01, and 19.5 ± 2.3 for Le-ZSF1-CTRL (median ± IQR). In old animals E/e’ was evaluated at 23.15 ± 4.45 for Ob-ZSF1-CTRL, 19.5 ± 5 for Ob-ZSF1-SAR247799 p<0.01, and 16.69 ± 1.7 for Le-ZSF1-CTRL, p<0.01 (median ± IQR). In old animals, SAR247799 reduced cardiac hypertrophy (mean ± SEM of heart weight/tibia length 0.053 ± 0.001 for Ob-ZSF1-CTRL vs 0.046 ± 0.002 for Ob-ZSF1-SAR247799 p<0.01, Le-ZSF1-CTRL 0.035 ± 0.001) and myocardial perivascular collagen content (p<0.001), independently of any changes in microvascular density. In young animals, SAR247799 improved endothelial function as assessed by the very low frequency bands of systolic blood pressure variability (mean ± SEM 67.8 ± 3.41 for Ob-ZSF1-CTRL  55.8 ± 4.27 or Ob-ZSF1-SAR247799, p<0.05  and 57.3 ± 1.82 Le-ZSF1-CTRL), independently of any modification of arterial blood pressure. In old animals, SAR247799 reduced urinary protein/creatinine ratio, an index of glomerular injury, (10.3 ± 0.621 vs 8.17 ± 0.231 for Ob-ZSF1-CTRL vs Ob-ZSF1-SAR247799, respectively, p<0.05 and 0.294 ± 0.029 for Le-ZSF1-CTRL, mean ± SEM) and the fractional excretion of electrolytes. Circulating lymphocytes were not decreased by SAR247799, confirming lack of S1P 1 desensitization.   Conclusions: These experimental findings suggest that S1P 1 activation with SAR247799 could improve LVH, cardiac diastolic and renal function in HFpEF patients .

scholarly journals A G-protein-biased S1P1 agonist, SAR247799, improved LVH and diastolic function in a rat model of metabolic syndrome

PLoS ONE ◽  
2022 ◽  
Vol 17 (1) ◽  
pp. e0257929
Author(s):  
Maria Francesca Evaristi ◽  
Bruno Poirier ◽  
Xavier Chénedé ◽  
Anne-Marie Lefebvre ◽  
Alain Roccon ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Cardiac Hypertrophy ◽  
Diastolic Dysfunction ◽  
Diastolic Function ◽  
G Protein ◽  
Rat Model ◽  
Left Ventricular ◽  
Heart Weight ◽  
Functional Components

