Central effects of leptin on cardiovascular and  neurohormonal responses in conscious rabbits

Matsumura, Kiyoshi; Abe, Isao; Tsuchihashi, Takuya; Fujishima, Masatoshi

doi:10.1152/ajpregu.2000.278.5.r1314

Cited by 73 publications

(73 citation statements)

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“…24 On the other hand, these neuropeptides involved in feeding behavior have been suggested to participate in central cardiovascular and sympathetic regulations. 16,17,[32][33][34] ICV administration of leptin activates sympathetic nervous system, resulting in an increase in arterial pressure. 33,34 In contrast, in the present study, ICV administration of ghrelin suppressed the sympathetic nervous system, resulting in a decrease in arterial pressure.…”

Section: Parameters and Maximum Gain Of Baroreflex Control Of Rsna Anmentioning

confidence: 99%

“…16,17,[32][33][34] ICV administration of leptin activates sympathetic nervous system, resulting in an increase in arterial pressure. 33,34 In contrast, in the present study, ICV administration of ghrelin suppressed the sympathetic nervous system, resulting in a decrease in arterial pressure. Based on these findings, leptin and ghrelin may interact with each other and play roles in central cardiovascular and sympathetic regulations and in food intake and energy expenditure.…”

Section: Parameters and Maximum Gain Of Baroreflex Control Of Rsna Anmentioning

confidence: 99%

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Central Ghrelin Modulates Sympathetic Activity in Conscious Rabbits

et al. 2002

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Abstract-Ghrelin is an orexigenic peptide originally isolated from the stomach. Intravenous administration of ghrelin has been shown to elicit a decrease in arterial pressure without a significant change in heart rate (HR), suggesting that ghrelin may act on the central nervous system to modulate sympathetic activity. The aim of the present study was to determine the central effects of ghrelin on cardiovascular and sympathetic responses in conscious rabbits. Key Words: baroreceptors Ⅲ blood pressure Ⅲ central nervous system Ⅲ ghrelin Ⅲ nervous system, sympathetic renal G hrelin, an acylated 28-residue peptide originally isolated from the rat stomach, is an endogenous ligand for the growth hormone (GH) secretagogue receptor. 1,2 Although ghrelin is likely to regulate pituitary GH secretion along with GH-releasing hormone and somatostatin, 2,3 GH secretagogue receptors have also been identified in hypothalamic neurons and in the brainstem. 4,5 Intracerebroventricular (ICV) administration of ghrelin has been shown to generate a dose-dependent increase in food intake and body weight, 6,7 suggesting that ghrelin participates in the regulation of food intake and GH secretion. Furthermore, ICV administration of ghrelin has been shown to increase plasma vasopressin level without a significant change in arterial pressure in conscious rats. 8 It has also been reported that intravenous injection of human ghrelin elicits a decrease in blood pressure without an increase in heart rate (HR) in healthy men. 9 In addition, plasma ghrelin concentration is increased in patients with cachexia associated with chronic heart failure. 10 These previous findings suggest that ghrelin may participate not only in feeding behavior but also in cardiovascular and sympathetic regulation. Although ghrelin has been reported to have a vasodilatory effect in humans, 11 the underlying mechanisms of depressor response induced by intravenous injection of ghrelin have not yet been determined. Because the depressor response was not accompanied by tachycardia, it is likely that mechanisms other than direct vasodilating effects, at least in part, are involved in this depressor response. To clarify the mechanisms for this depressor response, the effects of ghrelin on sympathetic activity and on the baroreceptor reflex should be determined. We hypothesized that intravenous administration of ghrelin acts at the central nervous system to modulate the sympathetic nervous system, resulting in a decrease in arterial pressure without tachycardia. Accordingly, in the present study, we focused on the central effect of ghrelin on sympathetic activity and baroreceptor reflex. To evaluate the sympathetic nervous system precisely, the present study was conducted on conscious rabbits with direct recording of renal sympathetic nerve activity (RSNA), because the sympathetic nervous system and baroreceptor reflex are greatly affected by anesthesia. 12,13

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Section: Parameters and Maximum Gain Of Baroreflex Control Of Rsna Anmentioning

confidence: 99%

Section: Parameters and Maximum Gain Of Baroreflex Control Of Rsna Anmentioning

confidence: 99%

Central Ghrelin Modulates Sympathetic Activity in Conscious Rabbits

et al. 2002

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“…[12][13][14] The following experiments were performed on conscious rabbits. On the day of the experiment, catheters were inserted into the ear artery and vein of each animal, which had been given 1% lidocaine local anesthesia.…”

