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

Relationship between renal sympathetic nerve activity and renal blood flow during natural behavior in rats

2004 ◽  
Vol 286 (5) ◽  
pp. R881-R887 ◽  
Author(s):  
Misa Yoshimoto ◽  
Tamaki Sakagami ◽  
Satsuki Nagura ◽  
Kenju Miki
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Rem Sleep ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nrem Sleep ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Behavioral Activities ◽  
Renal Sympathetic

The purpose of the present study was to determine the relationship between renal sympathetic nerve activity (RSNA) and renal blood flow (RBF) during normal daily activity in conscious, chronically instrumented Wistar rats ( n = 8). The animal's behavior was classified as rapid eye movement (REM) sleep, non-REM (NREM) sleep, quiet awake, moving, and grooming states. On average RSNA was lowest during REM sleep, which was decreased by 39.0 ± 3.2% ( P < 0.05) relative to NREM sleep, and rose linearly with an increase in activity level in the order of quiet awake (by 10.9 ± 1.8%, P < 0.05), moving (by 29.4 ± 2.9%, P < 0.05), and grooming (by 65.3 ± 3.9%, P < 0.05) relative to NREM sleep. By contrast, RBF was highest during REM sleep, which was increased by 4.8 ± 0.7% ( P < 0.05) relative to NREM sleep and decreased significantly ( P < 0.05) by 5.5 ± 0.6 and 6.6 ± 0.5% during moving and grooming states, respectively, relative to NREM sleep. There was a significant ( P < 0.05) inverse linear relationship between the percent changes in RSNA and RBF and between those in RSNA and renal vascular conductance. Furthermore, renal denervation ( n = 8) abolished the changes in RBF induced by different natural behavioral activities. These results suggest that the changes in RSNA induced by natural behavioral activities had a significant influence on RBF.

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.

Cerebral sympathetic nerve activity has a major regulatory role in the cerebral circulation in REM sleep

2009 ◽  
Vol 106 (4) ◽  
pp. 1050-1056 ◽  
Author(s):  
Priscila A. Cassaglia ◽  
Robert I. Griffiths ◽  
Adrian M. Walker
Keyword(s):  
Arterial Pressure ◽  
Blood Vessels ◽  
Rem Sleep ◽  
Sympathetic Nerve ◽  
Cerebral Circulation ◽  
Sympathetic Nerve Activity ◽  
Nrem Sleep ◽  
Protective Mechanism ◽  
Nerve Activity ◽  
Phasic Rem Sleep

Sympathetic nerve activity (SNA) in neurons projecting to skeletal muscle blood vessels increases during rapid-eye-movement (REM) sleep, substantially exceeding SNA of non-REM (NREM) sleep and quiet wakefulness (QW). Similar SNA increases to cerebral blood vessels may regulate the cerebral circulation in REM sleep, but this is unknown. We hypothesized that cerebral SNA increases during phasic REM sleep, constricting cerebral vessels as a protective mechanism against cerebral hyperperfusion during the large arterial pressure surges that characterize this sleep state. We tested this hypothesis using a newly developed model to continuously record SNA in the superior cervical ganglion (SCG) before, during, and after arterial pressure surges occurring during REM in spontaneously sleeping lambs. Arterial pressure (AP), intracranial pressure (ICP), cerebral blood flow (CBF), cerebral vascular resistance [CVR = (AP − ICP)/CBF], and SNA from the SCG were recorded in lambs ( n = 5) undergoing spontaneous sleep-wake cycles. In REM sleep, CBF was greatest (REM > QW = NREM, P < 0.05) and CVR was least (REM < QW = NREM, P < 0.05). SNA in the SCG did not change from QW to NREM sleep but increased during tonic REM sleep, with a further increase during phasic REM sleep (phasic REM > tonic REM > QW = NREM, P < 0.05). Coherent averaging revealed that SNA increases preceded AP surges in phasic REM sleep by 12 s ( P < 0.05). We report the first recordings of cerebral SNA during natural sleep-wake cycles. SNA increases markedly during tonic REM sleep, and further in phasic REM sleep. As SNA increases precede AP surges, they may serve to protect the brain against potentially damaging intravascular pressure changes or hyperperfusion in REM sleep.

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.

scholarly journals Selective α1-adrenergic blockade disturbs the regional distribution of cerebral blood flow during static handgrip exercise

2016 ◽  
Vol 310 (11) ◽  
pp. H1541-H1548 ◽  
Author(s):  
Igor A. Fernandes ◽  
João D. Mattos ◽  
Monique O. Campos ◽  
Alessandro C. Machado ◽  
Marcos P. Rocha ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Sympathetic Nerve ◽  
Adrenergic Receptor ◽  
Sympathetic Nerve Activity ◽  
Flow Distribution ◽  
Receptor Blockade ◽  
Blood Flow Distribution ◽  
Nerve Activity ◽  
Adrenergic Receptor Blockade

Handgrip-induced increases in blood flow through the contralateral artery that supplies the cortical representation of the arm have been hypothesized as a consequence of neurovascular coupling and a resultant metabolic attenuation of sympathetic cerebral vasoconstriction. In contrast, sympathetic restraint, in theory, inhibits changes in perfusion of the cerebral ipsilateral blood vessels. To confirm whether sympathetic nerve activity modulates cerebral blood flow distribution during static handgrip (SHG) exercise, beat-to-beat contra- and ipsilateral internal carotid artery blood flow (ICA; Doppler) and mean arterial pressure (MAP; Finometer) were simultaneously assessed in nine healthy men (27 ± 5 yr), both at rest and during a 2-min SHG bout (30% maximal voluntary contraction), under two experimental conditions: 1) control and 2) α1-adrenergic receptor blockade. End-tidal carbon dioxide (rebreathing system) was clamped throughout the study. SHG induced increases in MAP (+31.4 ± 10.7 mmHg, P < 0.05) and contralateral ICA blood flow (+80.9 ± 62.5 ml/min, P < 0.05), while no changes were observed in the ipsilateral vessel (−9.8 ± 39.3 ml/min, P > 0.05). The reduction in ipsilateral ICA vascular conductance (VC) was greater compared with contralateral ICA (contralateral: −0.8 ± 0.8 vs. ipsilateral: −2.6 ± 1.3 ml·min−1·mmHg−1, P < 0.05). Prazosin was effective to induce α1-blockade since phenylephrine-induced increases in MAP were greatly reduced ( P < 0.05). Under α1-adrenergic receptor blockade, SHG evoked smaller MAP responses (+19.4 ± 9.2, P < 0.05) but similar increases in ICAs blood flow (contralateral: +58.4 ± 21.5 vs. ipsilateral: +54.3 ± 46.2 ml/min, P > 0.05) and decreases in VC (contralateral: −0.4 ± 0.7 vs. ipsilateral: −0.4 ± 1.0 ml·min−1·mmHg−1, P > 0.05). These findings indicate a role of sympathetic nerve activity in the regulation of cerebral blood flow distribution during SHG.

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