Limits...
Leptin into the rostral ventral lateral medulla (RVLM) augments renal sympathetic nerve activity and blood pressure.

Barnes MJ, McDougal DH - Front Neurosci (2014)

Bottom Line: While this hormone normally acts to reduce feeding behavior and increase energy expenditure, in obesity, resistance to these effects occurs even though the hormone is released in large amounts.Sympathetic control of blood pressure is maintained principally by autonomic reflex control circuits in the caudal brainstem.The rostral ventral-lateral medulla (RVLM) is the primary regulator of the sympathetic nervous system, sending excitatory fibers to sympathetic preganglionic neurons to regulate sympathetic control over resistance vessels and blood pressure.

View Article: PubMed Central - PubMed

Affiliation: Nutrition and Neural Signaling Laboratory, Pennington Biomedical Research Center Baton Rouge, LA, USA.

ABSTRACT
Leptin is a hormone released from adipose tissue. While this hormone normally acts to reduce feeding behavior and increase energy expenditure, in obesity, resistance to these effects occurs even though the hormone is released in large amounts. Although leptin no longer works to suppress feeding in the obese, leptin retains its potent effects on other autonomic functions such as blood pressure regulation. Leptin has been associated with hypertension and increased sympathetic autonomic activity. Therefore, leptin is emerging as a major contributor to the hypertensive state observed in obesity. Sympathetic control of blood pressure is maintained principally by autonomic reflex control circuits in the caudal brainstem. The rostral ventral-lateral medulla (RVLM) is the primary regulator of the sympathetic nervous system, sending excitatory fibers to sympathetic preganglionic neurons to regulate sympathetic control over resistance vessels and blood pressure. Previous studies from our laboratory have shown that neurons in the ventral lateral medulla express leptin receptors (ObRb). Our present study using pseudo-rabies multi-synaptic retrograde tract tracing and immunohistochemical methods revealed that neurons within the RVLM that send sympathetic projections to the kidney express leptin receptors. Acute microinjection of leptin (1 and 3 μg; 40 nL) into the RVLM evoked a significant increase in Mean Arterial Pressure (MAP) and renal sympathetic nerve activity (RSNA). When the 3 μg dose of leptin was preceded with a leptin antagonist, (SLAN-4; 1 ng), it attenuated the cardiovascular response of leptin. Taken together, these data suggest that leptin's actions within the RVLM may influence blood pressure and renal sympathetic nerve activity.

No MeSH data available.


Related in: MedlinePlus

Nano-injection of leptin into the RVLM increased MAP and RSNA. Nano-injection of leptin (1 and 3 μg; 40 nL) into the RVLM increased MAP (A). Analysis of percent change in MAP was conducted with One-Way ANOVA which compared the MAP at 12 min following injection between each experimental condition (B). Peak response of leptin (1 and 3 μg) was 8.9 ± 2.9% and 7.6 ± 2.1% respectively. The MAP response to these treatments was significantly different from saline (−1.6 ± 1.6%) and leptin (0.3 μg) (−2.4 ± 1.0%). Leptin (1 and 3 μg) increased RSNA (C) 49 and 34%, respectively. (Bonferroni t-tests; *p < 0.05); arrows indicate time of first (−15 min) and second (0 min) injection. Analysis of percent change following the first inject was not statistically different from values obtained prior to the first injection.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4125949&req=5

Figure 4: Nano-injection of leptin into the RVLM increased MAP and RSNA. Nano-injection of leptin (1 and 3 μg; 40 nL) into the RVLM increased MAP (A). Analysis of percent change in MAP was conducted with One-Way ANOVA which compared the MAP at 12 min following injection between each experimental condition (B). Peak response of leptin (1 and 3 μg) was 8.9 ± 2.9% and 7.6 ± 2.1% respectively. The MAP response to these treatments was significantly different from saline (−1.6 ± 1.6%) and leptin (0.3 μg) (−2.4 ± 1.0%). Leptin (1 and 3 μg) increased RSNA (C) 49 and 34%, respectively. (Bonferroni t-tests; *p < 0.05); arrows indicate time of first (−15 min) and second (0 min) injection. Analysis of percent change following the first inject was not statistically different from values obtained prior to the first injection.

Mentions: Long Evan rats received one of three doses of leptin into the RVLM to observe the effect on MAP and RSNA (Figure 4). Figure 4A displays the percent change in MAP over time in response to saline, 0.3, 1, or 3 μg of leptin injected into the RVLM. Analysis of percent change in MAP was conducted with one-way ANOVA which compared the MAP at 12 min following injection between each experimental condition (Figure 4B). In response to leptin (1 and 3 μg) MAP increased 8.3 ± 2.9% and 7.6 ± 2.1% respectively. The MAP response to these treatments was significantly different from saline (−1.7 ± 1.6%) and leptin (0.3 μg) (−2.4 ± 1.0%) [F(3, 14) = 8.019; p < 0.05]. One-way analysis of MAP prior to and following the first injection (saline) was not statistically different (data not shown).


