Altered leptin signaling is sufficient, but not required,  for hypotension associated with caloric restriction

Swoap, Steven J.

doi:10.1152/ajpheart.2001.281.6.h2473

Cited by 44 publications

(51 citation statements)

References 33 publications

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“…In several studies BP was evaluated 48 h after surgery, a time-frame not sufficient for stabilizing BP and day/night circadian rhythm. In contrast to previous findings but more according to our data, Swoap reported slightly increased blood pressure in ob/ob mice with levels of 108±2 mmHg compared to 100±2 mmHg in controls [32]. In that study, BP was also measured by telemetry like in ours.…”

Section: Discussioncontrasting

confidence: 99%

Autonomic dysregulation in ob/ob mice is improved by inhibition of angiotensin-converting enzyme

et al. 2009

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The leptin deficient ob/ob mice are insulin resistant and obese. However, the control of blood pressure in this model is not well defined. The goal of this study was to evaluate the role of leptin and of the renin-angiotensin system in the cardiovascular abnormalities observed in obesity using a model lacking leptin. To this purpose, we measured blood pressure in ob/ob and control animals by radiotelemetry combined with fast Fourier transformation before and after both leptin and enalapril treatment. Autonomic function was assessed pharmacologically. Blood pressure during daytime was slightly higher in the ob/ob compared to control mice while no difference in heart rate was observed. Blood pressure response to trimetaphane and heart rate response to metoprolol were greater in ob/ob mice than in control littermates indicating an activated sympathetic nervous system. Heart rate response to atropine was attenuated. Baroreflex sensitivity and heart rate variability were blunted in ob/ob mice, while low frequency of systolic blood pressure variability was found increased. Chronic leptin replacement reduced blood pressure and reversed the impaired autonomic function observed in ob/ob mice. Inhibition of angiotensin converting enzyme by enalapril treatment had similar effects, prior to the loss of weight. These findings suggest that the renin-angiotensin system is involved in the autonomic dysfunction caused by the lack of leptin in ob/ob mice and support a role of this interplay in the pathogenesis of obesity, hypertension, and metabolic syndrome.

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Section: Discussioncontrasting

confidence: 99%

Autonomic dysregulation in ob/ob mice is improved by inhibition of angiotensin-converting enzyme

et al. 2009

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“…Seven mice were anesthetized initially with 5% isoflurane in an oxygen stream and maintained on 1-2% isoflurane. Mice were kept on a heating pad (38°C) throughout implantation of the blood pressure telemeter (PAC20; Data Sciences International) in the left common carotid artery (24). Implantation of the blood pressure telemeter into the abdominal aorta of seven rats (PAC40; Data Sciences International) was performed as described previously (24).…”

Section: Animalsmentioning

confidence: 99%

“…Mice were kept on a heating pad (38°C) throughout implantation of the blood pressure telemeter (PAC20; Data Sciences International) in the left common carotid artery (24). Implantation of the blood pressure telemeter into the abdominal aorta of seven rats (PAC40; Data Sciences International) was performed as described previously (24). Mice and rats were maintained on a heating pad for 48 h after the surgery and then housed individually at 30°C for 1 wk to allow time for recovery.…”

Section: Animalsmentioning

confidence: 99%

Effect of ambient temperature on cardiovascular parameters in rats and mice: a comparative approach

