Hemodynamic regulation: investigation by spectral analysis

1985 ◽  
Vol 249 (4) ◽  
pp. H867-H875 ◽  
Author(s):  
S. Akselrod ◽  
D. Gordon ◽  
J. B. Madwed ◽  
N. C. Snidman ◽  
D. C. Shannon ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spectral Analysis ◽  
Pressure Fluctuations ◽  
Low Frequency ◽  
Cardiovascular Control ◽  
Respiratory Frequency ◽  
Atrial Pacing ◽  
Loop Model ◽  
Short Term ◽  
Renin Angiotensin

We investigated the hypothesis that beat-to-beat variability in hemodynamic parameters reflects the dynamic interplay between ongoing perturbations to circulatory function and the compensatory response of short-term cardiovascular control systems. Spontaneous fluctuations in heart rate (HR), arterial blood pressure, and respiration were analyzed by spectral analysis in the 0.02- to 1-Hz frequency range. A simple closed-loop model of short-term cardiovascular control was proposed and evaluated in a series of experiments: pharmacological blockades of the parasympathetic, alpha-sympathetic, beta-sympathetic, and renin-angiotensin systems were used to open the principal control loops in order to examine changes in the spectral pattern of the fluctuations. Atrial pacing was used to examine blood pressure variability in the absence of HR variability. We found that respiratory frequency fluctuations in HR are parasympathetically mediated and that blood pressure fluctuations at this frequency result almost entirely from the direct effect of centrally mediated HR fluctuations. The sympathetic nervous system appears to be too sluggish to mediate respiratory frequency variations. Low-frequency (0.02-0.09 Hz) fluctuations in HR are jointly mediated by the parasympathetic and beta-sympathetic systems and appear to compensate for blood pressure fluctuations at this frequency. Low-frequency blood pressure fluctuations are probably due to variability in vasomotor activity which is normally damped by renin-angiotensin system activity. Blockade of the alpha-adrenergic system, however, does not significantly alter low-frequency blood pressure fluctuations.

Spectral analysis of hemodynamics during infusions of epinephrine and norepinephrine in men

1994 ◽  
Vol 76 (5) ◽  
pp. 1914-1921 ◽  
Author(s):  
J. H. Tulen ◽  
A. J. Man in ′t Veld ◽  
A. M. Van Roon ◽  
P. Moleman ◽  
H. G. Van Steenis ◽  
...  
Keyword(s):  
Spectral Analysis ◽  
Plasma Concentrations ◽  
Power Spectra ◽  
Low Frequency ◽  
Cardiovascular Control ◽  
Control Mechanisms ◽  
Short Term ◽  
Arterial Blood ◽  
Frequency Fluctuations ◽  
Infusion Of Norepinephrine

Spectral analysis of fluctuations in heart rate (HR) and arterial blood pressure (BP) during a 6-h infusion of epinephrine (15 ng.kg-1.min-1) or norepinephrine (30 ng.kg-1.min-1) in 10 normotensive males was used to analyze effects of peripheral sympathetic nervous system activity and adrenal medullary discharge on cardiovascular variability. Power spectra were calculated for each 5-min period for HR, systolic BP, and diastolic BP to yield power values for three frequency bands: low (0.02–0.06 Hz), mid (0.07–0.14 Hz), and high (0.15–0.40 Hz). Infusion of epinephrine and norepinephrine induced plasma concentrations of epinephrine and norepinephrine, respectively, within the high physiological range. Spectral analysis showed that low-frequency fluctuations of BP during infusions of epinephrine and midfrequency fluctuations of BP during infusion of norepinephrine changed in opposite directions. These fluctuations may represent different components of short-term cardiovascular control mechanisms during situations that mimic increased sympathoadrenal activity. No changes were observed in HR fluctuations or high-frequency fluctuations of BP after either catecholamine. Our data imply that changes in concentrations of circulating catecholamines cannot be unequivocally labeled as indexes of an altered sympathoadrenal involvement in short-term cardiovascular control.

The role of central vasopressin receptors in the modulation of autonomic cardiovascular controls: a spectral analysis study

2006 ◽  
Vol 291 (6) ◽  
pp. R1579-R1591 ◽  
Author(s):  
Sanja Milutinović ◽  
David Murphy ◽  
Nina Japundžić-Žigon
Keyword(s):  
Blood Pressure ◽  
Spectral Analysis ◽  
Low Frequency ◽  
Systolic Arterial Pressure ◽  
Short Term ◽  
Vasopressin Receptors ◽  
The Central Nervous System ◽  
Respiratory Stimulation ◽  
Stimulation Of

