Reduced parasympathetic control of heart rate in obese dogs

Vliet, Bruce N. Van; Hall, John E.; Mizelle, H. L.; Montani, Jean‐Pierre; Smith, M. J.

doi:10.1152/ajpheart.1995.269.2.h629

Cited by 68 publications

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“…A high fat diet in dogs also markedly raised heart rate and cardiac output, with little change in stroke volume. The rise in resting heart rate in obesity was due primarily to withdrawal of parasympathetic tone rather than increased sympathetic activity or increased intrinsic heart rate (18). Total peripheral vascular resistance decreased during the high fat diet, but when indexed for body weight (total peripheral vascular resistance index) there was a slight increase (16), similar to that observed in obese humans (19).…”

Section: Mechanisms Of Obesity Hypertension Hemodynamic Changes In Obmentioning

confidence: 52%

“…In dogs placed on a high fat diet for five weeks with a constant intake of sodium, protein, and carbohydrates, there were parallel increases in body weight and blood pressure, with arterial pressure increasing [15][16][17][18][19][20] (Figure 2). This is similar to the modest changes in blood pressure observed in the first few weeks after rapid weight gain or weight loss in humans.…”

Section: Mechanisms Of Obesity Hypertension Hemodynamic Changes In Obmentioning

confidence: 99%

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Role of sympathetic nervous system and neuropeptides in obesity hypertension

Hall

Brands

Hildebrandt

et al. 2000

Braz J Med Biol Res

125

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Obesity is the most common cause of human essential hypertension in most industrialized countries. Although the precise mechanisms of obesity hypertension are not fully understood, considerable evidence suggests that excess renal sodium reabsorption and a hypertensive shift of pressure natriuresis play a major role. Sympathetic activation appears to mediate at least part of the obesity-induced sodium retention and hypertension since adrenergic blockade or renal denervation markedly attenuates these changes. Recent observations suggest that leptin and its multiple interactions with neuropeptides in the hypothalamus may link excess weight gain with increased sympathetic activity. Leptin is produced mainly in adipocytes and is believed to regulate energy balance by acting on the hypothalamus to reduce food intake and to increase energy expenditure via sympathetic activation. Short-term administration of leptin into the cerebral ventricles increases renal sympathetic activity, and long-term leptin infusion at rates that mimic plasma concentrations found in obesity raises arterial pressure and heart rate via adrenergic activation in nonobese rodents. Transgenic mice overexpressing leptin also develop hypertension. Acute studies suggest that the renal sympathetic effects of leptin may depend on interactions with other neurochemical pathways in the hypothalamus, including the melanocortin-4 receptor (MC4-R). However, the role of this pathway in mediating the long-term effects of leptin on blood pressure is unclear. Also, it is uncertain whether there is resistance to the chronic renal sympathetic and blood pressure effects of leptin in obese subjects. In addition, leptin also has other cardiovascular and renal actions, such as stimulation of nitric oxide formation and improvement of insulin sensitivity, which may tend to reduce blood pressure in some conditions. Although the role of these mechanisms in human obesity has not been elucidated, this remains a fruitful area for further investigation, especially in view of the current epidemic of obesity in most industrialized countries. Correspondence

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Section: Mechanisms Of Obesity Hypertension Hemodynamic Changes In Obmentioning

confidence: 52%

Section: Mechanisms Of Obesity Hypertension Hemodynamic Changes In Obmentioning

confidence: 99%

Role of sympathetic nervous system and neuropeptides in obesity hypertension

Hall

Brands

Hildebrandt

et al. 2000

Braz J Med Biol Res

125

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“…Possible explanations include activation of the sympathetic nervous system or withdrawal of parasympathetic tone; evidence exists to support both these mechanisms. 2,[15][16][17] However, in heart transplant recipients, other factors may play a substantial role. Transplantation of the heart results in sympathetic and parasympathetic cardiac denervation.…”

