Dietary polyunsaturated fatty acid and antioxidant modulation of vascular dysfunction in the spontaneously hypertensive rat

2001 ◽  
Vol 65 (2) ◽  
pp. 91-97 ◽  
Author(s):  
M.Y. Abeywardena ◽  
R.J. Head
Keyword(s):  
Fatty Acid ◽  
Polyunsaturated Fatty Acid ◽  
Spontaneously Hypertensive Rat ◽  
Vascular Dysfunction ◽  
Spontaneously Hypertensive ◽  
Dietary Polyunsaturated Fatty Acid ◽  
Hypertensive Rat

scholarly journals Longitudinal Evaluation of Fatty Acid Metabolism in Normal and Spontaneously Hypertensive Rat Hearts with Dynamic MicroSPECT Imaging

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Bryan W. Reutter ◽  
Ronald H. Huesman ◽  
Kathleen M. Brennan ◽  
Rostyslav Boutchko ◽  
Stephen M. Hanrahan ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Spontaneously Hypertensive Rat ◽  
Projection Data ◽  
Ct Scanner ◽  
Pinhole Spect ◽  
Time Activity ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat

The goal of this project is to develop radionuclide molecular imaging technologies using a clinical pinhole SPECT/CT scanner to quantify changes in cardiac metabolism using the spontaneously hypertensive rat (SHR) as a model of hypertensive-related pathophysiology. This paper quantitatively compares fatty acid metabolism in hearts of SHR and Wistar-Kyoto normal rats as a function of age and thereby tracks physiological changes associated with the onset and progression of heart failure in the SHR model. The fatty acid analog, 123I-labeled BMIPP, was used in longitudinal metabolic pinhole SPECT imaging studies performed every seven months for 21 months. The uniqueness of this project is the development of techniques for estimating the blood input function from projection data acquired by a slowly rotating camera that is imaging fast circulation and the quantification of the kinetics of 123I-BMIPP by fitting compartmental models to the blood and tissue time-activity curves.

Vascular dysfunction in the stroke-prone spontaneously hypertensive rat is dependent on constrictor prostanoid activity and Y chromosome lineage

2018 ◽  
Vol 132 (1) ◽  
pp. 131-143 ◽  
Author(s):  
Shanzana I. Khan ◽  
Karen L. Andrews ◽  
Ann-Maree Jefferis ◽  
Garry L. Jennings ◽  
Amanda K. Sampson ◽  
...  
Keyword(s):  
Y Chromosome ◽  
Vascular Function ◽  
Disease Risk ◽  
Spontaneously Hypertensive Rat ◽  
Vascular Dysfunction ◽  
Cardiovascular Disease Risk ◽  
Spontaneously Hypertensive ◽  
Downstream Target ◽  
Hypertensive Rat ◽  
Artery Disease

Vascular dysfunction is a hallmark of hypertension and the strongest risk factor to date for coronary artery disease. As Y chromosome lineage has emerged as one of the strongest genetic predictors of cardiovascular disease risk to date, we investigated if Y chromosome lineage modulated this important facet in the stroke-prone spontaneously hypertensive rat (SHRSP) using consomic strains. Here, we show that vascular dysfunction in the SHRSP is attributable to differential cyclooxygenase (COX) activity with nitric oxide (NO) levels playing a less significant role. Measurement of prostacyclin, the most abundant product of COX in the vasculature, confirmed the augmented COX activity in the SHRSP aorta. This was accompanied by functional impairment of the vasodilatory prostacyclin (IP) receptor, while inhibition of the thromboxane (TP) receptor significantly ameliorated vascular dysfunction in the SHRSP, suggesting this is the downstream target responsible for constrictor prostanoid activity. Importantly, Y chromosome lineage was shown to modulate vascular function in the SHRSP through influencing COX activity, prostacyclin levels and IP dysfunction. Vascular dysfunction in the renal and intrarenal arteries was also found to be prostanoid and Y chromosome dependent. Interestingly, despite no apparent differences in agonist-stimulated NO levels, basal NO levels were compromised in the SHRSP aorta, which was also Y chromosome dependent. Thus, in contrast with the widely held view that COX inhibition is deleterious for the vasculature due to inhibition of the vasodilator prostacyclin, we show that COX inhibition abolishes vascular dysfunction in three distinct vascular beds, with IP dysfunction likely being a key mechanism underlying this effect. We also delineate a novel role for Y chromosome lineage in regulating vascular function through modulation of COX and basal NO levels.

Abstract 485: Mito-Targeted Antioxidant Superior to Non-Targeted Isoform in Modulating Energy Metabolism and Preventing Cardiovascular Remodelling in Spontaneously Hypertensive Rat

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Sherin Saheera ◽  
Ajay Godwin Potnuri ◽  
Raunak R Nair
Keyword(s):  
Fatty Acid ◽  
Energy Metabolism ◽  
Spontaneously Hypertensive Rat ◽  
Heart Diseases ◽  
Left Ventricular ◽  
Metabolic Switch ◽  
Spontaneously Hypertensive ◽  
Beneficial Effects ◽  
Hypertensive Rat ◽  
2D Echocardiography

Hypertension induced left ventricular hypertrophy (LVH) augments the risk of cardiovascular anomalies. Oxidative stress leads to the activation of the hypertrophic program with a metabolic switch from fatty acid to glucose oxidation. Mitochondria, the major source of free radicals, exhibit alterations in hypertensive heart diseases. Targeted antioxidants are expected to reduce mitochondrial reactive oxygen species more effectively than general antioxidants. This study was designed to assess whether mito-targeted antioxidant, MitoTempol is more effective than general oxidant, Tempol on hypertension, hypertrophy and cardiac energy metabolism. Spontaneously Hypertensive Rat were administered either Tempol (20mg/kg/day) or Mito Tempol (2mg/kg/day) orally for 30 days. Post treatment, animals were subjected to 2D-echocardiography. The Myocardial lysates were subjected to Insolution digestion followed by RPLC - LTQ-Orbitrap-MS analysis. Mid-ventricular sections were probed for markers of energy metabolism and fibrosis. The beneficial effect on cardiovascular structure and function was significantly higher for Mito Tempol. Increase in mitochondrial antioxidants and stimulation of fatty acid metabolism with significant improvement in cardiovascular function was apparent in SHR treated with Mito Tempol. The study indicates that Mito Tempol is superior to its non- targeted isoform in preventing hypertension induced LVH, and the beneficial effects on heart are possibly mediated by reversal of metabolic remodelling.

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