Characterization of the role of endogenous nitric oxide in myogenic vascular oscillations during cooling-evoked hemodynamic perturbations of rats

2017 ◽  
Vol 95 (7) ◽  
pp. 803-810 ◽  
Author(s):  
Yi-Hsien Lin ◽  
Yia-Ping Liu ◽  
Yu-Chieh Lin ◽  
Po-Lei Lee ◽  
Che-Se Tung
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Cold Stress ◽  
Low Frequency ◽  
Sympathetic Activation ◽  
Nitric Oxide Synthase Inhibitor ◽  
Dicrotic Notch ◽  
Endogenous Nitric Oxide

Rapid immersion of a rat’s limbs into 4 °C water, a model of cold stress, can elicit hemodynamic perturbations (CEHP). We previously reported that CEHP is highly relevant to sympathetic activation and nitric oxide production. This study identifies the role of nitric oxide in CEHP. Conscious rats were pretreated with the nitric oxide synthase inhibitor L-NAME (NG-nitro-l-arginine methyl ester) alone or following the removal of sympathetic influences using hexamethonium or guanethidine. Rats were then subjected to a 10 min cold-stress trial. Hemodynamic indices were telemetrically monitored throughout the experiment. The analyses included measurements of systolic blood pressure; heart rate; dicrotic notch; short-term cardiovascular oscillations and coherence between blood pressure variability and heart rate variability in regions of very low frequency (0.02–0.2 Hz), low frequency (0.2–0.6 Hz), and high frequency (0.6–3.0 Hz). We observed different profiles of hemodynamic reaction between hexamethonium and guanethidine superimposed on L-NAME, suggesting an essential role for a functional adrenal medulla release of epinephrine under cold stress. These results indicate that endogenous nitric oxide plays an important role in the inhibition of sympathetic activation and cardiovascular oscillations in CEHP.

Sympathetic-Parasympathetic Activation During Spontaneous Attacks of Cluster Headache: Evaluation by Spectral Analysis of Heart-Rate Fluctuations

Cephalalgia ◽  
1995 ◽  
Vol 15 (6) ◽  
pp. 504-510 ◽  
Author(s):  
M De Marinis ◽  
S Strano ◽  
M Granata ◽  
C Urani ◽  
S Lino ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Spectral Analysis ◽  
Cluster Headache ◽  
Low Frequency ◽  
Sympathetic Activation ◽  
Autonomic Balance ◽  
Spectral Parameters ◽  
Rate Fluctuation ◽  
Head Up Tilt

Twenty-four hour ECG Holter and blood-pressure monitorings were performed in eight patients suffering from cluster headache. Spectral analysis of heart-rate fluctuation was used to assess the autonomic balance under basal conditions, after head-up tilt, and during a spontaneous attack. Normal autonomic balance was found at rest and during sympathetic activation obtained with head-up tilt in the interparoxysmal period. Before the onset of headache, an increase in the low-frequency (LF) component of the power spectrum was apparent in all patients. This sign of sympathetic activation was followed by an increase in the high-frequency (HF) component that developed about 2000 beats after the onset of headache and rapidly overcame the LF component until the end of pain. Significant differences were found when comparing the spectral parameters [total spectral values (TP), power of the LF and HF components and LF/HF ratio] obtained before, during and after headache. During the attack, blood pressure increased and heart rate decreased in all subjects. There appears to be a primary activation of both sympathetic and parasympathetic functions in cluster headache attacks. The sympathetic component seems to be involved mostly in the development of the attack, whereas the parasympathetic activation seems to occur, following the onset of the attack, independently of the pain.

Neurogenic-nitric oxide interactions affecting brachial artery mechanics in humans: roles of vessel distensibility vs. diameter

2008 ◽  
Vol 295 (4) ◽  
pp. R1181-R1187 ◽  
Author(s):  
Deborah A. Salzer ◽  
Philip J. Medeiros ◽  
Rosemary Craen ◽  
J. Kevin Shoemaker
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Brachial Artery ◽  
Lower Body Negative Pressure ◽  
Cold Pressor ◽  
Sympathetic Outflow ◽  
Sympathetic Activation ◽  
Baseline Diameter ◽  
Conduit Vessel

