Obese Zucker rats are normotensive on normal and increased sodium intake.

Pawloski, C. M.; Kanagy, Nancy L.; Mortensen, Luke H.; Fink, Greg D.

doi:10.1161/01.hyp.19.1_suppl.i90

Cited by 34 publications

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“…9,[22][23][24] In contrast, the majority of studies using normoglycemic, hyperinsulinemic obese Zucker rats have found no increase in arterial pressure. 14,18 These results support the hypothesis that hyperglycemia contributes to hypertension in obese Zucker rats. It should be noted that most studies examining arterial pressure control in obese Zucker rats have not reported blood glucose concentrations, 7,8,10,12,13,[15][16][17] thus precluding an estimation of the contribution of glycemic levels to elevated arterial pressure.…”

Section: Discussionsupporting

confidence: 80%

Elevated Sympathetic Activity Contributes to Hypertension and Salt Sensitivity in Diabetic Obese Zucker Rats

et al. 2000

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Abstract-Zucker rats are a useful model in which to define the mechanisms that link obesity to diabetes and associated cardiovascular disease. The present study tests the hypothesis that diabetic obese (compared with nondiabetic lean) Zucker rats are hypertensive and display a further increase in arterial pressure when fed a high salt diet. Male, nondiabetic lean and diabetic obese Zucker rats were chronically instrumented with telemetry probes and fed a basal salt diet for 3 weeks followed by exposure to a high salt diet for 11 days. On the basal diet, obese (vs lean) rats had significantly higher arterial pressures (Ϸ13 mm Hg), and the high salt diet significantly elevated mean arterial pressure (MAP) in obese (but not lean) Zucker rats (Ϸ12 mm Hg). Blockade of the sympathetic nervous system with hexamethonium caused a significantly larger decrease in MAP in obese (vs lean) Zucker rats fed the basal diet (51 vs 33 mm Hg), but the high salt diet did not increase the hexamethonium-induced reduction in arterial pressure in obese rats. Acute blockade of angiotensin receptors with losartan resulted in similar decreases in MAP in both groups on either diet. Acetylcholine-induced vasodilatory capacity of the carotid artery was significantly less in the obese (vs lean) Zucker rats. Together these data indicate that increased sympathetic nervous system activity and decreased vascular reactivity may contribute to elevated arterial pressure in type 2 diabetic, obese Zucker rats, but the sympathetic nervous system does not appear to contribute to the dietary salt-sensitive hypertension in this model. which results in numerous pathological changes, including nephropathy, retinopathy, neuropathy, and cardiovascular disease. Of these factors, cardiovascular disease is the single largest cause of death in diabetes mellitus, accounting for an estimated 80% of deaths in diabetic individuals. 2 The risk of cardiovascular disease in diabetic individuals is increased by concomitant hypertension, which occurs in an estimated 70% of type 2 diabetic patients. 3 Results from the Framingham 4 and MRFIT 5 trials indicate that the coexistence of the 2 diseases triples the risk of cardiovascular disease. Moreover, the presence of hypertension probably accelerates diabetic nephropathy, which in turn exacerbates the hypertension, creating a vicious feedforward cycle that contributes to the extremely high occurrence of end-stage kidney failure in type 2 diabetic patients. 6

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Section: Discussionsupporting

confidence: 80%

Elevated Sympathetic Activity Contributes to Hypertension and Salt Sensitivity in Diabetic Obese Zucker Rats

et al. 2000

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“…Zucker rats have been described as being both hypertensive and normotensive. Several studies indicate that ZFR are hypertensive compared with phenotypically normal heterozygous insulin-sensitive ZLR (1,10,24,50), whereas other studies show a normotensive state of ZFR (30,35,36). Several studies (10,19,45,47) indicate higher levels of SNA in homozygous Zucker rats than in phenotypically normal heterozygous Zucker rats (fa/Ϫ), and it has been suggested that alterations in sympathetic function in obese Zucker rats can be tissue specific (30).…”