Swoap

Overton²,

Garber³

2004

American Journal of Physiology-Regulatory, Integrative and Comp

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111

109

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of Ͻ6°C or Ͼ29°C have been shown to induce large changes in arterial blood pressure and heart rate in homeotherms. The present study was designed to investigate whether small incremental changes in T a, such as those found in typical laboratory settings, would have an impact on blood pressure and other cardiovascular parameters in mice and rats. We predicted that small decreases in T a would impact the cardiovascular parameters of mice more than rats due to the increased thermogenic demands resulting from a greater surface area-to-volume ratio in mice relative to rats. Cardiovascular parameters were measured with radiotelemetry in mice and rats that were housed in temperaturecontrolled environments. The animals were exposed to different T a every 72 h, beginning at 30°C and incrementally decreasing by 4°C at each time interval to 18°C and then incrementally increasing back up to 30°C. As T a decreased, mean blood pressure, heart rate, and pulse pressure increased significantly for both mice (1.6 mmHg/°C, 14.4 beats ⅐ min Ϫ1 ⅐°C Ϫ1 , and 0.8 mmHg/°C, respectively) and rats (1.2 mmHg/°C, 8.1 beats ⅐ min Ϫ1 ⅐°C Ϫ1 , and 0.8 mmHg/°C, respectively). Thus small changes in T a significantly impact the cardiovascular parameters of both rats and mice, with mice demonstrating a greater sensitivity to these Ta changes. blood pressure; heart rate; standard deviation of the interbeat interval; radiotelemetry THE EXTERNAL ENVIRONMENT can have a substantial impact on the cardiovascular system. Exposure of humans (1,7,18,32), rats (2,3,14,20), and mice (22) to cold ambient temperature (T a ) results in elevated blood pressure and heart rate. It appears as if the tachycardia and hypertension are the indirect result of sympathetic nervous system (SNS) activation of thermoregulatory mechanisms because elevated plasma norepinephrine (NE) levels correlate with elevated blood pressure in the cold (7,14,17,32). Furthermore, propranolol, a ␤-adrenergic blocking agent, can blunt or completely reverse the cardiovascular effects of cold exposure (21). Cold-induced activation of the SNS, in turn, appears to elevate blood pressure through activation of the renin-angiotensin system (RAS). Blockade of the RAS systemically (19), centrally (15,16,22), or genetically in an angiotensinogen knockout mouse model (23) blunts or prevents cold-induced hypertension, suggesting that RAS signaling pathways are necessary for T a -induced effects on blood pressure.Elevation of T a beyond typical housing temperatures also impacts the cardiovascular system. Warming rats (31) and mice (30, 31) from 23°C to 28 -31°C, closer to, if not within, their thermoneutral zone (TNZ) results in a drop in heart rate and blood pressure. Metabolic rate in homeotherms is at its minimum in the TNZ, which is approximately 28 -31°C for rodents (4). Animals with smaller body sizes have higher surface area-to-volume ratios and thus typically exhibit warmer TNZs. At temperatures below the TNZ, nonshivering thermogenesis is stimulated by increased sympathetic activity to offset the...

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“…Studies in rat kidneys have shown that the brush border membranes of CR animals had decreased content of several phospholipids (phosphatidylserine, phosphatidylcholine, phosphatidylethanolamine, and sphingomyelin) and cholesterol (44). In addition to modulating renal lipid metabolism, other mechanisms may be involved in CR effects on age-related renal disease, such as modulating BP, which definitely plays an important role in the progression of renal disease (45)(46)(47)(48).…”

Section: Role Of Altered Lipid Metabolism In Renal Diseasementioning

confidence: 99%

Calorie Restriction Modulates Renal Expression of Sterol Regulatory Element Binding Proteins, Lipid Accumulation, and Age-Related Renal Disease

Jiang¹,

Liebman²,

Lucia³

et al. 2005

Journal of the American Society of Nephrology

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Sterol regulatory element binding proteins (SREBP) are major regulators of fatty acid and cholesterol synthesis. This study found that age-related renal matrix deposition and proteinuria were associated with increased renal expression of SREBP-1 and SREBP-2 and increased renal accumulation of triglyceride and cholesterol. Because calorie restriction (CR) modulates age-related renal disease, it then was determined whether the effects of CR are mediated partially by modulation of renal lipid metabolism. Compared with ad libitum (AL)-fed 24-month-old (24m) F344BN rats, CR resulted in significant decreases in extracellular matrix accumulation (periodic acid-Schiff staining and immunofluorescence of type IV collagen and fibronectin) and proteinuria. A significant decrease was also observed in the renal expression of growth factors (connective tissue growth factor and vascular endothelial growth factor) and matrix metalloproteinase inhibitor (plasminogen activator inhibitor-1). These structural and functional changes were associated with significant decreases in renal nuclear SREBP-1 (5.2 in 24m AL versus 3.3 densitometry units in 24m CR; P < 0.01) and SREBP-2 (7.1 in 24m AL versus 4.1 densitometry units in 24m CR; P < 0.01) protein abundance and renal triglyceride and cholesterol contents. It is interesting that serum leptin level was significantly increased as a function of aging, and CR resulted in significant reduction in serum leptin level. Because it was shown previously that increased renal expression of SREBP-1a per se caused renal lipid accumulation, glomerulosclerosis, and proteinuria, the results suggest that CR modulates age-related renal disease in part by modulation of renal SREBP expression and renal lipid accumulation.

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Altered leptin signaling is sufficient, but not required, for hypotension associated with caloric restriction

Cited by 44 publications

References 33 publications

Autonomic dysregulation in ob/ob mice is improved by inhibition of angiotensin-converting enzyme

Autonomic dysregulation in ob/ob mice is improved by inhibition of angiotensin-converting enzyme

Effect of ambient temperature on cardiovascular parameters in rats and mice: a comparative approach

Calorie Restriction Modulates Renal Expression of Sterol Regulatory Element Binding Proteins, Lipid Accumulation, and Age-Related Renal Disease

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