Insulin-induced endothelin release and vasoreactivity in hypertriglyceridemic and hypertensive rats

Nava, Pilar; Guarner, Verónica; Posadas, Rosalinda; Pérez, Israel; Baños, Guadalupe

doi:10.1152/ajpheart.1999.277.1.h399

Cited by 11 publications

(12 citation statements)

References 26 publications

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“…But after the HTG rats drink the 30% sucrose solution, their levels of insulin may increase significantly. With reference to this we have shown that even a moderate insulin increase can induce in vitro endothelin release in rat aorta and femoral arteries (25), an effect that could extend to HTG coronary vessels and modify their function.…”

Section: General Characteristicsmentioning

confidence: 70%

Isolated Heart Function after Ischemia and Reperfusion in Sucrose-Fed Rats: Influence of Gender and Treatment

Cárdenas

Torres

Zamora

et al. 2006

Clinical and Experimental Hypertension

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Sucrose-fed rats (HTG) develop hypertension, hypertriglyceridemia, and other features of the metabolic syndrome. This condition, nowadays a world epidemic, is more prevalent in males and increases the risk of cardiovascular diseases. Weanling male and female rats were given either tap water in control (C) or 30% sucrose solution in HTG groups and commercial rat chow for 3, 5, or 8 months. We studied possible variations in cardiac function, due to gender and length of treatment, in isolated heart after ischemia-reperfusion, since an impaired performance may be more easily detected under stress. Together, sucrose treatment and age affected all cardiac variables. Gender had significant effect on coronary vascular resistance and postischemic levels of the enzyme CK-MB; the percentages of retained cardiac enzymes after ischemia were higher in C and HTG females. C and HTG males had a higher incidence of arrhythmias than females, but only HTG males suffered lethal ventricular fibrillation.

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Section: General Characteristicsmentioning

confidence: 70%

Isolated Heart Function after Ischemia and Reperfusion in Sucrose-Fed Rats: Influence of Gender and Treatment

Cárdenas

Torres

Zamora

et al. 2006

Clinical and Experimental Hypertension

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“…It has been suggested that the imbalance between vasoconstriction and vasodilatation and the development of high SBP and MS may be partly due to an increase in vasoconstrictors dependent on the sympathetic system, as well as a deficiency in the expression of eNOS and in the antioxidant system [11,12,29].…”

Section: Discussionmentioning

confidence: 99%

Association of renal damage and oxidative stress in a rat model of metabolic syndrome. Influence of gender

Pérez-Torres¹,

Roque²,

Hafidi

et al. 2009

Free Radical Research

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This study investigated the association between nephropathy and oxidative stress, by measurement of systolic blood pressure, lipid peroxidation, activities of catalase, manganese- and copper-zinc-superoxide dismutase and endothelial nitric oxide synthase expression and concentrations of nitrates/nitrites in kidneys from rats with Metabolic Syndrome. Weaning female or male rats had 30% sucrose to drink for 24 weeks (Metabolic Syndrome). Modulation by sex hormones was investigated by gonadectomy and hormone replacement. In Metabolic Syndrome, Castrated Metabolic Syndrome + Testosterone males and Ovariectomized Metabolic Syndrome females had increased blood pressure, proteinuria and lipid peroxidation. Nitrates/nitrites and activities of catalase, manganese and copper-zinc-superoxide dismutase decreased vs intact Control, Castrated Metabolic Syndrome males, intact Metabolic Syndrome and Ovariectomized Metabolic Syndrome + Estradiol females. The results suggest that sex hormones modulate the activity of superoxide-dismutase, catalase and endothelial nitric oxide-synthase. Ovariectomy decreased the protection against oxidative stress in females; the opposite occurred in castrated males.

