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.

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.

scholarly journals A Reduction in ADAM17 Expression Is Involved in the Protective Effect of the PPAR-α Activator Fenofibrate on Pressure Overload-Induced Cardiac Hypertrophy

PPAR Research ◽  
2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Si-Yu Zeng ◽  
Hui-Qin Lu ◽  
Qiu-Jiang Yan ◽  
Jian Zou
Keyword(s):  
Body Weight ◽  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Wall Thickness ◽  
Protective Action ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Heart Weight ◽  
Hypertensive Rats ◽  
Protein Levels

The peroxisome proliferator-activated receptor-α (PPAR-α) agonist fenofibrate ameliorates cardiac hypertrophy; however, its mechanism of action has not been completely determined. Our previous study indicated that a disintegrin and metalloproteinase-17 (ADAM17) is required for angiotensin II-induced cardiac hypertrophy. This study aimed to determine whether ADAM17 is involved in the protective action of fenofibrate against cardiac hypertrophy. Abdominal artery constriction- (AAC-) induced hypertensive rats were used to observe the effects of fenofibrate on cardiac hypertrophy and ADAM17 expression. Primary cardiomyocytes were pretreated with fenofibrate (10 μM) for 1 hour before being stimulated with angiotensin II (100 nM) for another 24 hours. Fenofibrate reduced the ratios of left ventricular weight to body weight (LVW/BW) and heart weight to body weight (HW/BW), left ventricular anterior wall thickness (LVAW), left ventricular posterior wall thickness (LVPW), and ADAM17 mRNA and protein levels in left ventricle in AAC-induced hypertensive rats. Similarly, in vitro experiments showed that fenofibrate significantly attenuated angiotensin II-induced cardiac hypertrophy and diminished ADAM17 mRNA and protein levels in primary cardiomyocytes stimulated with angiotensin II. In summary, a reduction in ADAM17 expression is associated with the protective action of PPAR-α agonists against pressure overload-induced cardiac hypertrophy.

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.

Genistein prevents isoproterenol-induced cardiac hypertrophy in rats

2012 ◽  
Vol 90 (8) ◽  
pp. 1117-1125 ◽  
Author(s):  
Subir Kumar Maulik ◽  
Pankaj Prabhakar ◽  
Amit Kumar Dinda ◽  
Sandeep Seth
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Body Weight ◽  
Nitric Oxide Synthase ◽  
Cardiac Hypertrophy ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Heart Weight ◽  
Once Daily ◽  
Oxide Synthase

Genistein, an isoflavone and a rich constituent of soy, possesses important regulatory effects on nitric oxide (NO) synthesis and oxidative stress. Transient and low release of NO by endothelial nitric oxide synthase (eNOS) has been shown to be beneficial, while high and sustained release by inducible nitric oxide synthase (iNOS) may be detrimental in pathological cardiac hypertrophy. The present study was designed to evaluate whether genistein could prevent isoproterenol-induced cardiac hypertrophy in male Wistar rats (150–200 g, 10–12 weeks old) rats. Isoproterenol (5 mg·(kg body weight)–1) was injected subcutaneously once daily for 14 days to induced cardiac hypertrophy. Genistein (0.1 and 0.2 mg·kg–1, subcutaneous injection once daily) was administered along with isoproterenol. Heart tissue was studied for myocyte size and fibrosis. Myocardial thiobarbituric acid reactive substances (TBARS), glutathione (GSH), superoxide dismutase (SOD), catalase levels, and 1-OH proline (collagen content) were also estimated. Genistein significantly prevented any isoproterenol-induced increase in heart weight to body weight ratio, left ventricular mass (echocardiographic), myocardial 1-OH proline, fibrosis, myocyte size and myocardial oxidative stress. These beneficial effects of genistein were blocked by a nonselective NOS inhibitor (L-NAME), but not by a selective iNOS inhibitor (aminoguanidine). Thus, the present study suggests that the salutary effects of genistein on isoproterenol-induced cardiac hypertrophy may be mediated through inhibition of iNOS and potentiation of eNOS activities.