Section: Preparation Of Animalsmentioning

confidence: 99%

“…RSNA was recorded and analyzed as described previously. [12][13][14] Experiments were started at 9:00 AM and finished before 2:00 PM. All drugs for ICV injection were dissolved in artificial cerebrospinal fluid (aCSF).…”

Section: Preparation Of Animalsmentioning

confidence: 99%

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Central Human Cocaine- and Amphetamine-Regulated Transcript Peptide 55–102 Increases Arterial Pressure in Conscious Rabbits

2001

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Abstract-We determined cardiovascular and neurohormonal responses to intracerebroventricular administration of human cocaine-and amphetamine-regulated transcript (CART) peptide 55᎑102 in conscious rabbits. Intracerebroventricular injection of CART 55᎑102 elicited dose-related increases in mean arterial pressure and renal sympathetic nerve activity. Key Words: peptides Ⅲ catecholamines Ⅲ central nervous system Ⅲ glucose Ⅲ renal sympathetic nerve activity A ppetite and feeding behavior are regulated by many neuropeptides, such as neuropeptide Y, corticotrophinreleasing factor, ␣-melanocyte stimulating hormone, and melanin-concentrating hormone. 1,2 Cocaine-and amphetamine-regulated transcript (CART) was originally described as mRNA induced in rat striatum after acute administration of cocaine or amphetamine. 3 At least 6 CART proteins and peptides have been identified in rodents and humans, and some have been purified and sequenced. 4,5 CART peptides have been found in brain areas known to be involved in physiological control of feeding behavior. 4,5 Moreover, intracerebroventricular (ICV) administration of CART peptide fragment 55᎑86, other fragments (54᎑102, 55᎑102, 61᎑102, and 62᎑102), and recombinant CART peptide 55᎑102 cause dose-dependent inhibition of food intake in mice or rats, 6,7 which suggests that these peptides participate in regulation of food intake and feeding behaviors. Amino acid sequences of CART peptides in rat and human are similar, and 95% identity exists between them. 4,5 In the C-terminal region of peptide (55᎑102), a difference of only 1 amino acid exists: a Val3 Ile substitution at position 55. 4,5 CART-immunoreactive cells have been shown to be present not only in hypothalamic nuclei, but also in the medulla, particularly in the nucleus of the solitary tract and area postrema 8 ; these regions of the medulla constitute one of the most important cardiovascular centers of the brain. In addition, ICV administration of CART has been shown to cause increases in plasma corticosterone, oxytocin, and glucose concentrations. 9 We anticipated that CART peptides would be found to participate in cardiovascular and neuroendocrine regulations in addition to feeding behavior in the brain, and we hypothesized that central administration of CART peptides would modulate the hypothalamic-pituitary adrenal axis and change arterial pressure. Accordingly, the present study was designed to investigate the central effects of CART peptides on blood pressure, sympathetic nervous system, and blood variables, including plasma catecholamines, vasopressin, insulin, cortisol, and glucose concentrations. Experiments were conducted in conscious rabbits and included a direct recording of renal sympathetic nerve activity (RSNA), because sympathetic nerve activity or the baroreceptor reflex is strongly influenced by anesthesia. 10,11

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Leptin: A Metabolic Perspective

Penn

Rooks

Harris

2007

Handbook of Contemporary Neuropharmacology

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The history of discovery of leptin is given and current knowledge on the factors that regulate ob gene expression and leptin protein secretion is summarized. The chapter focuses on the metabolic effects of leptin, the pathways involved in the suppression of food intake and stimulation of energy expenditure are described. The role of central activation of sympathetic outflow to peripheral tissues, compared with direct effects of leptin on insulin‐sensitive tissues, in mediating metabolic responses to leptin is discussed. Recent work elucidating the cellular basis for the shift in metabolism of adipose and non‐adipose tissue to lipid oxidation and triglyceride depletion is reviewed.

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Central effects of leptin on cardiovascular and neurohormonal responses in conscious rabbits

Cited by 73 publications

References 32 publications

Central Ghrelin Modulates Sympathetic Activity in Conscious Rabbits

Central Ghrelin Modulates Sympathetic Activity in Conscious Rabbits

Central Human Cocaine- and Amphetamine-Regulated Transcript Peptide 55–102 Increases Arterial Pressure in Conscious Rabbits

Leptin: A Metabolic Perspective

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