scholarly journals Total Spectral Power and High Frequency Blood Pressure Variability is Reduced in Male Bmal1‐Collecting Duct Knock‐Out Mice During the Inactive Period

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Megan K Rhoads ◽  
Dingguo Zhang ◽  
Bryan K Becker ◽  
David M Pollock
Keyword(s):  
Blood Pressure ◽  
High Frequency ◽  
Blood Pressure Variability ◽  
Spectral Power ◽  
Collecting Duct ◽  
Knock Out ◽  
Inactive Period ◽  
Total Spectral Power ◽  
Knock Out Mice

Autonomic and ventilatory components of heart rate and blood pressure variability in freely behaving rats

1995 ◽  
Vol 269 (5) ◽  
pp. H1729-H1734 ◽  
Author(s):  
S. Perlini ◽  
F. Giangregorio ◽  
M. Coco ◽  
A. Radaelli ◽  
P. L. Solda ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
High Frequency ◽  
Blood Pressure Variability ◽  
Spectral Power ◽  
Relative Role ◽  
Freely Behaving ◽  
Intravenous Atropine ◽  
Autoregressive Analysis

The relative role of parasympathetic, sympathetic, and ventilatory influences in the genesis of blood pressure and R-R interval variability is controversial. In 13 freely behaving WKY rats instrumented with venous and arterial catheters and chest electrodes, mean arterial pressure (MAP, mmHg), R-R interval (ms), and respiratory fluctuations were monitored for 90 min in the control condition and after intravenous atropine (0.75 mg/kg) and/or propranolol (1 mg/kg). Spectral power (pw) in the 0.25- to 0.75-Hz (midfrequency, MF) and the 0.75- to 3.0-Hz (high-frequency, HF, respiratory-synchronous) bands was computed in sequences of 400 heartbeats by use of a combined autoregressive analysis. Atropine reduced but did not abolish HF R-R interval pw (from 1.73 +/- 0.50 to 0.39 +/- 0.27 ms2, P < 0.01) and halved HF MAP pw (from 0.41 +/- 0.30 to 0.21 +/- 0.12 mmHg2, P < 0.05), whereas propranolol did not affect HF pw of the R-R interval or MAP. Propranolol also failed to significantly modify MF R-R interval pw (from 0.48 +/- 0.44 to 0.40 +/- 0.34 ms2, P = NS) or MF MAP pw (from 0.54 +/- 0.39 to 0.42 +/- 0.20 mmHg2, P = NS), whereas atropine virtually abolished MF R-R interval pw (from 0.48 +/- 0.44 to 0.01 +/- 0.01 ms2, P < 0.01) and also significantly reduced MF MAP pw (from 0.54 +/- 0.39 to 0.33 +/- 0.24 mmHg2, P < 0.01). The effects of combined blockade were similar to those of atropine alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Absence of orthogonal arrays in kidney, brain and muscle from transgenic knockout mice lacking water channel aquaporin-4

1997 ◽  
Vol 110 (22) ◽  
pp. 2855-2860 ◽  
Author(s):  
J.M. Verbavatz ◽  
T. Ma ◽  
R. Gobin ◽  
A.S. Verkman
Keyword(s):  
Cho Cells ◽  
Collecting Duct ◽  
Water Channel ◽  
Freeze Fracture ◽  
Orthogonal Arrays ◽  
Knock Out ◽  
Orthogonal Arrays Of Particles ◽  
Freeze Fracture Electron Microscopy ◽  
Knock Out Mice ◽  
And Function

Freeze-fracture electron microscopy (FFEM) of kidney collecting duct, muscle, astrocytes in brain, and other mammalian tissues has revealed regular square arrays of intramembrane particles called orthogonal arrays of particles (OAPs). Their possible role in membrane structure and transport have been proposed, and their absence or decrease has been noted in a variety of hereditary and acquired diseases. A transgenic mouse lacking water channel AQP4 was used to show that AQP4 is the OAP protein. FFEM was done on kidney, skeletal muscle, and brain from AQP4 wild-type [+/+], heterozygous [+/−] and knock-out [-/-] mice. The [-/-] mice did not express detectable AQP4 protein, but were grossly indistinguishable from [+/+] mice. FFEM was done on blinded samples of kidney, brain and muscle from 9 mice. In all 6 kidney samples from [+/+] and [+/−] mice, OAPs similar to those in AQP4-transfected CHO cells were found in basolateral membranes of collecting duct principal cells. In all muscle and brain samples from [+/+] and [+/−] mice, OAPs of identical ultrastructure to those in kidney were seen, but in smaller patch sizes. OAPs were not seen in any sample from [-/-] mice. Label-fracture analysis using a peptide-derived AQP4 polyclonal antibody showed immunogold labeling of OAPs in AQP4-expressing CHO cells. These studies provide direct evidence that AQP4 is required for formation of OAPs and is a component of OAPs, thus establishing the identity and function of OAPs.