Although it has been suggested that vasopressin (VP) acts within the central nervous system to modulate autonomic cardiovascular controls, the mechanisms involved are not understood. Using nonpeptide, selective V1a, V1b, and V2 antagonists, in conscious rats, we assessed the roles of central VP receptors, under basal conditions, after the central application of exogenous VP, and after immobilization, on cardiovascular short-term variability. Equidistant sampling of blood pressure (BP) and heart rate (HR) at 20 Hz allowed direct spectral analysis in very-low frequency (VLF-BP), low-frequency (LF-BP), and high-frequency (HF-BP) blood pressure domains. The effect of VP antagonists and of exogenous VP on body temperature (Tb) was also investigated. Under basal conditions, V1a antagonist increased HF-BP and Tb, and this was prevented by metamizol. V1b antagonist enhanced HF-BP without affecting Tb, and V2 antagonist increased VLF-BP variability which could be prevented by quinapril. Immobilization increased BP, LF-BP, HF-BP, and HF-HR variability. V1a antagonist prevented BP and HR variability changes induced by immobilization and potentiated tachycardia. V1b antagonist prevented BP but not HR variability changes, whereas V2 antagonist had no effect. Exogenous VP increased systolic arterial pressure (SAP) and HF-SAP variability, and this was prevented by V1a and V1b but not V2 antagonist pretreatment. Our results suggest that, under basal conditions, VP, by stimulation of V1a, V1b, and cognate V2 receptors, buffers BP variability, mostly due to thermoregulation. Immobilization and exogenous VP, by stimulation of V1a or V1b, but not V2 receptors, increases BP variability, revealing cardiorespiratory adjustment to stress and respiratory stimulation, respectively.

MO443EFFECTS OF SHORT-TERM POTASSIUM CHLORIDE SUPPLEMENTATION IN PATIENTS WITH CHRONIC KIDNEY DISEASE*

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Martin Gritter ◽  
Rosa Wouda ◽  
Stanley Ming Hol Yeung ◽  
Liffert Vogt ◽  
Martin De Borst ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Ammonium Excretion ◽  
Short Term ◽  
Open Label ◽  
High Potassium ◽  
Renin Angiotensin ◽  
Lower Baseline

Abstract Background and Aims A high potassium (K+) diet is part of a healthy lifestyle and reduces blood pressure. Indeed, salt substitution (replacing NaCl by KCl) reduces the incidence of hypertension. Furthermore, emerging data show that high urinary K+ excretion in patients with chronic kidney disease (CKD) is associated with better kidney outcomes. This suggests that higher dietary K+ intake is also beneficial for patients with CKD, but a potential concern is hyperkalemia. Thus, there is a need for data on the effects of KCl supplementation in patients with CKD. Methods The effect of KCl supplementation (40 mEq/day) was studied by analyzing the 2-week open-label run-in phase of an ongoing randomized clinical trial studying the renoprotective effects of 2-year K+ supplementation in patients with progressive CKD and hypertension. The aims were to (1) analyze the effects of KCl supplementation on whole-blood K+ (WBK+) and acid-base balance, (2) identify factors associated with a rise in WBK+, and (3) identify risk factors for hyperkalemia (WBK+ > 5.5 mEq/L) . Results In 200 patients (68 ± 11 years, 74% males, eGFR 32 ± 9 mL/min/1.73 m2, 84% on renin-angiotensin inhibitors, 39% with diabetes mellitus), KCl supplementation increased urinary K+ excretion from 73 ± 24 to 106 ± 29 mEq/day, urinary chloride excretion from 144 ± 63 to 174 ± 60 mEq/day, WBK+ from 4.3 ± 0.5 to 4.7 ± 0.6 mEq/L, and plasma aldosterone from 294 to 366 ng/L (P < 0.01 for all). Plasma chloride increased from 104 ± 4 to 106 ± 4 mEq/L, while plasma bicarbonate decreased from 24.4 ± 3.4 to 23.6 ± 3.5 mEq/L and venous pH from 7.36 ± 0.03 to 7.34 ± 0.04 (P < 0.001 for all); urinary ammonium excretion did not increase (stable at 17.2 mEq/day). KCl supplementation had no significant effect on plasma renin (33 to 39 pg/mL), urinary sodium excretion (156 ± 63 to 155 ± 65 mEq/day), systolic blood pressure (134 ± 16 to 133 ± 17 mm Hg), eGFR (32 ± 9 to 31 ± 8 mL/min/1.73 m2) or albuminuria (stable at 0.2 g/day). Multivariable linear regression identified that age, female sex, and renin-angiotensin inhibitor use were associated with an increase in WBK+, while diuretic use, baseline WBK+, and baseline bicarbonate were inversely associated with a change in WBK+ after KCl supplementation (Table 1). The majority of patients (n = 181, 91%) remained normokalemic (WBK+ 4.6 ± 0.4 mEq/L). The 19 patients who did develop hyperkalemia (WBK+ 5.9 ± 0.4 mEq/L) were older (75 ± 8 vs. 67 ± 11 years), had lower eGFR (24 ± 8 vs. 32 ± 8 mL/min/1.73 m2), lower baseline bicarbonate (22.3 ± 3.6 vs. 24.6 ± 3.3 mEq/L), higher baseline WBK+ (4.8 ± 0.4 vs. 4.2 ± 0.4 mEq/L), and lower baseline urinary K+ excretion (64 ± 16 vs. 73 ± 25 mEq/day, P < 0.05 for all). Conclusions The majority of patients with advanced CKD remains normokalemic upon KCl supplementation, despite low eGFR, diabetes mellitus, or the use of renin-angiotensin inhibitors. This short-term study illustrates the feasibility of investigating the renoprotective potential of increased K+ intake or KCl-enriched salt in patients with CKD and provides the characteristics of patients in whom this is safe. Our study also shows that KCl supplementation causes a tendency towards metabolic acidosis, possibly by preventing an increase in ammoniagenesis. Longer-term studies are required to study the anti-hypertensive and renoprotective potential of K+ supplementation.

