scholarly journals Peripheral and Cerebral Resistance Arteries in the Spontaneously Hypertensive Heart Failure Rat: Effects of Stilbenoid Polyphenols

Molecules ◽  
2017 ◽  
Vol 22 (3) ◽  
pp. 380 ◽  
Author(s):  
Danielle Lee ◽  
Crystal Acosta ◽  
Christopher Anderson ◽  
Hope Anderson
Keyword(s):  
Heart Failure ◽  
Resistance Arteries ◽  
Spontaneously Hypertensive ◽  
Spontaneously Hypertensive Heart Failure ◽  
Cerebral Resistance

scholarly journals Long‐Term Dipeptidyl Peptidase 4 Inhibition Worsens Hypertension and Renal and Cardiac Abnormalities in Obese Spontaneously Hypertensive Heart Failure Rats

2021 ◽  
Author(s):  
Edwin K. Jackson ◽  
Zaichuan Mi ◽  
Delbert G. Gillespie ◽  
Dongmei Cheng ◽  
Stevan P. Tofovic
Keyword(s):  
Heart Failure ◽  
Collagen Iv ◽  
Spontaneously Hypertensive ◽  
Dipeptidyl Peptidase 4 ◽  
Dpp4 Inhibitor ◽  
Arterial Blood ◽  
Spontaneously Hypertensive Heart Failure ◽  
Blood Pressures ◽  
Renal Vascular

Background The long‐term effects of dipeptidyl peptidase 4 (DPP4) inhibitors on blood pressure and cardiovascular and renal health remain controversial. Herein, we investigated the extended (>182 days) effects of DPP4 inhibition in a model of spontaneous hypertension, heart failure, diabetes mellitus, obesity and hyperlipidemia. Methods and Results Adult obese spontaneously hypertensive heart failure rats (SHHF) were implanted with radio transmitters for measurement of arterial blood pressures. Two weeks later, SHHF were randomized to receive either a DPP4 inhibitor (sitagliptin, 80 mg/kg per day in drinking water) or placebo. At the end of the radiotelemetry measurements, renal and cardiac function and histology, as well as other relevant biochemical parameters, were assessed. For the first 25 days, mean arterial blood pressures were similar in sitagliptin‐treated versus control SHHF; afterwards, mean arterial blood pressures increased more in sitagliptin‐treated SHHF ( P <0.000001). The time‐averaged mean arterial blood pressures from day 26 through 182 were 7.2 mm Hg higher in sitagliptin‐treated SHHF. Similar changes were observed for systolic (8.6 mm Hg) and diastolic (6.1 mm Hg) blood pressures, and sitagliptin augmented hypertension throughout the light‐dark cycle. Long‐term sitagliptin treatment also increased kidney weights, renal vascular resistances, the excretion of kidney injury molecule‐1 (indicates injury to proximal tubules), renal interstitial fibrosis, glomerulosclerosis, renal vascular hypertrophy, left ventricular dysfunction, right ventricular degeneration, and the ratios of collagen IV/collagen III and collagen IV/laminin in the right ventricle. Conclusions These findings indicate that, in some genetic backgrounds, long‐term DPP4 inhibitor treatment is harmful and identify an animal model to study mechanisms of, and test ways to prevent, DPP4 inhibitor–induced pathological conditions.

Beneficial Effect of TMAO in Spontaneously Hypertensive Heart Failure Rats is Associated with Diuretic and Hypotensive Actions.

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Marcin Ufnal ◽  
Marek Konop ◽  
Marta Gawrys-Kopczynska ◽  
Klaudia Maksymiuk ◽  
Krzysztof Sozanski ◽  
...  
Keyword(s):  
Heart Failure ◽  
Beneficial Effect ◽  
Spontaneously Hypertensive ◽  
Spontaneously Hypertensive Heart Failure

scholarly journals Gut Microbiota Profile Identifies Transition From Compensated Cardiac Hypertrophy to Heart Failure in Hypertensive Rats

Hypertension ◽  
2020 ◽  
Vol 76 (5) ◽  
pp. 1545-1554
Author(s):  
Elena Gutiérrez-Calabrés ◽  
Adriana Ortega-Hernández ◽  
Javier Modrego ◽  
Rubén Gómez-Gordo ◽  
Alicia Caro-Vadillo ◽  
...  
Keyword(s):  
Heart Failure ◽  
Gut Microbiota ◽  
Spontaneously Hypertensive Rat ◽  
Spontaneously Hypertensive ◽  
Metabolic Functions ◽  
Hypertensive Rat ◽  
Spontaneously Hypertensive Heart Failure ◽  
Wistar Kyoto ◽  
And Function ◽  
Gut Microbial Community