Fractal Component of Variability of Heart Rate and Systolic Blood Pressure in Congestive Heart Failure

1997 ◽  
Vol 92 (6) ◽  
pp. 543-550 ◽  
Author(s):  
Gary C. Butler ◽  
Shin-Ichi Ando ◽  
John S. Floras
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Systolic Blood Pressure ◽  
Spectral Power ◽  
Normal Subjects ◽  
Total Spectral Power ◽  
Systolic Blood Pressure Variability ◽  
Harmonic Components

1. There is a substantial non-harmonic or fractal component to the variability of both heart rate and blood pressure in normal subjects. Heart rate is the more complex of these two signals, with respect to the slope, β, of the 1/fβ relationship. In congestive heart failure, heart rate spectral power is attenuated, but the fractal and harmonic components of heart rate and systolic blood pressure variability have not been characterized. 2. Two groups, each comprising 20 men, were studied during 15 min of supine rest and spontaneous respiration: one with functional class II—IV heart failure (age 52 ± 2 years; mean ± SEM) and a second group of healthy men (age 46 ± 2 years). 3. Total spectral power for heart rate was significantly reduced in heart failure (P < 0.02), whereas total spectral power for systolic blood pressure was similar in the two groups. In both heart failure and normal subjects, 65–80% of total spectral power in these two signals displayed fractal characteristics. 4. In heart failure, the slope of the 1/fβ relationship for heart rate was significantly steeper than in normal subjects (1.40 ± 0.08 compared with 1.14 ± 0.05; P < 0.05), indicating reduced complexity of the fractal component of heart rate variability. There was no significant difference in the 1/fβ slope for systolic blood pressure variability between these two groups, but the blood pressure signals were less complex than heart rate variations in both heart failure (2.31 ± 0.15; P < 0.006) and normal subjects (2.47 ± 0.15; P < 0.0001). 5. Parasympathetic nervous system activity, as estimated from heart rate variability was reduced (P < 0.01) in patients with heart failure, whereas trends towards increased sympathetic nervous system activity and decreased non-harmonic power were not significant. 6. The non-harmonic components of cardiac frequency are reduced in heart failure. Non-harmonic power is not attenuated, but the complexity of the heart rate signal is less than in subjects with normal ventricular function. A reduction in parasympathetic modulation appears to contribute to this loss of complexity of heart rate. Consequently, the heart rate signal comes to resemble that of blood pressure. In contrast, the variability and complexity of the systolic blood pressure signal is similar in heart failure and normal subjects. This reduced complexity of heart rate variability may have adverse implications for patients with heart failure.

Changes in Electroencephalogram and Autonomic Cardiovascular Activity during Induction of Anesthesia with Sevoflurane Compared with Halothane in Children 

1999 ◽  
Vol 91 (6) ◽  
pp. 1604-1604 ◽  
Author(s):  
Isabelle Constant ◽  
Marie-Claude Dubois ◽  
Véronique Piat ◽  
Marie-Laure Moutard ◽  
Maggie McCue ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Spectral Power ◽  
Low Frequency ◽  
Relative Increase ◽  
Slow Waves ◽  
Cardiovascular Activity ◽  
Additional Group ◽  
Finger Blood Pressure ◽  
Total Spectral Power