Aim Heart failure with preserved ejection fraction (HFpEF) is a major cause of death worldwide with no approved treatment. Left ventricular hypertrophy (LVH) and diastolic dysfunction represent the structural and functional components of HFpEF, respectively. Endothelial dysfunction is prevalent in HFpEF and predicts cardiovascular events. We investigated if SAR247799, a G-protein-biased sphingosine-1-phosphate receptor 1 (S1P1) agonist with endothelial-protective properties, could improve cardiac and renal functions in a rat model of metabolic syndrome LVH and diastolic function. Methods 31- and 65-week-old obese ZSF1 (Ob-ZSF1) rats, representing adult and aged animals with LVH and diastolic dysfunction, were randomized to a chow diet containing 0.025% (w/w) of SAR247799, or control (CTRL) chow for 4 weeks. Age-matched lean ZSF1 (Le-ZSF1) rats were fed control chow. Echocardiography, telemetry, biochemical and histological analysis were performed to evaluate the effect of SAR247799. Results Echocardiography revealed that Ob-ZSF1 rats, in contrast to Le-ZSF1 rats, developed progressive diastolic dysfunction and cardiac hypertrophy with age. SAR247799 blunted the progression of diastolic dysfunction in adult and aged animals: in adult animals E/e’ was evaluated at 21.8 ± 1.4 for Ob-ZSF1-CTRL, 19.5 ± 1.2 for Ob-ZSF1-SAR247799 p<0.01, and 19.5 ± 2.3 for Le-ZSF1-CTRL (median ± IQR). In aged animals E/e’ was evaluated at 23.15 ± 4.45 for Ob-ZSF1-CTRL, 19.5 ± 5 for Ob-ZSF1-SAR247799 p<0.01, and 16.69 ± 1.7 for Le-ZSF1-CTRL, p<0.01 (median ± IQR). In aged animals, SAR247799 reduced cardiac hypertrophy (g/mm mean ± SEM of heart weight/tibia length 0.053 ± 0.001 for Ob-ZSF1-CTRL vs 0.046 ± 0.002 for Ob-ZSF1-SAR247799 p<0.01, Le-ZSF1-CTRL 0.035 ± 0.001) and myocardial perivascular collagen content (p<0.001), independently of any changes in microvascular density. In adult animals, SAR247799 improved endothelial function as assessed by the very low frequency bands of systolic blood pressure variability (mean ± SEM 67.8 ± 3.41 for Ob-ZSF1-CTRL 55.8 ± 4.27 or Ob-ZSF1-SAR247799, p<0.05 and 57.3 ± 1.82 Le-ZSF1-CTRL), independently of any modification of arterial blood pressure. In aged animals, SAR247799 reduced urinary protein/creatinine ratio, an index of glomerular injury, (10.3 ± 0.621 vs 8.17 ± 0.231 for Ob-ZSF1-CTRL vs Ob-ZSF1-SAR247799, respectively, p<0.05 and 0.294 ± 0.029 for Le-ZSF1-CTRL, mean ± SEM) and the fractional excretion of electrolytes. Circulating lymphocytes were not decreased by SAR247799, confirming lack of S1P1 desensitization. Conclusions These experimental findings suggest that S1P1 activation with SAR247799 may be considered as a new therapeutic approach for LVH and diastolic dysfunction, major components of HFpEF.

Abstract 16165: Inorganic Arsenic Induces Sex-Dependent Pathological Cardiac Hypertrophy

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Raihan Kabir ◽  
Prithvi Sinha ◽  
Sumita Mishra ◽  
Obialunanma V Ebenebe ◽  
Nicole Taube ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Hypertrophy ◽  
Inorganic Arsenic ◽  
Left Ventricular ◽  
Luciferase Assay ◽  
Heart Weight ◽  
Left Ventricular Geometry ◽  
Wall Thickening ◽  
Pathological Cardiac Hypertrophy ◽  
Relevant Dose

Exposure to inorganic arsenic (iAS) through drinking water is well-associated with adverse cardiovascular outcomes, yet the mechanisms through which it induces these effects are not fully understood. Recent epidemiological findings highlight an association between iAS exposure and altered left ventricular geometry in both the presence and absence of hypertension. We therefore tested the hypothesis that iAS exposure has a bimodal impact on cardiac-intrinsic and hemodynamic mechanisms that together induce pathological remodeling of the myocardium. Adult male and female mice were exposed to an environmentally relevant dose of 615 μg/L NaAsO 2 for eight weeks. Males (n=9-10 mice/group) exhibited increased systolic blood pressure (115.1±3.0 vs. 106.0±2.3 mmHg, p=0.0350) via tail cuff photoplethysmography, left ventricular wall thickening (0.98±0.01 vs. 0.88±0.01 mm, p<0.0001) via transthoracic echocardiography, increased heart weight to tibia length (8.56±0.21 vs. 7.15±0.24 mg/mm; n=24 mice/group), and increased plasma atrial natriuretic peptide (47.85±12.0 vs. 15.14±3.73 pg/mL, p=0.0379) via enzyme immunoassay. Myocardial mRNA transcript levels (n=10 hearts/group) of Acta1 (1.36±0.18 vs. 0.73±0.11, p=0.0037), Myh7 (1.53±0.15 vs. 1.04±0.10, p=0.0138), and Nppa (2.40±0.29 vs. 1.02±0.07, p=0.0001) were increased, and Myh6 (0.92±0.17 vs. 1.14±0.23, p=0.0001) was decreased, evidencing pathological hypertrophy in the male heart. Female hearts, however, were largely protected at this eight-week timepoint as similar changes were not detected. Further investigation found that Rcan1 was upregulated (1.47±0.19 vs. 0.97±0.04, p=0.0161; n=10 hearts/group) in male hearts, suggesting that calcineurin-NFAT was activated. Interestingly, iAS was sufficient to activate NFAT (0.82±0.11 vs. 0.46±0.05, p=0.0214; n=8 wells/group) independent of blood pressure via luciferase assay. In conclusion, these results demonstrate for the first time that iAS may cause pathological cardiac hypertrophy not only by increasing hemodynamic load, but also by activating calcineurin-NFAT and inducing fetal gene expression in the male heart, thus providing novel mechanistic insight into the threat of iAS exposure to the cardiovascular system.

