Endogenous leptin contributes to baroreflex suppression within the solitary tract nucleus of aged rats

Arnold, Amy C.; Diz, Debra I.

doi:10.1152/ajpheart.00282.2014

Cited by 11 publications

(8 citation statements)

References 47 publications

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“…Baseline BRS in older SD rats was impaired to a similar level relative to young SD rats, as previously reported (13, 15). Microinjection of SR141716A (36 pmol) into the NTS significantly improved BRS by approximately 89%, from a baseline of 0.56 ± 0.06 ms/mmHg to 1.06 ± 0.05 ms/mmHg (P < 0.05; Figure 1A and 1B), in aged SD rats after 60 minutes.…”

Section: Resultssupporting

confidence: 89%

“…As described previously (13, 15), aged SD rats (60– to 69-weeks-old; mean age = 64 ± 1 weeks; n = 4) were anesthetized with combination urethane-chloralose (750 and 35 mg/kg, respectively) via intraperitoneal injections with supplemental doses given intravenously as needed (diluted to 3:7 with saline). Polyethylene catheters (Clay Adams) were inserted into the femoral artery and vein, with the venous catheter positioned near the right atrium.…”

Section: Methodsmentioning

confidence: 99%

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Alterations in the Medullary Endocannabinoid System Contribute to Age-related Impairment of Baroreflex Sensitivity

Schaich

Shaltout

Grabenauer

et al. 2015

Journal of Cardiovascular Pharmacology

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As they age, Sprague-Dawley (SD) rats develop elevated systolic blood pressure associated with impaired baroreflex sensitivity (BRS) for control of heart rate. We previously demonstrated in young hypertensive (mRen2)27 rats that impaired BRS is restored by CB1 cannabinoid receptor blockade in the solitary tract nucleus (NTS), consistent with elevated content of the endocannabinoid 2-arachidonoylglycerol (2-AG) in dorsal medulla relative to normotensive SD rats. There is no effect of CB1 receptor blockade in young SD rats. We now report in older SD rats that dorsal medullary 2-AG levels are two-fold higher at 70 versus 15 weeks of age (4.22 ± 0.61 vs. 1.93 ± 0.22 ng/mg tissue; P < 0.05). Furthermore, relative expression of CB1 receptor mRNA is significantly lower in aged rats, while CB2 receptor mRNA is significantly higher. In contrast to young adult SD rats, microinjection of the CB1 receptor antagonist SR141716A (36 pmol) into the NTS of older SD rats normalized BRS in animals exhibiting impaired baseline BRS (0.56 ± 0.06 baseline vs. 1.06 ± 0.05 ms/mmHg after 60 min; P < 0.05). Therefore, this study provides evidence for alterations in the endocannabinoid system within the NTS of older SD rats that contribute to age-related impairment of BRS.

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Section: Resultssupporting

confidence: 89%

Section: Methodsmentioning

confidence: 99%

Alterations in the Medullary Endocannabinoid System Contribute to Age-related Impairment of Baroreflex Sensitivity

Schaich

Shaltout

Grabenauer

et al. 2015

Journal of Cardiovascular Pharmacology

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“…The hypothalamic arcuate nucleus (ARC) was initially considered the main site of leptin actions in modulating energy balance and sympathetic activity; however, increasing evidence suggests that leptin may also act on a more extensive brain network that includes hindbrain areas such as the NTS and the ventral surface of the medulla (Grill et al . ; Ciriello & Moreau, ; Barnes & McDougal, ; Arnold & Diz, ; Ciriello & Caverson, ; Bassi et al . a ).…”

Section: Introductionmentioning

confidence: 99%

“…In addition, leptin in the NTS attenuated the arterial baroreflex response (Arnold et al . ; Arnold & Diz, ) and enhanced basal respiration activity (Inyushkin et al . ; Inyushkina et al .…”

Section: Introductionmentioning

confidence: 99%

Facilitation of breathing by leptin effects in the central nervous system

Bassi

Furuya

Zoccal

et al. 2015

The Journal of Physiology

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With the global epidemic of obesity, breathing disorders associated with excess body weight have markedly increased. Respiratory dysfunctions caused by obesity were originally attributed to mechanical factors; however, recent studies have suggested a pathophysiological component that involves the central nervous system (CNS) and hormones such as leptin produced by adipocytes as well as other cells. Leptin is suggested to stimulate breathing and leptin deficiency causes an impairment of the chemoreflex, which can be reverted by leptin therapy. This facilitation of the chemoreflex may depend on the action of leptin in the hindbrain areas involved in the respiratory control such as the nucleus of the solitary tract (NTS), a site that receives chemosensory afferents, and the ventral surface of the medulla that includes the retrotrapezoid nucleus (RTN), a central chemosensitive area, and the rostral ventrolateral medulla (RVLM). Although the mechanisms and pathways activated by leptin to facilitate breathing are still not completely clear, evidence suggests that the facilitatory effects of leptin on breathing require the brain melanocortin system, including the POMC–MC4R pathway, a mechanism also activated by leptin to modulate blood pressure. The results of all the studies that have investigated the effect of leptin on breathing suggest that disruption of leptin signalling as caused by obesity‐induced reduction of central leptin function (leptin resistance) is a relevant mechanism that may contribute to respiratory dysfunctions associated with obesity.

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“…Therefore, it is of importance to note that the increase in heart rate in obesity is a function of the reduction of the parasympathetic function of the heart. A report has suggested that during aging, endogenously produced leptin contributed to reduce the BRS (Arnold et al 2014). The chief determining factor for reduced BRS was due to the dominant role of sympathetic activity over parasympathetic.…”

Section: Baroreflex Sensitivitymentioning

confidence: 99%

The Role of Leptin in Obesity-Induced Hypertension

Miraaj-Raza¹

2016

TIJMD

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Obesity is linked with the growth of white adipose tissue and associated chronic hyperleptinemia. Leptin is a hormone-like cytokine or adipokine secreted mainly from adipose tissue. High leptin state in obesity rapidly causes selective resistance, focused in the arcuate nucleus of the hypothalamus, and centered round leptin's role in food intake and satiety. This resistance lowers the body's reaction to food intake and prevents the anorexigenic effects of leptin. As this resistance builds up, the intake of food increases causing an enhancement in body adiposity and leptin levels. However, some pathways do not build resistance to leptin and continue to exhibit the stimulatory effects, which cause a persistent stimulation of sympathetic nervous system (SNS), particularly in the kidneys and skeletal muscles. The increase in SNS activity in the kidney, along with the endothelial dysfunction and oxidative stress, lead to an increase in blood pressure. Apart from leptin's effects on SNS and renal function, this adipokine influences vascular health and hypertension through several phenomena or mechanisms such as baroreflex sensitivity, release of nitric oxide and cardiac hormones. In this review, an attempt has been made to highlight different aspects of leptin biology, which are relevant to hypertension.

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Endogenous leptin contributes to baroreflex suppression within the solitary tract nucleus of aged rats

Cited by 11 publications

References 47 publications

Alterations in the Medullary Endocannabinoid System Contribute to Age-related Impairment of Baroreflex Sensitivity

Alterations in the Medullary Endocannabinoid System Contribute to Age-related Impairment of Baroreflex Sensitivity

Facilitation of breathing by leptin effects in the central nervous system

The Role of Leptin in Obesity-Induced Hypertension

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