Background This study was design to assess clinical agitation, electroencephalogram (EEG) and autonomic cardiovascular activity changes in children during induction of anesthesia with sevoflurane compared with halothane using noninvasive recording of EEG, heart rate, and finger blood pressure. Methods Children aged 2-12 yr premedicated with midazolam were randomly assigned to one of three induction techniques: 7% sevoflurane in 100% O2 (group SevoRAPID); 2%, 4%, 6%, and 7% sevoflurane in 100% O2 (group SevoINCR); or 1%, 2%, 3%, and 3.5% halothane in 50% N2O-50% O2 (group HaloN2O). An additional group of children who received 7% sevoflurane in 50% N2O-50% O2 (group SevoN2O) was enrolled after completion of the study. Induction was videotaped. EEG, heart rate, and finger blood pressure were continuously recorded during induction until 5 min after tracheal intubation and analyzed in frequency domain using spectral analysis. Results Agitation was more frequent when anesthesia was induced with 100% O2 compared to the mixture of oxygen and nitrous oxide. No seizures were recorded in any group. In the four groups, induction of anesthesia was associated with an increase in EEG total spectral power and a shift toward the low-frequency bands. Sharp slow waves were present on EEG tracings of the three sevoflurane groups, whereas slow waves and fast rhythms (spindles) were observed in the halothane group. Sevoflurane induced a greater withdrawal of parasympathetic activity than halothane and a transient relative increase in sympathetic vascular tone at loss of eyelash reflex. Conclusions Agitation observed during sevoflurane induction was not associated with seizures. Sevoflurane induction induced a marked inhibition of parasympathetic control of heart rate.

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.

Identification of low and high frequency ranges for heart rate variability and blood pressure variability analyses using pharmacological autonomic blockade with atropine and propranolol in swine

2011 ◽  
Vol 103 (2) ◽  
pp. 188-196 ◽  
Author(s):  
Rosangela Poletto ◽  
Andrew M. Janczak ◽  
Ruth M. Marchant-Forde ◽  
Jeremy N. Marchant-Forde ◽  
Donald L. Matthews ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
High Frequency ◽  
Blood Pressure Variability ◽  
Autonomic Blockade

scholarly journals A role for the A3 adenosine receptor in determining tissue levels of cAMP and blood pressure: studies in knock-out mice

2000 ◽  
Vol 1500 (3) ◽  
pp. 280-290 ◽  
Author(s):  
Zhihui Zhao ◽  
Konstantinos Makaritsis ◽  
Cynthia E Francis ◽  
Haralambos Gavras ◽  
Katya Ravid
Keyword(s):  
Blood Pressure ◽  
Adenosine Receptor ◽  
Knock Out ◽  
Tissue Levels ◽  
A3 Adenosine Receptor ◽  
Knock Out Mice

scholarly journals Effect of Losartan, an Angiotensin II Type 1 Receptor Antagonist on Cardiac Autonomic Functions of Rats During Acute and Chronic Inhibition of Nitric Oxide Synthesis

2012 ◽  
pp. 135-144
Author(s):  
M. CHASWAL ◽  
S. DAS ◽  
J. PRASAD ◽  
A. KATYAL ◽  
A. K. MISHRA ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
High Frequency ◽  
Spectral Power ◽  
Pressor Response ◽  
Low Frequency ◽  
Renin Angiotensin System ◽  
Nitric Oxide Synthesis ◽  
Total Spectral Power ◽  
The Difference

We studied the effect of losartan on baroreflex sensitivity (BRS) and heart rate variability (HRV) of adult Wistar rats during acute and chronic inhibition of nitric oxide synthesis by NG-nitro-L-arginine methyl ester (L-NAME). Chronic L-NAME administration (50 mg/kg per day for 7 days, orally through gavage) increased mean arterial pressure (MAP), heart rate but significantly decreased BRS. In addition, a significant fall of standard deviation of normal RR intervals, total spectral power, high frequency spectral power and a rise of low frequency to high frequency (LF: HF) ratio was seen. Acute L-NAME administration (30 mg/kg, i.v. bolus dose) also raised MAP and impaired HRV but it was associated with augmented BRS for bradycardia reflex. Losartan treatment (10 mg/kg, i.v.) in both acute and chronic L-NAME treated rats, decreased MAP but the difference was not significant. On the other hand, losartan administration normalized depressed BRS for bradycardia reflex and significantly reduced LF to HF ratio in chronic L-NAME treated rats. But this improvement was not observed in acute L-NAME group. These results indicate importance of mechanisms other than renin-angiotensin system in the pressor response of both acute as well as chronic L-NAME. However, autonomic dysregulation especially following chronic L-NAME appears to be partly angiotensin dependent.

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