Abstract 2280: Urine Albumin/creatinine Ratio, Cardiac Structure And Diastolic Function In Patients With Hypertension And Diastolic Dysfunction: The Validd Study

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Anil Verma ◽  
Rajesh Janardhanan ◽  
William L Daley ◽  
Susan Ritter ◽  
William A Kaye ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Diastolic Dysfunction ◽  
Diastolic Function ◽  
Organ Damage ◽  
Left Ventricular ◽  
Creatinine Ratio ◽  
Albumin Creatinine Ratio ◽  
End Organ Damage ◽  
Urine Albumin ◽  
Urine Albumin Creatinine Ratio

Background: Increasing urine albumin/creatinine ratio (ACR) is associated with systemic microvascular damage and increased cardiovascular morbidity and mortality. However, the relationship between albuminuria and left ventricular (LV) diastolic function, an early measure of myocardial end-organ damage in hypertension, has not been well defined. Methods: Urine ACR and echocardiographic measures of LV structure and function were assessed in 384 patients enrolled in the VALsartan In Diastolic Dysfunction (VALIDD) trial with mild hypertension and no heart failure and evidence of diastolic dysfunction based on Doppler assessment of myocardial relaxation velocities. Results: Urine ACR was undetected in 151 (39.3%) subjects, between 1 to 30 mg/g in 194 (50.5%), and > 30mg/g in 39 (10.2%). The mean blood pressure in the cohort was 143.8 ± 16.1/86.2 ± 10.3 mmHg and LV hypertrophy was present in < 4% of enrolled patients. Higher urine ACR was associated with lower annular relaxation velocity (E′), higher E/E′ (Figure ), higher prevalence of concentric LV remodeling and higher NT-ProBNP even after adjusting for age, diabetes, systolic BP, eGFR and LV mass index (LVMi) (p < 0.02 for all associations). Conclusion: Albuminuria is associated with worsening diastolic function in patients with hypertension, and both measures may represent important and modifiable markers of early end-organ damage even in patients with mild blood pressure elevation. E′ stratified by urine albumin creatinine ratio E/E′ stratified by urine albumin creatinine ratio

Rat model of exercise-induced cardiac hypertrophy: hemodynamic characterization using left ventricular pressure-volume analysis

2013 ◽  
Vol 305 (1) ◽  
pp. H124-H134 ◽  
Author(s):  
Tamás Radovits ◽  
Attila Oláh ◽  
Árpád Lux ◽  
Balázs Tamás Németh ◽  
László Hidi ◽  
...  
Keyword(s):  
Exercise Training ◽  
Cardiac Hypertrophy ◽  
Rat Model ◽  
Left Ventricular ◽  
Heart Weight ◽  
Stroke Work ◽  
Functional Changes ◽  
Exercise Induced