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“…At the end of each week, during glycine treatment, systolic arterial BP was measured by connecting the tail cuff to a pneumatic pulse transducer and a programmed electrosphygmomanometer (Narco Biosystems) as described previously (39). Recordings were made in triplicate by means of a Grass polygraph (Grass Medical Instruments, Quincy, MA).…”

Section: Methodsmentioning

confidence: 99%

Glycine intake decreases plasma free fatty acids, adipose cell size, and blood pressure in sucrose-fed rats

Hafidi¹,

Pérez²,

Zamora³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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106

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os. Glycine intake decreases plasma free fatty acids, adipose cell size, and blood pressure in sucrose-fed rats. Am J Physiol Regul Integr Comp Physiol 287: R1387-R1393, 2004. First published August 26, 2004 doi:10.1152/ajpregu.00159.2004The study investigated the mechanism by which glycine protects against increased circulating nonesterified fatty acids (NEFA), fat cell size, intra-abdominal fat accumulation, and blood pressure (BP) induced in male Wistar rats by sucrose ingestion. The addition of 1% glycine to the drinking water containing 30% sucrose, for 4 wk, markedly reduced high BP in sucrose-fed rats (SFR) (122.3 Ϯ 5.6 vs. 147.6 Ϯ 5.4 mmHg in SFR without glycine, P Ͻ 0.001). Decreases in plasma triglyceride (TG) levels (0.9 Ϯ 0.3 vs. 1.4 Ϯ 0.3 mM, P Ͻ 0.001), intra-abdominal fat (6.8 Ϯ 2.16 vs. 14.8 Ϯ 4.0 g, P Ͻ 0.01), and adipose cell size were observed in SFR treated with glycine compared with SFR without treatment. Total NEFA concentration in the plasma of SFR was significantly decreased by glycine intake (0.64 Ϯ 0.08 vs. 1.11 Ϯ 0.09 mM in SFR without glycine, P Ͻ 0.001). In control animals, glycine decreased glucose, TGs, and total NEFA but without reaching significance. In SFR treated with glycine, mitochondrial respiration, as an indicator of the rate of fat oxidation, showed an increase in the state IV oxidation rate of the ␤-oxidation substrates octanoic acid and palmitoyl carnitine. This suggests an enhancement of hepatic fatty acid metabolism, i.e., in their transport, activation, or ␤-oxidation. These findings imply that the protection by glycine against elevated BP might be attributed to its effect in increasing fatty acid oxidation, reducing intra-abdominal fat accumulation and circulating NEFA, which have been proposed as links between obesity and hypertension. obesity; mitochondrial oxygen uptake; fatty acid oxidation OBESITY is a significant human health problem; its incidence is reaching epidemic proportions in many Western countries (2, 31). Obesity with fat accumulation predominantly in the abdominal cavity is more frequently associated with disorders of glucose and lipid metabolism than is subcutaneous fat obesity (6, 17). It is well known that increased intra-abdominal fat accumulation is also associated with elevated circulating nonesterified fatty acids (NEFA) (33), resulting from the increased lipolytic activity in adipose tissue. High levels of circulating NEFA have been assumed to be a possible link between intra-abdominal fat accumulation and elevated blood pressure (BP) (9,34,46,49).Several factors are known to be involved in the development of intra-abdominal adiposity in both humans and animals, including genetic and environmental factors, such as excessive fat or carbohydrate intake and lack of physical exercise (8, 44). Thus several animal models of obesity have been developed to investigate the mechanism by which obesity induces hypertension, hyperinsulinemia, and insulin resistance.In our laboratory, we developed an animal model of intraabdominal fat accumulation, indu...

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Insulin-induced endothelin release and vasoreactivity in hypertriglyceridemic and hypertensive rats

Cited by 11 publications

References 26 publications

Isolated Heart Function after Ischemia and Reperfusion in Sucrose-Fed Rats: Influence of Gender and Treatment

Isolated Heart Function after Ischemia and Reperfusion in Sucrose-Fed Rats: Influence of Gender and Treatment

Association of renal damage and oxidative stress in a rat model of metabolic syndrome. Influence of gender

Glycine intake decreases plasma free fatty acids, adipose cell size, and blood pressure in sucrose-fed rats

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