The purpose of this investigation was to assess the interactive influence of sympathetic activation and supplemental nitric oxide (NO) on brachial artery distensibility vs. its diameter. It was hypothesized that 1) sympathetic activation and NO competitively impact muscular conduit artery (brachial artery) mechanics, and 2) neurogenic constrictor input affects conduit vessel stiffness independently of outright changes in conduit vessel diastolic diameter. Lower body negative pressure (LBNP) and a cold pressor stress (CPT) were used to study the changes in conduit vessel mechanics when the increased sympathetic outflow occurred with and without changes in heart rate (LBNP −40 vs. −15 mmHg) and blood pressure (CPT vs. LBNP). These maneuvers were performed in the absence and presence of nitroglycerin. Neither LBNP nor CPT altered brachial artery diastolic diameter; however, distensibility was reduced by 25 to 54% in each reflex (all P < 0.05). This impact of sympathetic activation on brachial artery distensibility was not altered by nitroglycerin supplementation (21–54%; P < 0.05), although baseline diameter was increased by the exogenous NO ( P < 0.05). The results indicate that sympathetic excitation can reduce the distensibility of the brachial artery independently of concurrent changes in diastolic diameter, heart rate, and blood pressure. However, exogenous NO did not minimize or reverse brachial stiffening during sympathetic activation. Therefore, sympathetic outflow appears to impact the stiffness of this conduit vessel rather than its diastolic diameter or, by inference, its local resistance to flow.

Very-low-frequency oscillations in heart rate and blood pressure in periodic breathing: role of the cardiovascular limb of the hypoxic chemoreflex

2000 ◽  
Vol 99 (2) ◽  
pp. 125 ◽  
Author(s):  
Darrel P. FRANCIS ◽  
L. Ceri DAVIES ◽  
Keith WILLSON ◽  
Piotr PONIKOWSKI ◽  
Andrew J.S. COATS ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Low Frequency ◽  
Periodic Breathing ◽  
Very Low Frequency ◽  
Low Frequency Oscillations

Repeatability of Spectral Components of Short-Term Blood Pressure and Heart Rate Variability during Acute Sympathetic Activation in Healthy Young Male Subjects

1997 ◽  
Vol 93 (1) ◽  
pp. 21-28 ◽  
Author(s):  
Laure Cloarec-Blanchard ◽  
Christian Funck-Brentano ◽  
Margorzata Lipski ◽  
Patrice Jaillon ◽  
Isabelle MacQuin-Mavier
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Clinical Studies ◽  
Low Frequency ◽  
Young Male ◽  
Sympathetic Activation ◽  
Spectral Components ◽  
Acute Changes ◽  
Normalized Units

1. Changes in the low-frequency (LF) components of blood pressure and heart rate variability and in the ratio of LF to high-frequency (HF) components of heart rate variability (LF/HF ratio) are used to assess acute changes in sympathetic control of blood pressure or heart rate and in sympathovagal balance that occur in response to physiological or pharmacological stimuli. Before these spectral indexes can be used to assess the effects of drug therapy or other clinical interventions on reflex sympathetic activity, their repeatability must be evaluated. 2. Intra-observer repeatability was studied by analysing changes in the LF components (expressed as absolute or normalized units) of cardiovascular variability and in the LF/HF ratio during sympathetic activation induced by nitroglycerin infusion (n = 10 subjects) or 60° head-up tilt (n = 13 subjects) repeated on two occasions, 2 days and 1 week apart respectively, in healthy young male volunteers. Repeatability was estimated as recommended by Bland and Altman. 3. Bland and Altman's plots of the repeatability of changes in the LF components and LF/HF ratio showed that measurements were sufficiently repeatable to be used over periods of time of up to 1 week in clinical studies. 4. The sample-size tables derived from our results show that expression of spectral components as normalized units, and use of a cross-over design, minimize the number of subjects to be included in clinical studies conducted using similar designs and LF component changes as endpoints.