Long-term exercise training is associated with characteristic structural and functional changes of the myocardium, termed athlete's heart. Several research groups investigated exercise training-induced left ventricular (LV) hypertrophy in animal models; however, only sporadic data exist about detailed hemodynamics. We aimed to provide functional characterization of exercise-induced cardiac hypertrophy in a rat model using the in vivo method of LV pressure-volume (P-V) analysis. After inducing LV hypertrophy by swim training, we assessed LV morphometry by echocardiography and performed LV P-V analysis using a pressure-conductance microcatheter to investigate in vivo cardiac function. Echocardiography showed LV hypertrophy (LV mass index: 2.41 ± 0.09 vs. 2.03 ± 0.08 g/kg, P < 0.01), which was confirmed by heart weight data and histomorphometry. Invasive hemodynamic measurements showed unaltered heart rate, arterial pressure, and LV end-diastolic volume along with decreased LV end-systolic volume, thus increased stroke volume and ejection fraction (73.7 ± 0.8 vs. 64.1 ± 1.5%, P < 0.01) in trained versus untrained control rats. The P-V loop-derived sensitive, load-independent contractility indexes, such as slope of end-systolic P-V relationship or preload recruitable stroke work (77.0 ± 6.8 vs. 54.3 ± 4.8 mmHg, P = 0.01) were found to be significantly increased. The observed improvement of ventriculoarterial coupling (0.37 ± 0.02 vs. 0.65 ± 0.08, P < 0.01), along with increased LV stroke work and mechanical efficiency, reflects improved mechanoenergetics of exercise-induced cardiac hypertrophy. Despite the significant hypertrophy, we observed unaltered LV stiffness (slope of end-diastolic P-V relationship: 0.043 ± 0.007 vs. 0.040 ± 0.006 mmHg/μl) and improved LV active relaxation (τ: 10.1 ± 0.6 vs. 11.9 ± 0.2 ms, P < 0.01). According to our knowledge, this is the first study that provides characterization of functional changes and hemodynamic relations in exercise-induced cardiac hypertrophy.

Angiotensin II type 2 receptor gene transfer elicits cardioprotective effects in an angiotensin II infusion rat model of hypertension

2004 ◽  
Vol 19 (3) ◽  
pp. 255-261 ◽  
Author(s):  
Beverly L. Falcón ◽  
Jillian M. Stewart ◽  
Erick Bourassa ◽  
Michael J. Katovich ◽  
Glenn Walter ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Gene Transfer ◽  
Cardiac Hypertrophy ◽  
Rat Model ◽  
Lentiviral Vector ◽  
Receptor Gene ◽  
Left Ventricular ◽  
Heart Weight ◽  
Sprague Dawley

The role of the angiotensin II type 2 receptor (AT2R) in cardiovascular physiology remains elusive. We have developed an in vivo lentiviral vector-mediated gene transfer system to study the physiological functions of the AT2R. Our objectives in this study were to determine whether the AT2R influences cardiac hypertrophy and myocardial and perivascular fibrosis in a nongenetic rat model of hypertension. Lentiviral vector containing the AT2R or saline was injected intracardially in 5-day-old Sprague-Dawley rats. This resulted in a persistent overexpression of the AT2R in cardiac tissues. At 15 wk of age, animals were infused with either 200 ng·kg−1·min−1 of angiotensin II or saline by implantation of a 4-wk osmotic minipump. This resulted in an increase in blood pressure (BP) that reached maximal by 2 wk of treatment and was associated with a 123% increase in left ventricular wall thickness (LVWT) and a 129% increase in heart weight to body weight ratios (HW/BW). In addition, the increase in cardiac hypertrophy was associated with a 300% and 158% increase in myocardial and perivascular fibrosis, respectively. Cardiac transduction of the AT2R resulted in an 85% attenuation of LVWT, 91% attenuation of HW/BW, and a 43% decrease in myocardial fibrosis induced by angiotensin infusion. These improvements in cardiac pathology were observed in the absence of attenuation of high BP. Thus our observations indicate that long-term expression of the AT2R in the heart attenuates cardiac hypertrophy and fibrosis in a nongenetic rat model of hypertension.