Section: Discussionmentioning

confidence: 99%

“…Homozygous Zucker rats are insulin resistant, hyperinsulinemic, and obese. Previous studies on the link between alterations of blood pressure and SNA in the presence of insulin resistance in this strain have yielded contradictory results (1,10,19,24,30,35,36,47,50) that might to be caused, in part, by limitations of the assessment of the degree of alterations of glucose kinetics.We showed previously in the spontaneously hypertensive rat (SHR) and its related control strain (33, 34) that a suitable characterization of the dynamics of glucose kinetics is obtained from the intravenous glucose tolerance test (IVGTT) interpreted with the minimal model (4, 16). On the other hand, an important index of SNA is provided by somatosympathetic reflexes, which are coordinated autonomic responses to activation of somatic afferents mediated by changes in sympathetic activity that cause a cardiovascular reaction to changes in the physical state of the body (14,40).…”

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confidence: 83%

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Enhanced sympathetic reactivity associates with insulin resistance in the young Zucker rat

Ruggeri¹,

Brunori²,

Cogo³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Somatosympathetic reflexes were studied in young hyperinsulinemic, insulin-resistant (Zucker fatty) rats (ZFR) and a related control (Zucker lean) strain (ZLR). Glucose metabolism was characterized by minimal model analysis of intravenous glucose tolerance test data. Seven-week-old ZFR (n ϭ 18) and ZLR (n ϭ 17) were studied under pentobarbital anesthesia. Mean body weight and plasma glucose and insulin concentration were significantly greater (P Ͻ 0.05) in ZFR than in ZLR, whereas basal values of mean arterial pressure (MAP) and heart rate (HR) were not significantly different. Increments of MAP (⌬MAP) and HR (⌬HR) elicited by electrical stimulation of the sciatic nerve (5-s trains of 100 pulses, 0.5-ms pulse duration, 100-to 400-A pulse intensity) were significantly higher (ANOVA, P Ͻ 0.05) in ZFR at each level of stimulus intensity. Regression analysis showed a linear increase in ⌬MAP and ⌬HR with increasing sciatic nerve stimulus intensity. Pressor responses to phenylephrine after ganglionic blockade demonstrated that vascular reactivity to adrenergic stimulation is not increased in ZFR compared with ZLR. Thus this factor does not contribute to enhancement of somatosympathetic reflexes observed in this strain. Insulin sensitivity in ZFR was onefourth (P Ͻ 0.05) that in ZLR. These results suggest that stronger sympathetic nervous reactivity in ZFR is associated with a severe insulin-resistant state before the onset of hypertension and support the hypothesis that insulin-mediated stimulation of the sympathetic nervous system is involved in the development of cardiovascular diseases related to alterations of glucose metabolism. sympathetic nervous activity; minimal model analysis; glucose kinetics; hypertension HYPERINSULINEMIA AND INSULIN resistance are considered important risk factors for development of hypertension (2, 39), and a number of studies have shown a significant association between hypertension and insulin resistance in obese and nonobese individuals (12,15,27,28,46). However, the pathophysiological relation among hyperinsulinemia, insulin resistance, and hypertension remains poorly understood.Some experimental reports suggest that an increase in sympathetic nervous system activity (SNA) may play a role in the association between insulin resistance and elevated blood pressure (39). This association might be due to a primary increase in sympathetic activity (22). Although an increase in sympathetic activity can cause hypertension and insulin resistance, studies performed on animal models indicate that the insulin resistance induced by a high-lipid diet occurs before the onset of hypertension (20), suggesting the primacy of the insulinmediated stimulation of the sympathetic nervous system. If this is true, a suitable animal model to investigate the mechanisms underlying insulin resistance and its associated pathologies is the obese Zucker rat, homozygous for the fa allele (fa/fa), in which a mutation of the leptin receptor-coding gene impairs the ability of leptin to suppress food intake. Homozygous ...