Leptin into the rostral ventral lateral medulla (RVLM) augments renal sympathetic nerve activity and blood pressure.

Barnes MJ, McDougal DH - Front Neurosci (2014)

Nano-injection of leptin into the RVLM increased MAP and RSNA. Nano-injection of leptin (1 and 3 μg; 40 nL) into the RVLM increased MAP (A). Analysis of percent change in MAP was conducted with One-Way ANOVA which compared the MAP at 12 min following injection between each experimental condition (B). Peak response of leptin (1 and 3 μg) was 8.9 ± 2.9% and 7.6 ± 2.1% respectively. The MAP response to these treatments was significantly different from saline (−1.6 ± 1.6%) and leptin (0.3 μg) (−2.4 ± 1.0%). Leptin (1 and 3 μg) increased RSNA (C) 49 and 34%, respectively. (Bonferroni t-tests; *p < 0.05); arrows indicate time of first (−15 min) and second (0 min) injection. Analysis of percent change following the first inject was not statistically different from values obtained prior to the first injection.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4125949&req=5

Figure 4: Nano-injection of leptin into the RVLM increased MAP and RSNA. Nano-injection of leptin (1 and 3 μg; 40 nL) into the RVLM increased MAP (A). Analysis of percent change in MAP was conducted with One-Way ANOVA which compared the MAP at 12 min following injection between each experimental condition (B). Peak response of leptin (1 and 3 μg) was 8.9 ± 2.9% and 7.6 ± 2.1% respectively. The MAP response to these treatments was significantly different from saline (−1.6 ± 1.6%) and leptin (0.3 μg) (−2.4 ± 1.0%). Leptin (1 and 3 μg) increased RSNA (C) 49 and 34%, respectively. (Bonferroni t-tests; *p < 0.05); arrows indicate time of first (−15 min) and second (0 min) injection. Analysis of percent change following the first inject was not statistically different from values obtained prior to the first injection.
Mentions: Long Evan rats received one of three doses of leptin into the RVLM to observe the effect on MAP and RSNA (Figure 4). Figure 4A displays the percent change in MAP over time in response to saline, 0.3, 1, or 3 μg of leptin injected into the RVLM. Analysis of percent change in MAP was conducted with one-way ANOVA which compared the MAP at 12 min following injection between each experimental condition (Figure 4B). In response to leptin (1 and 3 μg) MAP increased 8.3 ± 2.9% and 7.6 ± 2.1% respectively. The MAP response to these treatments was significantly different from saline (−1.7 ± 1.6%) and leptin (0.3 μg) (−2.4 ± 1.0%) [F(3, 14) = 8.019; p < 0.05]. One-way analysis of MAP prior to and following the first injection (saline) was not statistically different (data not shown).

Bottom Line: While this hormone normally acts to reduce feeding behavior and increase energy expenditure, in obesity, resistance to these effects occurs even though the hormone is released in large amounts.Sympathetic control of blood pressure is maintained principally by autonomic reflex control circuits in the caudal brainstem.The rostral ventral-lateral medulla (RVLM) is the primary regulator of the sympathetic nervous system, sending excitatory fibers to sympathetic preganglionic neurons to regulate sympathetic control over resistance vessels and blood pressure.

View Article: PubMed Central - PubMed

Affiliation: Nutrition and Neural Signaling Laboratory, Pennington Biomedical Research Center Baton Rouge, LA, USA.

ABSTRACT
Leptin is a hormone released from adipose tissue. While this hormone normally acts to reduce feeding behavior and increase energy expenditure, in obesity, resistance to these effects occurs even though the hormone is released in large amounts. Although leptin no longer works to suppress feeding in the obese, leptin retains its potent effects on other autonomic functions such as blood pressure regulation. Leptin has been associated with hypertension and increased sympathetic autonomic activity. Therefore, leptin is emerging as a major contributor to the hypertensive state observed in obesity. Sympathetic control of blood pressure is maintained principally by autonomic reflex control circuits in the caudal brainstem. The rostral ventral-lateral medulla (RVLM) is the primary regulator of the sympathetic nervous system, sending excitatory fibers to sympathetic preganglionic neurons to regulate sympathetic control over resistance vessels and blood pressure. Previous studies from our laboratory have shown that neurons in the ventral lateral medulla express leptin receptors (ObRb). Our present study using pseudo-rabies multi-synaptic retrograde tract tracing and immunohistochemical methods revealed that neurons within the RVLM that send sympathetic projections to the kidney express leptin receptors. Acute microinjection of leptin (1 and 3 μg; 40 nL) into the RVLM evoked a significant increase in Mean Arterial Pressure (MAP) and renal sympathetic nerve activity (RSNA). When the 3 μg dose of leptin was preceded with a leptin antagonist, (SLAN-4; 1 ng), it attenuated the cardiovascular response of leptin. Taken together, these data suggest that leptin's actions within the RVLM may influence blood pressure and renal sympathetic nerve activity.

No MeSH data available.


Related in: MedlinePlus