scholarly journals Sesame lignans increase sympathetic nerve activity and blood flow in rat skeletal muscles

2020 ◽  
pp. 253-260
Author(s):  
K. Egawa ◽  
Y. Horii ◽  
Y. Misonou ◽  
I. Yamasaki ◽  
D. Takemoto ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Autonomic Nerves ◽  
Nerve Activity ◽  
Beneficial Effects ◽  
Antioxidative Effects ◽  
Β2 Adrenergic Receptor ◽  
Sesame Lignans

Beneficial effects of sesame lignans, especially antioxidative effects, have been widely reported; however, its potential effects on autonomic nerves have not yet been investigated. Therefore, the current study aimed to investigate the effect of sesame lignans on the autonomic nervous system. The sympathetic nerve activity in rat skeletal muscle was measured using electrophysiological approaches, with blood flow determined using the laser Doppler method. Sesame lignans were administered intragastrically at 2 and 20 mg/kg, and after 60 min, the sympathetic nerve activity was observed to increase by 45.2 % and 66.1 %, respectively. A significant increase in blood flow (39.6 %) was also observed for the 20-mg/kg dose when measured at 55 min after administration. These sympathomimetic effects were completely prevented by subdiaphragmatic vagotomy, and the increase in blood flow was eliminated in the presence of the β2-adrenergic receptor inhibitor butoxamine. Thus, it is proposed that sesame lignans can increase the blood flow of skeletal muscle, possibly by exciting sympathetic nerve activity through the afferent vagal nerve.

Skeletal Muscle Vasculature and Systemic Hypoxia

Physiology ◽  
1995 ◽  
Vol 10 (6) ◽  
pp. 274-280
Author(s):  
JM Marshall
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Intravital Microscopy ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Blood Flow ◽  
Nerve Activity ◽  
Systemic Hypoxia

Studies involving recordings of gross muscle blood flow and intravital microscopy have been used to analyze the behavior of muscle vasculature during systemic hypoxia. The roles of sympathetic nerve activity, circulating hormones (e.g., catecholamines, angiotensin, vasopressin), and locally released adenosine and K+ in determining the behavior of arterial and venous vessels are considered.

Neural control of muscle blood flow during exercise

2004 ◽  
Vol 97 (2) ◽  
pp. 731-738 ◽  
Author(s):  
Gail D. Thomas ◽  
Steven S. Segal
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve ◽  
Neural Control ◽  
Sympathetic Nerve Activity ◽  
Muscle Blood Flow ◽  
Nerve Activity ◽  
Arterial Blood

Activation of skeletal muscle fibers by somatic nerves results in vasodilation and functional hyperemia. Sympathetic nerve activity is integral to vasoconstriction and the maintenance of arterial blood pressure. Thus the interaction between somatic and sympathetic neuroeffector pathways underlies blood flow control to skeletal muscle during exercise. Muscle blood flow increases in proportion to the intensity of activity despite concomitant increases in sympathetic neural discharge to the active muscles, indicating a reduced responsiveness to sympathetic activation. However, increased sympathetic nerve activity can restrict blood flow to active muscles to maintain arterial blood pressure. In this brief review, we highlight recent advances in our understanding of the neural control of the circulation in exercising muscle by focusing on two main topics: 1) the role of motor unit recruitment and muscle fiber activation in generating vasodilator signals and 2) the nature of interaction between sympathetic vasoconstriction and functional vasodilation that occurs throughout the resistance network. Understanding how these control systems interact to govern muscle blood flow during exercise leads to a clear set of specific aims for future research.

scholarly journals Attenuation of rapid onset vasodilation with advanced age : roles of adrenergic and endothelial signaling

2016 ◽  
Author(s):  
◽  
Shenghua Yuan Sinkler
Keyword(s):  
Physical Activity ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Blood Flow ◽  
Rapid Onset ◽  
Nerve Activity ◽  
Endothelium Dysfunction ◽  
Effects Of Aging