Section: Discussionmentioning

confidence: 99%

Independent Association Between Plasma Leptin Levels and Heart Rate in Heart Transplant Recipients

et al. 2001

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Background-Leptin, the protein product of the ob gene, has been linked to a faster heart rate in animal and human studies.The interaction between leptin and heart rate in the denervated heart is not known. Therefore, we studied the relationship between plasma leptin levels and heart rate in heart transplant recipients. Methods and Results-We studied 32 male patients (mean age, 56.5Ϯ9.3 years; range, 41 to 74 years) after orthotopic heart transplantation. All subjects underwent a physical examination, anthropometric measurements, blood chemistry analysis, and office blood pressure measurements. A blood sample was collected from each subject while fasting. In univariate analysis, heart rate was related to leptin levels (rϭ0.47, Pϭ0.007) but heart rate was not related to systolic or diastolic blood pressure, mean arterial pressure, body mass index, or catecholamines. Leptin levels were only strongly associated with heart rate and body mass index (rϭ0. 73, PϽ0.0001). In multivariate analysis, heart rate was independently and positively associated with leptin levels (Fϭ2.61, Pϭ0.017). We also observed a strong, independent association between leptin levels and body mass index (Fϭ5.8, PϽ0.00001). Conclusions-We show an independent association between leptin levels and heart rate in heart transplant recipients. We speculate that this may be due, in part, to a direct effect of leptin on heart rate, conceivably mediated through cardiac leptin receptors. Key Words: leptin Ⅲ heart rate Ⅲ transplantation H eart rate is emerging as an important cardiovascular risk factor, and it may predict the development of sustained hypertension. 1 Autonomic neural and humoral mechanisms contribute to the control of heart rate. Leptin, the 167 amino acid product of the ob gene, 2 has also been linked to cardiovascular risk. 3,4 Animal studies show that chronic leptin infusion increases heart rate and blood pressure. 5,6 High leptin levels are linked to poor prognosis in the setting of myocardial infarction. 4 In human studies, plasma leptin levels correlate strongly with heart rate, most strikingly during sleep. [7][8][9] The effects of leptin on heart rate are presumably mediated by the central effects of leptin as it modulates autonomic neural control of the heart. 5,6 However, there is emerging evidence that leptin may have direct, non-neural effects on cardiovascular function. Leptin receptors or their mRNA have been detected in blood vessels and in the heart. 10 -13 The interaction between leptin and heart rate in the denervated heart is not known. Therefore, we studied the relationship between plasma leptin levels and heart rate in heart transplant recipients. Methods SubjectsWe studied 32 male patients (aged 56.5Ϯ9.3 years; range, 41 to 74 years). Subjects were selected across a broad spectrum of time intervals after transplantation (mean time after transplantation, 56Ϯ8 months; range, 1 to 132 months). Acute rejection, significant graft vasculopathy (stenoses Ն50%), and impaired systolic function were excluded by endomyocardial ...

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“…18 Finally, the combination of mild elevation of systolic blood pressure along with increased heart rate increases the double product (heart rate-pressure product), a determinant of myocardial oxygen consumption. 19,20 Since weight gain leads to a reduced parasympathetic control of heart rate with a decreased baroreflex gain, 21 small intermittent increases in blood pressure are not balanced by adequate decreases in heart rate and further increase heart work. high-fat diet.…”

Section: Ectopic Fat Storage In the Heartmentioning

confidence: 99%

Ectopic fat storage in heart, blood vessels and kidneys in the pathogenesis of cardiovascular diseases

et al. 2004

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In humans and most animal models, the development of obesity leads not only to increased fat depots in classical adipose tissue locations but also to significant lipid deposits within and around other tissues and organs, a phenomenon known as ectopic fat storage. The purpose of this review is to explore the possible locations of ectopic fat in key target-organs of cardiovascular control (heart, blood vessels and kidneys) and to propose how ectopic fat storage can play a role in the pathogenesis of cardiovascular diseases associated with obesity. In animals fed a high-fat diet, cardiac fat depots within and around the heart impair both systolic and diastolic functions, and may in the long-term promote heart failure. Accumulation of fat around blood vessels (perivascular fat) may affect vascular function in a paracrine manner, as perivascular fat cells secrete vascular relaxing factors, proatherogenic cytokines and smooth muscle cell growth factors. Furthermore, high amounts of perivascular fat could mechanically contribute to the increased vascular stiffness seen in obesity. Finally, accumulation of fat in the renal sinus may limit the outflow of blood and lymph from the kidney, which would alter intrarenal physical forces and promote sodium reabsorption and arterial hypertension. Taken together, ectopic fat storage in key target-organs of cardiovascular control may impair their functions, contributing to the increased prevalence of cardiovascular diseases in obese subjects.

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Reduced parasympathetic control of heart rate in obese dogs

Cited by 68 publications

References 0 publications

Role of sympathetic nervous system and neuropeptides in obesity hypertension

Role of sympathetic nervous system and neuropeptides in obesity hypertension

Independent Association Between Plasma Leptin Levels and Heart Rate in Heart Transplant Recipients

Ectopic fat storage in heart, blood vessels and kidneys in the pathogenesis of cardiovascular diseases

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