Short-term and long-term blood pressure and heart rate variability in the mouse

2000 ◽  
Vol 278 (1) ◽  
pp. R215-R225 ◽  
Author(s):  
Ben J. A. Janssen ◽  
Peter J. A. Leenders ◽  
Jos F. M. Smits
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Pressure Fluctuations ◽  
Sympathetic Nerves ◽  
Pulse Interval ◽  
Control Mechanisms ◽  
Short Term ◽  
Endogenous Nitric Oxide ◽  
Short Term Variability

Knowledge on murine blood pressure and heart rate control mechanisms is limited. With the use of a tethering system, mean arterial pressure (MAP) and pulse interval (PI) were continuously recorded for periods up to 3 wk in Swiss mice. The day-to-day variation of MAP and PI was stable from 5 days after surgery. Within each mouse ( n = 9), MAP and PI varied by 21 ± 6 mmHg and 17 ± 4 ms around their respective 24-h averages (97 ± 3 mmHg and 89 ± 3 ms). Over 24-h periods, MAP and PI were bimodally distributed and clustered around two preferential states. Short-term variability of MAP and PI was compared between the resting (control) and active states using spectral analysis. In resting conditions, variability of MAP was mainly confined to frequencies <1 Hz, whereas variability of PI was predominantly linked to the respiration cycle (3–6 Hz). In the active state, MAP power increased in the 0.08- to 3-Hz range, whereas PI power fell in the 0.08- to 0.4-Hz range. In both conditions, coherence between MAP and PI was high at 0.4 Hz with MAP leading the PI fluctuations by 0.3–0.4 s, suggesting that reflex coupling between MAP and PI occurred at the same frequency range as in rats. Short-term variability of MAP and PI was studied after intravenous injection of autonomic blockers. Compared with the resting control state, MAP fell and PI increased after ganglionic blockade with hexamethonium. Comparable responses of MAP were obtained with the α-blocker prazosin, whereas the β-blocker metoprolol increased PI similarly. Muscarinic blockade with atropine did not significantly alter steady-state levels of MAP and PI. Both hexamethonium and prazosin decreased MAP variability in the 0.08- to 1-Hz range. In contrast, after hexamethonium and metoprolol, PI variability increased in the 0.4- to 3-Hz range. Atropine had no effect on MAP fluctuations but decreased those of PI in the 0.08- to 1-Hz range. These data indicate that, in mice, blood pressure and its variability are predominantly under sympathetic control, whereas both vagal and sympathetic nerves control PI variability. Blockade of endogenous nitric oxide formation by N G-nitro-l-arginine methyl ester increased MAP variability specifically in the 0.08- to 0.4-Hz range, suggesting a role of nitric oxide in buffering blood pressure fluctuations.

scholarly journals Mechanisms of blood pressure and heart rate variability: an insight from low-level paraplegia

2007 ◽  
Vol 292 (4) ◽  
pp. R1502-R1509 ◽  
Author(s):  
Paolo Castiglioni ◽  
Marco Di Rienzo ◽  
Arsenio Veicsteinas ◽  
Gianfranco Parati ◽  
Giampiero Merati
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Low Frequency ◽  
Neural Oscillator ◽  
Sympathetic Activation ◽  
Arterial Blood ◽  
Baroreflex Function ◽  
Cord Injury

It is still unclear whether the low-frequency oscillation in heart rate is generated by an endogenous neural oscillator or by a baroreflex resonance. Our aim was to investigate this issue by analyzing blood pressure and heart rate variability and the baroreflex function in paraplegic subjects with spinal cord injury below the fourth thoracic vertebra. These subjects were selected because they represent a model of intact central neural drive to the heart, with a partially impaired autonomic control of the vessels. In our study, arterial blood pressure and ECG were recorded in 33 able-bodied controls and in 33 subjects with spinal cord lesions between the fifth thoracic and the fourth lumbar vertebra 1) during supine rest (lowest sympathetic activation), 2) sitting on a wheelchair (light sympathetic activation), and 3) during exercise (moderate sympathetic activation). Blood pressure and heart rate spectra, coherence, and baroreflex function (sequence technique) were estimated in each condition. Compared with controls, paraplegic subjects showed a reduction of the low-frequency power of blood pressure and heart rate, and, unlike controls, a 0.1-Hz peak did not appear in their spectra. Sympathetic activation increased the 0.1-Hz peak of blood pressure and heart rate and the coherence at 0.1 Hz in controls only. Paraplegic subjects also had significantly lower baroreflex effectiveness and greater blood pressure variability. In conclusion, the disappearance of the 10-s oscillation of heart rate and blood pressure in subjects with spinal cord lesion supports the hypothesis of the baroreflex nature of this phenomenon.