scholarly journals Inhibition of Cardiac Hypertrophy Effects in D-Galactose-Induced Senescent Hearts byAlpinate Oxyphyllae FructusTreatment

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Yung-Ming Chang ◽  
Hen-Hong Chang ◽  
Hung-Jen Lin ◽  
Chin-Chuan Tsai ◽  
Chuan-Te Tsai ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Rat Model ◽  
Cerebrovascular Disorders ◽  
Treated Group ◽  
Left Ventricular ◽  
Heart Weight ◽  
Dependent Manner ◽  
Signaling Mechanism ◽  
Aging Rat ◽  
Whole Heart

Aging is a complex physiological phenomenon accelerated by ROS accumulation, with multisystem decline and increasing vulnerability to degenerative diseases and death. Cardiac hypertrophy is a key pathophysiological component that accompanies the aging process. Alpinate Oxyphyllae Fructus (Alpinia oxyphyllaMIQ, AOF) is a traditional Chinese medicine, which provides cardioprotective activity against aging, hypertension, and cerebrovascular disorders. In this study, we found the protective effect of AOF against cardiac hypertrophy in D-galactose-induced aging rat model. The results showed that treating rats with D-galactose resulted in pathological hypertrophy as evident from the morphology change, increased left ventricular weight/whole heart weight, and expression of hypertrophy-related markers (MYH7 and BNP). Both concentric and eccentric cardiac hypertrophy signaling proteins were upregulated in aging rat model. However, these pathological changes were significantly improved in AOF treated group (AM and AH) in a dose-dependent manner. AOF negatively modulated D-galactose-induced cardiac hypertrophy signaling mechanism to attenuate ventricular hypertrophy. These enhanced cardioprotective activities following oral administration of AOF reflect the potential use of AOF for antiaging treatments.

Effect of exercise training on diastolic function in metabolic syndrome

2013 ◽  
Vol 38 (5) ◽  
pp. 545-550 ◽  
Author(s):  
Sophie Lalande ◽  
Robert J. Petrella ◽  
J. Kevin Shoemaker
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Exercise Training ◽  
Flow Velocity ◽  
Diastolic Function ◽  
Left Ventricular ◽  
Aerobic Exercise Training ◽  
Cardiometabolic Health ◽  
Maximal Aerobic Capacity ◽  
Lv Diastolic Function

It has been reported that metabolic syndrome (MetS) impairs left ventricular (LV) diastolic function. The objective of this study was to determine whether exercise training can improve LV diastolic function in individuals with MetS. Twenty-eight individuals with MetS (9 males, aged 60 ± 5 years) underwent a 1-year combined endurance and resistance exercise training program; maximal aerobic capacity (V̇O2max), blood pressure, blood markers, and LV diastolic function were measured at weeks 0, 12, 24, and 52 throughout the training. Pulsed wave Doppler echocardiography across the mitral valve was used to assess peak early flow velocity (E) and peak atrial flow velocity (A) to determine the E/A ratio. Individuals with MetS had a reversed E/A ratio, suggesting impaired LV relaxation, the first stage of LV diastolic dysfunction. Exercise training reduced systolic blood pressure (SBP) (129 ± 14 to 120 ± 12 mm Hg; p < 0.01) and increased V̇O2max (29.2 ± 6.3 to 33.4 ± 6.5 mL·kg−1·min−1; p < 0.01) and high-density lipoprotein cholesterol (1.04 ± 0.21 to 1.12 ± 0.25 mmol·L−1; p = 0.02), but did not improve LV diastolic function. Individuals with an E/A ratio <1 at the start of training had a tendency toward an increased E/A ratio (p = 0.12) accompanied by significant decreases in SBP and increases in V̇O2max with exercise training. Combined resistance and aerobic exercise training improved cardiometabolic health but did not improve the impaired LV diastolic function of individuals with MetS.

scholarly journals Remodelling and left ventricular diastolic function in relation to blood pressure variability in patients with arterial hypertension and coronary heart disease