Rapid onset vasodilation (ROV) occurs immediately in response to skeletal muscle contraction and initiates a prompt increase in blood flow and oxygen delivery that facilitate the transition to exercise. Muscle blood flow is attenuated during aging which limits physical activity. Understanding the mechanisms that attenuate ROV requires invasive measurements that cannot be performed in human subjects. Published studies indicate that the effects of aging on muscle blood flow are similar in mice and in humans. Using our established mouse model to study the actual blood vessels that control blood flow in living skeletal muscle, the focus of my research is to understand where and how aging affects ROV in light of enhanced sympathetic nerve activity and endothelium dysfunction. A mouse was anesthetized and a skeletal muscle was prepared for studying individual microvessels using a microscope. The muscle was stimulated to contract with the amount and speed of vessel opening (vasodilation) recorded. I used selective interventions to modulate sympathetic or endothelial function and compared ROV for each vessel branch between Young (4 months) and Old (24 months) mice to resolve the effects of aging. I found that sympathetic activation attenuates ROV and that endothelium is integral to ROV. Thus, enhanced sympathetic nerve activity and endothelium dysfunction with aging attenuates ROV. These effects are greater effects in larger upstream vessels, which can restrict blood flow into active muscles. My research provides new insight for improving muscle blood flow, thereby promoting physical activity to improve the quality of life for aging individuals.

scholarly journals Effect of acute hypoxia on regional cerebral blood flow: effect of sympathetic nerve activity

2014 ◽  
Vol 116 (9) ◽  
pp. 1189-1196 ◽  
Author(s):  
Nia C. S. Lewis ◽  
Laura Messinger ◽  
Brad Monteleone ◽  
Philip N. Ainslie
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Sympathetic Nerve ◽  
Regional Difference ◽  
Sympathetic Nerve Activity ◽  
Acute Hypoxia ◽  
Adrenergic Blockade ◽  
Percentage Increase ◽  
Nerve Activity ◽  
Global Cerebral Blood Flow

We examined 1) whether global cerebral blood flow (CBF) would increase across a 6-h bout of normobaric poikilocapnic hypoxia and be mediated by a larger increase in blood flow in the vertebral artery (VA) than in the internal carotid artery (ICA); and 2) whether additional increases in global CBF would be evident following an α1-adrenergic blockade via further dilation of the ICA and VA. In 11 young normotensive individuals, ultrasound measures of ICA and VA flow were obtained in normoxia (baseline) and following 60, 210, and 330 min of hypoxia (FiO2 = 0.11). Ninety minutes prior to final assessment, participants received an α1-adrenoreceptor blocker (prazosin, 1 mg/20 kg body mass) or placebo. Compared with baseline, following 60, 220, and 330 min of hypoxia, global CBF [(ICAFlow + VAFlow) ∗ 2] increased by 160 ± 52 ml/min (+28%; P = 0.05), 134 ± 23 ml/min (+23%; P = 0.02), and 113 ± 51 (+19%; P = 0.27), respectively. Compared with baseline, ICAFlow increased by 23% following 60 min of hypoxia ( P = 0.06), after which it progressively declined. The percentage increase in VA flow was consistently larger than ICA flow during hypoxia by ∼20% ( P = 0.002). Compared with baseline, ICA and VA diameters increased during hypoxia by ∼9% and ∼12%, respectively ( P ≤ 0.05), and were correlated with reductions in SaO2. Flow and diameters were unaltered following α1 blockade ( P ≥ 0.10). In conclusion, elevations in global CBF during acute hypoxia are partly mediated via greater increases in VA flow compared with ICA flow; this regional difference was unaltered following α1 blockade, indicating that a heightened sympathetic nerve activity with hypoxia does not constrain further dilation of larger extracranial blood vessels.

scholarly journals Lumbar sympathetic nerve activity and hindquarter blood flow during REM sleep in rats

2004 ◽  
Vol 557 (1) ◽  
pp. 261-271 ◽  
Author(s):  
Kenju Miki ◽  
Michiyo Oda ◽  
Nozomi Kamijyo ◽  
Kazumi Kawahara ◽  
Misa Yoshimoto
Keyword(s):  
Blood Flow ◽  
Rem Sleep ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity

scholarly journals Bradykinin does not acutely sensitize the reflex pressor response during hindlimb skeletal muscle stretch in decerebrate rats

2017 ◽  
Vol 313 (4) ◽  
pp. R463-R472 ◽  
Author(s):  
Korynne S. Rollins ◽  
Joshua R. Smith ◽  
Peter J. Esau ◽  
Evan A. Kempf ◽  
Tyler D. Hopkins ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Femoral Artery ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Nerve Activity ◽  
Muscle Stretch ◽  
Renal Sympathetic Nerve Activity ◽  
Hindlimb Muscle

