Effects of centrally administered atrial natriuretic polypeptide on sympathetic nerve activity and blood flow to the kidney in conscious rats

1990 ◽  
Vol 116 (1-2) ◽  
pp. 123-129 ◽  
Author(s):  
H. Kannan ◽  
Y. Ueta ◽  
T. Nakamura ◽  
H. Yamashita ◽  
Y. Hayashida
Keyword(s):  
Blood Flow ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Conscious Rats ◽  
Atrial Natriuretic Polypeptide ◽  
Atrial Natriuretic

Effects of centrally administered angiotensin on sympathetic nerve activity and blood flow to the kidney in conscious rats

1991 ◽  
Vol 34 (2-3) ◽  
pp. 201-210 ◽  
Author(s):  
Hiroshi Kannan ◽  
Tadashi Nakamura ◽  
Xin Ji Jin ◽  
Yoshiaki Hayashida ◽  
Hiroshi Yamashita
Keyword(s):  
Blood Flow ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Conscious Rats

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

Discharge Pattern of Renal Sympathetic Nerve Activity in the Conscious Rat: Spectral Analysis of Integrated Activity

2000 ◽  
Vol 84 (6) ◽  
pp. 2859-2867 ◽  
Author(s):  
Takato Kunitake ◽  
Hiroshi Kannan
Keyword(s):  
Heart Rate ◽  
Power Spectrum ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Low Frequency ◽  
Heart Beat ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Conscious Rats ◽  
Renal Sympathetic

We investigated the periodic characteristics of bursting discharge in renal sympathetic nerve activity (RSNA) in conscious rats. Employing a discrete fast Fourier transform algorithm, a power spectrum analysis was used to quantify periodicities present in rectified and integrated RSNA whose signal-to-noise ratio in the recordings was greater than six. In conscious rats with intact baroreceptors, RSNA was characterized by four frequency components occurring at about 0.5, 1.5, 6, and 12 Hz, which corresponded to the low-frequency fluctuation of heart rate, respiration, and frequency of heart beat, and its harmonics, respectively. After intravenous infusion of sodium nitroprusside (SNP) to elicit reflex increases in RSNA and heart rate, the power for the component at 6 Hz followed the changes in heart beat frequency and was significantly increased, while those for the three other components were attenuated or experienced no change. In sino-aortic denervated (SAD) conscious rats, all four components were abolished, and the power spectrum was well fitted by a flat or Lorentzian curve, suggesting an almost random pattern. Only a respiratory-related component, which suggested common central modulation, appeared sporadically for short periods but was absent for the most part. Therefore most of this component together with the low-frequency component was also likely due to the baroreceptor-dependent peripheral modulation. The activity was sorted in 15 subgroups on the basis of spike amplitudes in the RSNA. Each subgroup showed frequency characteristics similar to the whole nerve activity. These results suggest that all periodicity in the RSNA of conscious rats with intact baroreceptors is caused by the baroreceptor input.

Role of nitric oxide in regulation of renal sympathetic nerve activity during hemorrhage in conscious rats

1999 ◽  
Vol 277 (1) ◽  
pp. H8-H14 ◽  
Author(s):  
Yoshihide Fujisawa ◽  
Naoko Mori ◽  
Kouichi Yube ◽  
Hiroshi Miyanaka ◽  
Akira Miyatake ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Saline Group ◽  
Baroreceptor Reflex ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Conscious Rats ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

The effect of inhibition of nitric oxide (NO) synthesis on the responses of blood pressure (BP), heart rate (HR), and renal sympathetic nerve activity (RSNA) during hemorrhaging was examined with the use of an NO synthase inhibitor, NG-nitro-l-arginine methyl ester (l-NAME), in conscious rats. In the 0.9% saline group, hemorrhage (10 ml/kg body wt) did not alter BP but significantly increased HR and RSNA by 88 ± 12 beats/min and 67 ± 12%, respectively. Intravenous infusion of l-NAME (50 μg ⋅ kg−1⋅ min−1) significantly attenuated these tachycardic and sympathoexcitatory responses to hemorrhage (14 ± 7 beats/min and 26 ± 12%, respectively). Pretreatment ofl-arginine (87 mg/kg) recovered the attenuation of HR and RSNA responses induced byl-NAME (92 ± 6 beats/min and 64 ± 10%, respectively).l-NAME by itself did not alter the baroreceptor reflex control of HR and RSNA. Hemorrhage increased the plasma vasopressin concentration, and its increment in thel-NAME-treated group was significantly higher than that in the 0.9% saline group. Pretreatment with the vascular arginine vasopressin V1-receptor antagonist OPC-21268 (5 mg/kg) recovered the attenuation of RSNA response induced byl-NAME (54 ± 7%). These results indicate that NO modulated HR and RSNA responses to hemorrhage but did not directly affect the baroreceptor reflex arch. It can be assumed that NO modulated the baroreflex function by altering the secretion of vasopressin induced by hemorrhage.

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