Impaired sympathetic response before intradialytic hypotension: a study based on spectral analysis of heart rate and pressure variability

1999 ◽  
Vol 96 (1) ◽  
pp. 23-31 ◽  
Author(s):  
Gualtiero PELOSI ◽  
Michele EMDIN ◽  
Clara CARPEGGIANI ◽  
Maria Aurora MORALES ◽  
Marcello PIACENTI ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Pressure Fluctuations ◽  
Power Spectra ◽  
Low Frequency ◽  
Autonomic Response ◽  
Dialysis Session ◽  
Intradialytic Hypotension ◽  
Sympathetic Response ◽  
A Minor

The purpose of this study was to evaluate the autonomic response to standard haemodialysis and the changes associated with the onset of intradialytic hypotension in 12 normotensive patients with uraemia. Power spectra of R–R interval and of blood pressure fluctuations were obtained during a standard dialysis session and estimated in the low-frequency (LF, 30–150 ;mHz) and high-frequency (HF, 150–400 ;mHz) range. The absolute power of the LF component of blood pressure variations and the LF/HF ratio of R–R interval were assumed as indexes of sympathetic activity. Standard haemodialysis induced hypotension in six patients (unstable) while a minor pressure decline was present in the other six (stable). Normalized blood volume before dialysis and percentage volume reduction were similar in the two groups. Tachycardia in response to pressure and volume decrease was more pronounced in stable than in unstable patients, as evidenced by a higher slope of the relation between R–R interval and systolic blood pressure (7.9 versus 0.9 ;ms/mmHg, P< 0.01). Sympathetic tone was enhanced during early dialysis in all patients (+2±1 for R–R LF/HF ratio, +2.4±0.6 ;mmHg2 and +7.2±2 ;mmHg2 for absolute LF power of diastolic and of systolic blood pressure respectively, P< 0.05), compared with baseline predialysis values. During late dialysis, unstable patients showed an impairment of sympathetic activation which preceded hypotension and was maximal during the crisis (-2.9±1.4 for R–R LF/HF ratio, -2.7±1.4 ;mmHg2 and -8.6±4.0 ;mmHg2 for absolute LF power of diastolic and of systolic blood pressure respectively, P< 0.05). On the contrary, stable patients showed constantly elevated indexes (+3.7±1.4 for R–R LF/HF ratio, +5.9±2.7 ;mmHg2 and +13.3±6.2 ;mmHg2 for LF of diastolic and of systolic blood pressure, P< 0.05). Values returned to predialysis levels after the end of the dialysis session in all patients. We conclude that standard haemodialysis activates a marked and reversible sympathetic response in both stable and unstable uraemic patients. However, in unstable patients, such activation is impaired in late dialysis, therefore contributing to the onset of the hypotensive crisis.

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.

scholarly journals Role of neurons and glia in the CNS actions of the renin-angiotensin system in cardiovascular control

2015 ◽  
Vol 309 (5) ◽  
pp. R444-R458 ◽  
Author(s):  
Annette D. de Kloet ◽  
Meng Liu ◽  
Vermalí Rodríguez ◽  
Eric G. Krause ◽  
Colin Sumners
Keyword(s):  
Blood Pressure ◽  
Glial Cell ◽  
Renin Angiotensin System ◽  
Cardiovascular Control ◽  
Health Concern ◽  
Ang Ii ◽  
Ongoing Research ◽  
Angiotensin System ◽  
Renin Angiotensin

Despite tremendous research efforts, hypertension remains an epidemic health concern, leading often to the development of cardiovascular disease. It is well established that in many instances, the brain plays an important role in the onset and progression of hypertension via activation of the sympathetic nervous system. Further, the activity of the renin-angiotensin system (RAS) and of glial cell-mediated proinflammatory processes have independently been linked to this neural control and are, as a consequence, both attractive targets for the development of antihypertensive therapeutics. Although it is clear that the predominant effector peptide of the RAS, ANG II, activates its type-1 receptor on neurons to mediate some of its hypertensive actions, additional nuances of this brain RAS control of blood pressure are constantly being uncovered. One of these complexities is that the RAS is now thought to impact cardiovascular control, in part, via facilitating a glial cell-dependent proinflammatory milieu within cardiovascular control centers. Another complexity is that the newly characterized antihypertensive limbs of the RAS are now recognized to, in many cases, antagonize the prohypertensive ANG II type 1 receptor (AT1R)-mediated effects. That being said, the mechanism by which the RAS, glia, and neurons interact to regulate blood pressure is an active area of ongoing research. Here, we review the current understanding of these interactions and present a hypothetical model of how these exchanges may ultimately regulate cardiovascular function.

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