Hindlimb skeletal muscle stretch (i.e., selective activation of the muscle mechanoreflex) in decerebrate rats evokes reflex increases in blood pressure and sympathetic nerve activity. Bradykinin has been found to sensitize mechanogated channels through a bradykinin B2 receptor-dependent mechanism. Moreover, bradykinin B2 receptor expression on sensory neurons is increased following chronic femoral artery ligation in the rat (a model of simulated peripheral artery disease). We tested the hypothesis that injection of bradykinin into the arterial supply of a hindlimb in decerebrate, unanesthetized rats would acutely augment (i.e., sensitize) the increase in blood pressure and renal sympathetic nerve activity during hindlimb muscle stretch to a greater extent in rats with a ligated femoral artery than in rats with a freely perfused femoral artery. The pressor response during static hindlimb muscle stretch was compared before and after hindlimb arterial injection of 0.5 µg of bradykinin. Injection of bradykinin increased blood pressure to a greater extent in “ligated” ( n = 10) than “freely perfused” ( n = 10) rats. The increase in blood pressure during hindlimb muscle stretch, however, was not different before vs. after bradykinin injection in freely perfused (14 ± 2 and 15 ± 2 mmHg for pre- and post-bradykinin, respectively, P = 0.62) or ligated (15 ± 3 and 14 ± 2 mmHg for pre- and post-bradykinin, respectively, P = 0.80) rats. Likewise, the increase in renal sympathetic nerve activity during stretch was not different before vs. after bradykinin injection in either group of rats. We conclude that bradykinin did not acutely sensitize the pressor response during hindlimb skeletal muscle stretch in freely perfused or ligated decerebrate rats.

scholarly journals Impact of gender on benefits of exercise training on sympathetic nerve activity and muscle blood flow in heart failure

2009 ◽  
Vol 12 (1) ◽  
pp. 58-65 ◽  
Author(s):  
Ligia M. Antunes-Correa ◽  
Ruth C. Melo ◽  
Thais S. Nobre ◽  
Linda M. Ueno ◽  
Fabio G.M. Franco ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Exercise Training ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Blood Flow ◽  
Nerve Activity

Spectral characteristics of skin sympathetic nerve activity in heat-stressed humans

2006 ◽  
Vol 290 (4) ◽  
pp. H1601-H1609 ◽  
Author(s):  
Jian Cui ◽  
Mithra Sathishkumar ◽  
Thad E. Wilson ◽  
Manabu Shibasaki ◽  
Scott L. Davis ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Heat Stress ◽  
Skin Blood Flow ◽  
Sympathetic Nerve ◽  
High Frequency ◽  
Sympathetic Nerve Activity ◽  
Spectral Power ◽  
Spectral Characteristics ◽  
Nerve Activity

Skin sympathetic nerve activity (SSNA) exhibits low- and high-frequency spectral components in normothermic subjects. However, spectral characteristics of SSNA in heat-stressed subjects are unknown. Because the main components of the integrated SSNA during heat stress (sudomotor/vasodilator activities) are different from those during normothermia and cooling (vasoconstrictor activity), we hypothesize that spectral characteristics of SSNA in heat-stressed subjects will be different from those in subjects subjected to normothermia or cooling. In 17 healthy subjects, SSNA, electrocardiogram, arterial blood pressure (via Finapres), respiratory activity, and skin blood flow were recorded during normothermia and heat stress. In 7 of the 17 subjects, these variables were also recorded during cooling. Spectral characteristics of integrated SSNA, R-R interval, beat-by-beat mean blood pressure, skin blood flow variability, and respiratory excursions were assessed. Heat stress and cooling significantly increased total SSNA. SSNA spectral power in the low-frequency (0.03–0.15 Hz), high-frequency (0.15–0.45 Hz), and very-high-frequency (0.45–2.5 Hz) regions was significantly elevated by heat stress and cooling. Interestingly, heat stress caused a greater relative increase of SSNA spectral power within the 0.45- to 2.5-Hz region than in the other spectral ranges; cooling did not show this effect. Differences in the SSNA spectral distribution between normothermia/cooling and heat stress may reflect different characteristics of central modulation of vasoconstrictor and sudomotor/vasodilator activities.

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