Mitochondrial Membrane Potential and Oxygen Consumption in Spontaneously Hypertensive Rats

2012 ◽  
Vol 3 (1) ◽  
pp. 61-68 ◽  
Author(s):  
Nataliya Dorofeyeva ◽  
Yulia V. Goshovska ◽  
Vadym F. Sagach
Keyword(s):  
Oxygen Consumption ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

scholarly journals Role of Ca+-dependent K-channels in the membrane potential and contractility of aorta from spontaneously hypertensive rats

1994 ◽  
Vol 113 (3) ◽  
pp. 1022-1028 ◽  
Author(s):  
Eneida G. Silva ◽  
Eugenio Frediani-Neto ◽  
Alice T. Ferreira ◽  
Antonio CM. Paiva ◽  
Therezinha B. Paiva
Keyword(s):  
Membrane Potential ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
K Channels

scholarly journals Mitochondrial dysfunction in insulin resistance: differential contributions of chronic insulin and saturated fatty acid exposure in muscle cells

2012 ◽  
Vol 32 (5) ◽  
pp. 465-478 ◽  
Author(s):  
Chenjing Yang ◽  
Cho Cho Aye ◽  
Xiaoxin Li ◽  
Angels Diaz Ramos ◽  
Antonio Zorzano ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Oxygen Consumption ◽  
Fatty Acid ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Saturated Fatty Acid ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Acid Exposure ◽  
High Insulin

Mitochondrial dysfunction has been associated with insulin resistance, obesity and diabetes. Hyperinsulinaemia and hyperlipidaemia are hallmarks of the insulin-resistant state. We sought to determine the contributions of high insulin and saturated fatty acid exposure to mitochondrial function and biogenesis in cultured myocytes. Differentiated C2C12 myotubes were left untreated or exposed to chronic high insulin or high palmitate. Mitochondrial function was determined assessing: oxygen consumption, mitochondrial membrane potential, ATP content and ROS (reactive oxygen species) production. We also determined the expression of several mitochondrial genes. Chronic insulin treatment of myotubes caused insulin resistance with reduced PI3K (phosphoinositide 3-kinase) and ERK (extracellular-signal-regulated kinase) signalling. Insulin treatment increased oxygen consumption but reduced mitochondrial membrane potential and ROS production. ATP cellular levels were maintained through an increased glycolytic rate. The expression of mitochondrial OXPHOS (oxidative phosphorylation) subunits or Mfn-2 (mitofusin 2) were not significantly altered in comparison with untreated cells, whereas expression of PGC-1α (peroxisome-proliferator-activated receptor γ co-activator-1α) and UCPs (uncoupling proteins) were reduced. In contrast, saturated fatty acid exposure caused insulin resistance, reducing PI3K (phosphoinositide 3-kinase) and ERK (extracellular-signal-regulated kinase) activation while increasing activation of stress kinases JNK (c-Jun N-terminal kinase) and p38. Fatty acids reduced oxygen consumption and mitochondrial membrane potential while up-regulating the expression of mitochondrial ETC (electron chain complex) protein subunits and UCP proteins. Mfn-2 expression was not modified by palmitate. Palmitate-treated cells also showed a reduced glycolytic rate. Taken together, our findings indicate that chronic insulin and fatty acid-induced insulin resistance differentially affect mitochondrial function. In both conditions, cells were able to maintain ATP levels despite the loss of membrane potential; however, different protein expression suggests different adaptation mechanisms.

Altered hemodynamic responses to acute hypoxemia in spontaneously hypertensive rats

1978 ◽  
Vol 234 (3) ◽  
pp. H275-H279 ◽  
Author(s):  
G. M. Walsh ◽  
M. Tsuchiya ◽  
A. C. Cox ◽  
A. J. Tobia ◽  
E. D. Frohlich
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Early Stage ◽  
Peripheral Resistance ◽  
Oxygen Availability ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Total Body Oxygen