Hypertension and Cardiac Hypertrophy in Growth Hormone-Deficient Rats

1994 ◽  
Vol 87 (2) ◽  
pp. 239-243 ◽  
Author(s):  
Stephen B. Harrap ◽  
Shari R. Datodi ◽  
Emma K. Crapper ◽  
Leon A. Bach
Keyword(s):  
Blood Pressure ◽  
Growth Hormone ◽  
Body Weight ◽  
Cardiac Hypertrophy ◽  
Weight Ratio ◽  
The Body ◽  
Hormone Deficiency ◽  
Heart Weight ◽  
Deoxycorticosterone Acetate ◽  
F344 Rats

1. Growth hormone may influence cardiac growth during post-natal maturation or in response to hypertension, and the growth-hormone deficient dwarf rat model offers an opportunity to study this question. 2. We compared the blood pressure and heart weight of dwarf rats and Fischer (F344) control rats in early adulthood, after two hypertensive stimuli: unilateral renal ischaemia (two-kidney, one-clip) or the administration of deoxycorticosterone acetate and saline drinking fluid. 3. In untreated animals at 13 weeks of age the body weight of dwarf rats was significantly less than that of F344 rats, but the mean arterial pressure was similar. Although the hearts of dwarf rats were smaller than those of F344 rats, the heart weight/body weight ratio was significantly greater in dwarf rats. 4. Both dwarf and F344 rats developed similar hypertensive mean arterial pressures 5 weeks after left renal artery clipping or treatment with deoxycorticosterone acetate salt. The heart weights of hypertensive dwarf and F344 rats were equivalent, indicating a proportionally greater increase in cardiac size in dwarf rats for the same rise in blood pressure. 5. The plasma insulin-like growth factor-I level was markedly lower in dwarf than in F344 rats, and hypertension did not have any significant effects on these levels. 6. These findings indicate that the developmental increase in blood pressure and heart size in growing animals and the adaptive cardiac hypertrophy accompanying hypertension are not affected by growth hormone deficiency.

RNA interference targeting the ACE gene reduced blood pressure and improved myocardial remodelling in SHRs

2009 ◽  
Vol 116 (3) ◽  
pp. 249-255 ◽  
Author(s):  
Junhua He ◽  
Yunfei Bian ◽  
Fen Gao ◽  
Maolian Li ◽  
Ling Qiu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Rna Interference ◽  
Serum Concentration ◽  
Systolic Blood Pressure ◽  
Normal Saline ◽  
Left Ventricular ◽  
Heart Weight ◽  
Wky Rats ◽  
Wistar Kyoto

The purpose of the present study was to investigate the effects on blood pressure and myocardial hypertrophy in SHRs (spontaneously hypertensive rats) of RNAi (RNA interference) targeting ACE (angiotensin-converting enzyme). SHRs were treated with normal saline as vehicle controls, with Ad5-EGFP as vector controls, and with recombinant adenoviral vectors Ad5-EGFP-ACE-shRNA, carrying shRNA (small hairpin RNA) for ACE as ACE-RNAi. WKY (Wistar–Kyoto) rats were used as normotensive controls treated with normal saline. The systolic blood pressure of the caudal artery was recorded. Serum levels of ACE and AngII (angiotensin II) were determined using ELISA. ACE mRNA and protein levels were determined in aorta, myocardium, kidney and lung. On day 32 of the experiment, the heart was pathologically examined. The ratios of heart weight/body weight and left ventricular weight/body weight were calculated. The serum concentration of ACE was lower in ACE-RNAi rats (16.37±3.90 ng/ml) compared with vehicle controls and vector controls (48.26±1.50 ng/ml and 46.67±2.82 ng/ml respectively; both P&lt;0.05), but comparable between ACE-RNAi rats and WKY rats (14.88±3.15 ng/ml; P&gt;0.05). The serum concentration of AngII was also significantly lower in ACE-RNAi rats (18.24±3.69 pg/ml) compared with vehicle controls and vector controls (46.21±5.06 pg/ml and 44.93±4.12 pg/ml respectively; both P&lt;0.05), but comparable between ACE-RNAi rats and WKY rats (16.06±3.11 pg/ml; P&gt;0.05). The expression of ACE mRNA and ACE protein were significantly reduced in the myocardium, aorta, kidney and lung in ACE-RNAi rats compared with that in vehicle controls and in vector controls (all P&lt;0.05). ACE-RNAi treatment resulted in a reduction in systolic blood pressure by 22±3 mmHg and the ACE-RNAi-induced reduction lasted for more than 14 days. In contrast, blood pressure was continuously increased in the vehicle controls as well as in the vector controls. The ratios of heart weight/body weight and left ventricular weight/body weight were significantly lower in ACE-RNAi rats (3.12±0.23 mg/g and 2.24±0.19 mg/g) compared with the vehicle controls (4.29±0.24 mg/g and 3.21±0.13 mg/g; P&lt;0.05) and the vector controls (4.43±0.19 mg/g and 3.13±0.12 mg/g; P&lt;0.05). The conclusion of the present study is that ACE-silencing had significant antihypertensive effects and reversed hypertensive-induced cardiac hypertrophy in SHRs, and therefore RNAi might be a new strategy in controlling hypertension.