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“…(28)(29)(30)(31)(32)(33)(34) Entretanto, estes animais podem não apresentar algumas anormalidades exibidas em humanos obesos, como hiperinsulinemia, hiperglicemia, hipertensão arterial e hipertrofia cardíaca. (35,36) A administração de uma dieta rica em gordura para roedores representa uma alternativa em modelos experimentais, uma vez que, reproduz muitas características da obesidade humana. (37,38) (19,(71)(72)(73) que, como referido anteriormente, pode ser causada por alterações nas proteínas do trânsito de cálcio miocárdico.…”

Section: -Introduçãounclassified

Influência do tempo de exposição à obesidade sobre a expressão gênica e protéica do sistema regulador do trânsito de cálcio miocárdico

Leopoldo¹

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+2Dedico este trabalho às pessoas mais importantes da minha vida, À toda minha famíliaQue soube compreender todos os momentos em que estive ausente, obrigada pelos constantes incentivos e torcida pelo meu futuro. Vocês são essenciais! Aos meus PaisSignificado de devoção e coragem, com o exemplo deles, aprendi que tudo é possível com força de vontade e pensamento positivo, e, sobretudo, a importância da dignidade e do caráter. Amor eterno! Ao meu marido, André, Pelo privilégio de ter você ao meu lado, sempre carinhoso, otimista e compreensivo até nos momentos mais difíceis. Pelos momentos de esperança que pensa, junto comigo, no nosso futuro. Amo você! Há três coisas fundamentais para a felicidade:alguma coisa para fazer, alguém para amar e algo para esperar. Joseph Addison AGRADECIMENTOS ESPE AGRADECIMENTOS ESPE AGRADECIMENTOS ESPE AGRADECIMENTOS ESPECIAIS CIAIS CIAIS CIAISAo meu orientador, Prof. Dr. Antonio Carlos Cicogna, pela oportunidade, credibilidade e por ter me ensinado que ciência não se faz em poucas horas, mas sim em investigação científica baseada na observação e experimentação, com perseverança e muita dedicação. ABSTRACTCurrently, greater than one billion people are overweight and 30% of the population is obese.Several structural and functional changes of the heart have often been associated with human obesity. Experimental models for high-fat diets have been used to study the relationship between obesity and the heart. Myocardial calcium (Ca 2+ ) handling has been extensively studied in several experimental models and has often been shown to be related to cardiac dysfunction. However, few studies have evaluated the relationship between the duration of exposure to obesity and a high-fat diet, and mRNA and proteins involved in homeostasis of myocardial Ca 2+ . Some studies have reported the influence of thyroid hormones on these proteins, which may cause changes in cardiac contraction and relaxation. The main objective of the current study was to test the hypothesis that the increased duration of exposure to obesity leads to a reduction in the expression and/or phosphorylation of proteins and mRNA levels related to myocardial Ca 2+ handling. This study had, as additional objective, to verify if the decrease in mRNA expression was accompanied by a reduction in thyroid hormone levels.The periods of exposure to a high-fat diet used in this study were effective in promoting obesity since the adiposity index used to characterize animals as obese was 79.5%, 82%, and 69.5% higher than controls after 15, 30, and 45 weeks, respectively. The duration of exposure to a high-fat diet did not change the total body fat between the obese groups. This result indicates that there was not an increase in the intensity of obesity over time. In this study, some co-morbidities often associated with experimental obesity existed, such as glucose intolerance, insulin resistance, hyperinsulinemia, hyperleptinemia, and dyslipidemia; however, the co-morbidities were not associated with changes in systolic blood pressure.Obesi...

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Obese Zucker rats are normotensive on normal and increased sodium intake.

Cited by 34 publications

References 0 publications

Elevated Sympathetic Activity Contributes to Hypertension and Salt Sensitivity in Diabetic Obese Zucker Rats

Elevated Sympathetic Activity Contributes to Hypertension and Salt Sensitivity in Diabetic Obese Zucker Rats

Enhanced sympathetic reactivity associates with insulin resistance in the young Zucker rat

Influência do tempo de exposição à obesidade sobre a expressão gênica e protéica do sistema regulador do trânsito de cálcio miocárdico

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