Conscious spontaneously hypertensive rats (SHR), 5--7 wk old, were studied hemodynamically by the direct Fick procedure to determine whether high total peripheral resistance (TPR) coexisted with increased oxygen consumption (QO2) at an early stage of hypertension development. Since under resting conditions cardiac output in SHR was not significantly different from normotensive controls, the elevated arterial pressure and QO2 were associated with increased TPR. Arterial hypoxemia was induced to reduce oxygen availability and to assess whether increased TPR in SHR could be reversed by this procedure. During hypoxemia, normotensive controls (WKY) responded with increased cardiac output and decreased arterial pressure and TPR. In contrast, arterial pressure and cardiac output fell in SHR; and the increased TPR persisted. QO2 fell in hypoxemic SHR demonstrating that the relationship between total body oxygen consumption and cardiac output was abnormal in young SHR, and that increased TPR in SHR was not dependent on resting levels of QO2 or oxygen availability. Although QO2 was elevated in SHR compared to age-matched WKY, this condition was not essential for maintained elevated vascular resistance.

scholarly journals Malnutrition impairs mitochondrial function and leukocyte activation

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Celia Bañuls ◽  
Aranzazu M. de Marañon ◽  
Silvia Veses ◽  
Iciar Castro-Vega ◽  
Sandra López-Domènech ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxygen Consumption ◽  
Membrane Potential ◽  
Adhesion Molecules ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Leukocyte Adhesion ◽  
Retinol Binding Protein ◽  
Rolling Velocity ◽  
Markers Of Inflammation

Abstract Background The aim of this study was to evaluate markers of inflammation, oxidative stress and endothelial function in a disease-related malnutrition (DRM) outpatient population. Methods For this cross-sectional study, a total of 83 subjects were included and clustered in 3 groups: 34 with normonutrition (NN), 21 with DRM without inflammation (DRM-I) and 28 with DRM and inflammation (DRM + I). Nutritional diagnosis was conducted for all subjects according to ASPEN. Biochemical parameters, proinflammatory cytokines, reactive oxygen species production, glutathione, mitochondrial membrane potential, oxygen consumption, adhesion molecules and leukocyte-endothelium interactions were evaluated. Results DRM + I patients showed lower albumin, prealbumin, transferrin, and retinol-binding protein levels with respect to the NN group (p < 0.05), differences that were less noticeable in the DRM-I group. DRM + I was associated with a significant increase in hsCRP and IL6 vs the NN and DRM-I groups, and TNFα was increased in both DRM vs NN. DRM was characterised by increased oxidative stress, which was marked by a significant increase in ROS levels and a decrease in mitochondrial membrane potential in the DRM + I group. An evident reduction in mitochondrial oxygen consumption and glutathione concentration was observed in both DRM groups, and was accompanied by increased leukocyte adhesion and adhesion molecules and decreased rolling velocity in the DRM + I group. Furthermore, percentage of weight loss was negatively correlated with albumin, prealbumin, transferrin, O2 consumption, glutathione and leukocyte rolling velocity, and positively correlated with hsCRP, IL6, TNFα, ROS, leukocyte adhesion, and VCAM-1. Conclusions Our results show that DRM is associated with oxidative stress and an inflammatory state, with a deterioration of endothelial dysfunction in the DRM + I population.

Increased oxidative metabolism in renal tubules from spontaneously hypertensive rats

1989 ◽  
Vol 257 (5) ◽  
pp. F818-F825 ◽  
Author(s):  
P. C. Brazy ◽  
P. E. Klotman
Keyword(s):  
Oxygen Consumption ◽  
Oxidative Metabolism ◽  
Spontaneously Hypertensive Rats ◽  
Antihypertensive Agents ◽  
Systemic Hypertension ◽  
Renal Tubules ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Consumption Rates ◽  
Relationship Of

Genetic hypertension in the rat is associated with abnormal renal function. This may be due to systemic hypertension or to intrinsic alterations in the kidney. Therefore, we examined intrinsic rates of oxidative metabolism in renal cortical tubules isolated from spontaneously hypertensive rats (SHR) and age-matched normotensive controls (WKY) before, during, and after the development of hypertension. We examined tubule function in SHR and WKY treated with antihypertensive agents to block the development of hypertension. During the early phase of hypertension (ages 7-8 wk), SHR tubules have intrinsic rates of oxygen consumption that are 15-25% greater than that of WKY. Ouabain-sensitive rates of oxygen consumption, an index of sodium entry, and Na+-K+-ATPase activity were not increased by 17%. Reduction of blood pressure with drugs did not abolish these differences in oxidative metabolism. Addition of exogenous arachidonic acid (1 microM) did reduce the metabolic differences between 8-wk-old SHR and WKY tubules. Norepinephrine (1 microM) had a greater stimulatory effect on oxygen consumption rates in tubules from hypertensive SHR. The relationship of these metabolic differences to the development of hypertension remains unclear.

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