2003 ◽  
Vol 9 (4) ◽  
pp. 124-127 ◽  
Author(s):  
A. A. Kozina ◽  
Yu. A. Vasyuk ◽  
Yc. N. Yushchuk ◽  
Ye. A. Nesterova ◽  
LA. .. Sadulayeva
Keyword(s):  
Blood Pressure ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Arterial Hypertension ◽  
Diastolic Dysfunction ◽  
Diastolic Function ◽  
Blood Pressure Variability ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
Postinfarction Cardiosclerosis

Sixty five patients (mean age 55.7 ± 8,7 years), including 51 patients with arterial hypertension (AH) (mean age 54,9 ± 8,6 years) and 14 patients with a combination of AG and coronary heart disease (CHD) with postinfarction cardiosclerosis (mean age 54,9 ± 8,6 years) were examined. According to the values of average daily blood pressure variability (HPV), the patients were divided into subgroups with normal (11 patients with AH and 3 patients with AH and CHD) and increased (39 patients with AH and 12 patients with AH and CUD) BPV. Patients with isolated AH were found to have developed concentric hypertrophy of the left ventricle (LV), and moderate LV diastolic dysfunction mainly with impaired relaxation and the patients with a combination of AH and CHD with postinfarction cardiosclerosis had more significant LV structural and geometric derangements with a tendency for the development of eccentric hypertrophy of the LV, as well as more marked diastolic dysfunction with a larger proportion of the pseudo-normal and restrictive types of LV diastolic function. Patients with increased average daily BPV were found to have more significant LV structural, geometrical, and diastolic impairments.

Reversibility of cold-induced hypertension after removal of rats from cold

1990 ◽  
Vol 68 (7) ◽  
pp. 830-835 ◽  
Author(s):  
Orit Shechtman ◽  
Paula E. Papanek ◽  
Melvin J. Fregly
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Cardiac Hypertrophy ◽  
Cold Exposure ◽  
Adrenal Glands ◽  
Treated Group ◽  
Left Ventricular ◽  
Male Rats ◽  
Heart Weight ◽  
Renal Hypertrophy

Chronic exposure of rats to cold air induces hypertension, including elevation of blood pressure and cardiac hypertrophy. The present study was designed to assess reversibility of these changes after removal from cold. Five groups of six male rats each were exposed to cold (5 ± 2 °C) for 39 days, while six control rats were maintained at 26 ± 2 °C. Systolic blood pressures of the rats in one of the cold-treated groups, as well as the controls, were measured twice weekly throughout the experiment. Blood pressure of the cold-exposed rats (150 ± 3 mmHg; 1 mmHg = 133.3 Pa) became elevated significantly above that of controls (129 ± 3 mmHg) within 4 weeks. On day 39 of cold exposure, one group (six rats) of the cold-treated rats was sacrificed while still in the cold. The remaining four groups of cold-treated rats were than removed from cold and kept at 26 ± 2 °C. One group of cold-treated rats was sacrificed weekly thereafter. During the last week, the six control rats were also sacrificed. At death, the heart, kidneys, and adrenal glands were removed and weighed. Mean heart weight of the cold-treated group (346 ± 7 mg/100 g body weight), sacrificed prior to removal from cold, was significantly (p < 0.01) greater than that of controls (268 ± 5 mg/100 g body weight). The increased heart weight of the cold-treated group appeared to result mainly from an increase in left ventricular weight. The weights (mg/100 g body weight) of the kidneys and adrenal glands of cold-treated rats, measured prior to removal from cold, were significantly (p < 0.01) greater than those of controls. Two weeks after removal from cold, blood pressure, heart weight, and left ventricular weight decreased from the levels observed prior to removal from cold. However, they were still significantly greater than those of controls through the fourth week after removal from cold. Thus, the hypertension accompanying a 39-day exposure to cold appears to be only partially reversible at 4 weeks after removal from cold.Key words: cold exposure, hypertension, blood pressure, reversibility of hypertension, renal hypertrophy, cardiac hypertrophy.

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