Lansoprazole alleviates pressure overload-induced cardiac hypertrophy and heart failure in mice by blocking the activation of β-catenin

2019 ◽  
Vol 116 (1) ◽  
pp. 101-113 ◽  
Author(s):  
Hairuo Lin ◽  
Yang Li ◽  
Hailin Zhu ◽  
Qiancheng Wang ◽  
Zhenhuan Chen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Body Weight ◽  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Neonatal Rat ◽  
Cardiac Remodelling ◽  
Heart Weight ◽  
Body Weight Ratio

Abstract Aims Proton pump inhibitors (PPIs) are widely used in patients receiving percutaneous coronary intervention to prevent gastric bleeding, but whether PPIs are beneficial for the heart is controversial. Here, we investigated the effects of lansoprazole on cardiac hypertrophy and heart failure, as well as the underlying mechanisms. Methods and results Adult male C57 mice were subjected to transverse aortic constriction (TAC) or sham surgery and then were treated with lansoprazole or vehicle for 5 weeks. In addition, cultured neonatal rat ventricular cardiomyocytes and fibroblasts were exposed to angiotensin II in the presence or absence of lansoprazole. At 5 weeks after TAC, the heart weight/body weight ratio was lower in lansoprazole-treated mice than in untreated mice, as was the lung weight/body weight ratio, while left ventricular (LV) fractional shortening and the maximum and minimum rates of change of the LV pressure were higher in lansoprazole-treated mice, along with less cardiac fibrosis. In cultured cardiomyocytes, lansoprazole inhibited angiotensin II-induced protein synthesis and hypertrophy, as well as inhibiting proliferation of fibroblasts. Lansoprazole decreased myocardial levels of phosphorylated Akt, phosphorylated glycogen synthase kinase 3β, and active β-catenin in TAC mice and in angiotensin II-stimulated cardiomyocytes. After overexpression of active β-catenin or knockdown of H+/K+-ATPase α-subunit, lansoprazole still significantly attenuated myocyte hypertrophy. Conclusion Lansoprazole inhibits cardiac remodelling by suppressing activation of the Akt/GSK3β/β-catenin pathway independent of H+/K+-ATPase inhibition, and these findings may provide a novel insight into the pharmacological effects of PPIs with regard to alleviation of cardiac remodelling.

Aminotriazole, thyroid function, and catecholamines in nephrogenic hypertension in rats

1969 ◽  
Vol 47 (5) ◽  
pp. 407-414 ◽  
Author(s):  
M. J. Fregly ◽  
A. H. Anton
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Adrenal Glands ◽  
Weight Ratio ◽  
Male Rats ◽  
Heart Weight ◽  
Threshold Pressure ◽  
Body Weight Ratio ◽  
Blood Pressures ◽  
Blood Pressure Range

Administration of graded doses of the antithyroid agent aminotriazole (ATZ) to male rats whose kidneys were bilaterally encapsulated with latex envelopes provided protection against the elevation of systolic blood pressure to the level of untreated, renal-encapsulated controls. The doses used were 5, 10, 50, and 250 p.p.m. mixed thoroughly into food. Blood pressures of the groups treated with either 50 or 250 p.p.m. ATZ were within the range of the non-encapsulated controls during the last 7 weeks of the 15-week experiment. Hypothyroidism accompanied administration of the highest dose of ATZ in that heart rate was reduced, and thyroid weight increased, beyond the levels observed for renal-encapsulated control rats. A sigmoid relationship was observed between heart to body weight ratio and systolic blood pressure for all rats. This relationship suggests that heart weight is unaffected by change in blood pressure until the threshold pressure of 150–159 mm Hg is reached. Beyond this threshold pressure, heart weight increased sharply to reach a level approximately 30% above that observed within the blood pressure range of 120–149 mm Hg. Treatment of hypertensive rats with ATZ failed to affect heart and adrenal norepinephrine and adrenal epinephrine concentrations, suggesting a lack of correlation between blood pressure and concentration of these catecholamines in the heart and adrenal glands.

scholarly journals The Programming of Cardiac Hypertrophy in the Offspring by Maternal Obesity Is Associated with Hyperinsulinemia, AKT, ERK, and mTOR Activation

Endocrinology ◽  
2012 ◽  
Vol 153 (12) ◽  
pp. 5961-5971 ◽  
Author(s):  
Denise S. Fernandez-Twinn ◽  
Heather L. Blackmore ◽  
Lee Siggens ◽  
Dino A. Giussani ◽  
Christine M. Cross ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Cardiac Hypertrophy ◽  
Maternal Obesity ◽  
Mammalian Target Of Rapamycin ◽  
Left Ventricular ◽  
Target Of Rapamycin ◽  
Heart Weight ◽  
Cardiac Phenotype ◽  
Pregnancy And Lactation