The role of nitric oxide in the development of neurogenic pulmonary edema in spinal cord-injured rats: the effect of preventive interventions

2009 ◽  
Vol 297 (4) ◽  
pp. R1111-R1117 ◽  
Author(s):  
Jiří Šedý ◽  
Josef Zicha ◽  
Jaroslav Kuneš ◽  
Aleš Hejčl ◽  
Eva Syková
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Pulmonary Edema ◽  
No Synthase ◽  
Neurogenic Pulmonary Edema ◽  
Therapeutic Effects ◽  
Cord Injury

Neurogenic pulmonary edema (NPE) is an acute life-threatening complication following an injury of the spinal cord or brain, which is associated with sympathetic hyperactivity. The role of nitric oxide (NO) in NPE development in rats subjected to balloon compression of the spinal cord has not yet been examined. We, therefore, pretreated Wistar rats with the NO synthase inhibitor N G-nitro-l-arginine methyl ester (l-NAME) either acutely (just before the injury) or chronically (for 4 wk prior to the injury). Acute (but not chronic) l-NAME administration enhanced NPE severity in rats anesthetized with 1.5% isoflurane, leading to the death of 83% of the animals within 10 min after injury. Pretreatment with either the ganglionic blocker pentolinium (to reduce blood pressure rise) or the muscarinic receptor blocker atropine (to lessen heart rate decrease) prevented or attenuated NPE development in these rats. We did not observe any therapeutic effects of atropine administered 2 min after spinal cord compression. Our data indicate that NPE development is dependent upon a marked decrease of heart rate under the conditions of high blood pressure elicited by the activation of the sympathetic nervous system. These hemodynamic alterations are especially pronounced in rats subjected to acute NO synthase inhibition. In conclusion, nitric oxide has a partial protective effect on NPE development because it attenuates sympathetic vasoconstriction and consequent baroreflex-induced bradycardia following spinal cord injury.

Mechanism of the acute pressor effect and bradycardia elicited by diaspirin crosslinked hemoglobin in anesthetized rats

1998 ◽  
Vol 76 (4) ◽  
pp. 434-442 ◽  
Author(s):  
Steve Moisan ◽  
Guy Drapeau ◽  
Kenneth E Burhop ◽  
Francis Rioux
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Pressor Effect ◽  
Endogenous Nitric Oxide ◽  
Pressor Activity ◽  
Vagal Reflex ◽  
Generating System ◽  
Hypertensive Episode ◽  
Diaspirin Crosslinked Hemoglobin

Diaspirin crosslinked hemoglobin (DCLHb) is a chemically stabilizedhemoglobin (Hb) that induces an increase in blood pressure and a decrease of heart rate wheninjected intravenously in some animals. The mechanism by which DCLHb elicits thesehemodynamic effects was studied in pentobarbital-anesthetized, vagotomized rats using a varietyof drugs known for their inhibitory action towards endogenous hemodynamically active systems.The hypertensive episode elicited by DCLHb (100 or 400 mg·kg–1) was attenuatedin animals pretreated with NG-nitro-L-arginine (inhibitor of nitric oxidesynthases) throughout the 30-min period of observation, but it was not reduced in thosepretreated with a variety of sympatholytic drugs (e.g., prazosin), atropine, BIBP-3226(neuropeptide Y antagonist), indomethacin,[1-(Beta-mercapto-Beta,Beta-cyclopentanemethylene propionic acid), 2-(0-methyl)tyrosine]-Arg8 vasopressin (vasopressin antagonist), losartan (angiotensin antagonist),bosentan (endothelin antagonist), or L-arginine- (nitric oxide precursor), compared withcontrol animals. With the exception of propranolol and BIBP-3226, none of the aforenamedinhibitors reduced the amplitude of the bradycardia associated with the pressor effect of DCLHb.These results suggest that: (i) the acute (<30 min) pressor activity of DCLHb inour animal model requires the presence of an endogenous nitric oxide generating system to beexpressed; (ii) the bradycardia elicited by DCLHb might involve the participation ofneuropeptide Y and (or) its NPY-1 receptors, but it is unlikely to involve abaroreceptor-mediated vagal reflex, at least in our animal model.Key words: hemoglobin, nitric oxide, blood pressure, heart rate,DCLHb.

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