Microcirculatory alterations displayed by patients with heart failure (HF) induce structural and functional intestinal changes that may affect normal gut microbial community. At the same time, gut microbiota can influence pathological mechanisms implicated in HF progression. However, it is unknown whether gut microbiota dysbiosis can precede the development of cardiac alterations in HF or it is only a mere consequence. Our aim was to investigate the potential relationship between gut microbiota composition and HF development by comparing spontaneously hypertensive heart failure and spontaneously hypertensive rat models. Gut microbiota from spontaneously hypertensive heart failure, spontaneously hypertensive rat, and normotensive Wistar Kyoto rats at 9 and 19 months of age was analyzed by sequencing the 16S ribosomal RNA gene, and KEGG metabolic pathways associated to 16S profiles were predicted. Beta diversity, Firmicutes / Bacteroidetes ratio, taxonomic abundances, and potential metabolic functions of gut microbiota were significantly different in spontaneously hypertensive heart failure with respect to spontaneously hypertensive rat before (9 months) and after (19 months) cardiac differences were presented. Nine-month-old spontaneously hypertensive heart failure showed a significant increase in the genera Paraprevotella, Oscillospira, Prevotella 9, Faecalitalea, Faecalibacterium, Ruminiclostridium 6, Phascolarctobacterium, Butyrivibrio, Parasutterella, and Parabacteroides compared with both Wistar Kyoto and spontaneously hypertensive rat, while Ruminiclostridium 9 , Oscillibacter , Ruminiclostridium , Mucispirillum, Intestinimonas , and Akkermansia were diminished. Of them, Akkermansia, Prevotella 9 , Paraprevotella , and Phascolarctobaterium were associated to changes in cardiac structure and function. Our results demonstrate an association between specific changes in gut microbiota and the development of HF in a hypertensive model of HF and further support the intervention to restore gut microbiota as an innovative therapeutic strategy for preventing HF.

scholarly journals Heart Failure Disturbs Gut–Blood Barrier and Increases Plasma Trimethylamine, a Toxic Bacterial Metabolite

2020 ◽  
Vol 21 (17) ◽  
pp. 6161
Author(s):  
Adrian Drapala ◽  
Mateusz Szudzik ◽  
Dawid Chabowski ◽  
Izabella Mogilnicka ◽  
Kinga Jaworska ◽  
...  
Keyword(s):  
Heart Failure ◽  
Plasma Levels ◽  
Ultra Performance Liquid Chromatography ◽  
Cardiovascular Pathology ◽  
Spontaneously Hypertensive ◽  
Plasma And Urine Samples ◽  
Spontaneously Hypertensive Heart Failure ◽  
Biochemical Measurements ◽  
Wistar Kyoto ◽  
Junction Proteins

Trimethylamine (TMA) is a gut bacteria product oxidized by the liver to trimethylamine-N-oxide (TMAO). Clinical evidence suggests that cardiovascular disease is associated with increased plasma TMAO. However, little headway has been made in understanding this relationship on a mechanistic and molecular level. We investigated the mechanisms affecting plasma levels of TMAO in Spontaneously Hypertensive Heart Failure (SHHF) rats. Healthy Wistar Kyoto (WKY) and SHHF rats underwent metabolic, hemodynamic, histopathological and biochemical measurements, including tight junction proteins analysis. Stool, plasma and urine samples were evaluated for TMA and TMAO using ultra performance liquid chromatography-mass spectrometry. SHHF presented disturbances of the gut–blood barrier including reduced intestinal blood flow, decreased thickness of the colonic mucosa and alterations in tight junctions, such as claudin 1 and 3, and zonula occludens-1. This was associated with significantly higher plasma levels of TMA and TMAO and increased gut-to-blood penetration of TMA in SHHF compared to WKY. There was no difference in kidney function or liver oxidation of TMA to TMAO between WKY and SHHF. In conclusion, increased plasma TMAO in heart failure rats results from a perturbed gut–blood barrier and increased gut-to-blood passage of TMAO precursor, i.e., TMA. Increased gut-to-blood penetration of bacterial metabolites may be a marker and a mediator of cardiovascular pathology.

Sign in / Sign up

Export Citation Format

Share Document