Abstract Human and animal studies suggest that suboptimal early nutrition during critical developmental periods impacts long-term health. For example, maternal overnutrition during pregnancy and lactation in mice programs insulin resistance, obesity, and endothelial dysfunction in the offspring. Here we investigated the effects of diet-induced maternal obesity on the offspring cardiac phenotype and explored potential underlying molecular mechanisms. Dams fed the obesogenic diet were heavier (P &lt; 0.01) and fatter (P &lt; 0.0001) than controls throughout pregnancy and lactation. There was no effect of maternal obesity on offspring body weight or body composition up to 8 wk of age. However, maternal obesity resulted in increased offspring cardiac mass (P &lt; 0.05), increased heart-body weight (P &lt; 0.01), heart weight-tibia length (P &lt; 0.05), increased left ventricular free wall thickness and area (P &lt; 0.01 and P &lt; 0.05, respectively), and increased myocyte width (P &lt; 0.001). Consistent with these structural changes, the expression of molecular markers of cardiac hypertrophy were also increased [Nppb(BNP), Myh7-Myh6(βMHC-αMHC) (both P &lt; 0.05) and mir-133a (P &lt; 0.01)]. Offspring were hyperinsulinemic and displayed increased insulin action through AKT (P &lt; 0.01), ERK (P &lt; 0.05), and mammalian target of rapamycin (P &lt; 0.05). p38MAPK phosphorylation was also increased (P &lt; 0.05), suggesting pathological remodeling. Increased Ncf2(p67phox) expression (P &lt; 0.05) and impaired manganese superoxide dismutase levels (P &lt; 0.01) suggested oxidative stress, which was consistent with an increase in levels of 4-hydroxy-2-trans-nonenal (a measure of lipid peroxidation). We propose that maternal diet-induced obesity leads to offspring cardiac hypertrophy, which is independent of offspring obesity but is associated with hyperinsulinemia-induced activation of AKT, mammalian target of rapamycin, ERK, and oxidative stress.

scholarly journals The HDAC Inhibitor Emodin Blocks Hypertension-Induced Cardiac Hypertrophy: A Mediating Role for the Gut?

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 396-396
Author(s):  
Levi Evans ◽  
Brad Ferguson
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Cardiac Hypertrophy ◽  
Parent Compound ◽  
Heart Weight ◽  
Female Mice ◽  
Blood Institute ◽  
Mediating Role ◽  
Funding Sources ◽  
Pathological Cardiac Hypertrophy

Abstract Objectives Evidence suggests that food bioactives impact the epigenome to prevent pathological cardiac hypertrophy. Recently, we showed that emodin, an anthraquinone, attenuated pathological cardiac hypertrophy and histone deacetylase (HDAC) activity. However, we only examined the cardioprotective effects of emodin's parent compound, not of emodin metabolites or of emodin-gut microbiome interactions. The microbiome has emerged as a key player in chronic diseases such as metabolic and cardiac disease. Thus, we hypothesized that emodin could reverse hypertension-induced changes in microbial communities. Methods Normo- and hypertensive (angiotensin ii) C57/BL6 female mice were randomly assigned to receive vehicle (Veh, DMSO: PEG 1:1) or emodin (Emod, 30 mg/kg) for 14 days. Body weight was collected pre- and post-treatment and blood pressure assessed via tail-cuff. At study end, mice were euthanized and assessed for heart weight and fibrosis. In addition, stool samples and cecal content were collected to elucidate changes in microbial populations using 16S rRNA sequencing. Lastly, tissue was lysed and RNA isolated for RNA sequencing. One-way ANOVA with Tukey's post-hoc was performed unless otherwise specified and P &lt; 0.05 considered significant. Results Emodin significantly attenuated cardiac hypertrophy and fibrosis in female mice. No significant changes were observed for body weight or systolic blood pressure in response to hypertension or emodin. Lastly, preliminary analysis suggests that hypertension altered the microbiome, with evidence to support that emodin effects gut microbiota. Conclusions Our data demonstrates that emodin attenuates pathological hypertrophy and fibrosis in female mice. Whether this attenuation in cardiac remodeling is driven, in part, by the actions of emodin on the gut the microbiome remains unclear and is currently an active topic of investigation in our lab. Funding Sources This work is supported by the USDA NIFA (Hatch-NEV00767), the Dennis Meiss & Janet Ralston Fund for Nutri-epigenetic Research, the National Institute for General Medical Sciences (NIGMS) of the NIH (P20 GM130459) and the National Heart, Lung, and Blood Institute of the NIH (R15 HL143496) to B.S.F. Core facilities used for Research were supported by NIGMS of the NIH (P20 GM103554).

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