The differential modulation of the baroreflex control mechanism in fight, flight or freeze behavior

2021 ◽  
Author(s):  
Sara AlMarabeh ◽  
Mohammed H. Abdulla
Keyword(s):  
Control Mechanism ◽  
Differential Modulation ◽  
Baroreflex Control

Baroreflex modulation by angiotensins at the rat rostral and caudal ventrolateral medulla

2006 ◽  
Vol 290 (4) ◽  
pp. R1027-R1034 ◽  
Author(s):  
Andréia C. Alzamora ◽  
Robson A. S. Santos ◽  
Maria J. Campagnole-Santos
Keyword(s):  
Heart Rate ◽  
Baroreflex Sensitivity ◽  
Opposite Effect ◽  
Ventrolateral Medulla ◽  
Ang Ii ◽  
Differential Modulation ◽  
Baroreflex Control ◽  
Caudal Ventrolateral Medulla ◽  
Angiotensin Peptides ◽  
Reflex Bradycardia

We determined the effect of microinjection of ANG-(1–7) and ANG II into two key regions of the medulla that control the circulation [rostral and caudal ventrolateral medulla (RVLM and CVLM, respectively)] on baroreflex control of heart rate (HR) in anesthetized rats. Reflex bradycardia and tachycardia were induced by increases and decreases in mean arterial pressure produced by intravenous phenylephrine and sodium nitroprusside, respectively. The pressor effects of ANG-(1–7) and ANG II (25 pmol) after RVLM microinjection (11 ± 0.8 and 10 ± 2 mmHg, respectively) were not accompanied by consistent changes in HR. In addition, RVLM microinjection of these angiotensin peptides did not alter the bradycardic or tachycardic component of the baroreflex. CVLM microinjections of ANG-(1–7) and ANG II produced hypotension (−11 ± 1.5 and −11 ± 1.9 mmHg, respectively) that was similarly not accompanied by significant changes in HR. However, CVLM microinjections of angiotensins induced differential changes in the baroreflex control of HR. ANG-(1–7) attenuated the baroreflex bradycardia (0.26 ± 0.06 ms/mmHg vs. 0.42 ± 0.08 ms/mmHg before treatment) and facilitated the baroreflex tachycardia (0.86 ± 0.19 ms/mmHg vs. 0.42 ± 0.10 ms/mmHg before treatment); ANG II produced the opposite effect, attenuating baroreflex tachycardia (0.09 ± 0.06 ms/mmHg vs. 0.31 ± 0.07 ms/mmHg before treatment) and facilitating the baroreflex bradycardia (0.67 ± 0.16 ms/mmHg vs. 0.41 ± 0.05 ms/mmHg before treatment). The modulatory effect of ANG II and ANG-(1–7) on baroreflex sensitivity was completely abolished by peripheral administration of methylatropine. These results suggest that ANG II and ANG-(1–7) at the CVLM produce a differential modulation of the baroreflex control of HR, probably through distinct effects on the parasympathetic drive to the heart.

Step baroreflex response in awake patients undergoing carotid surgery: time- and frequency-domain analysis

1998 ◽  
Vol 274 (5) ◽  
pp. H1590-H1597 ◽  
Author(s):  
Giora Landesberg ◽  
Dan Adam ◽  
Yacov Berlatzky ◽  
Solange Akselrod
Keyword(s):  
Control Mechanism ◽  
Time Window ◽  
Power Spectra ◽  
Frequency Domain Analysis ◽  
Atheromatous Plaque ◽  
Carotid Surgery ◽  
Baroreflex Control ◽  
Baroreceptor Stimulation ◽  
Before And After ◽  
Blood Pressures

Step baroreceptor stimulation can provide an insight into the baroreflex control mechanism, yet this has never been done in humans. During carotid surgery under regional anesthesia, a step increase in baroreceptor stimulation occurs at carotid declamping immediately after removal of the intra-arterial atheromatous plaque. In 10 patients, the R-R interval and systolic and diastolic blood pressures (BP) were continuously recorded, and signals obtained within the time window from 10 min before until 10 min after carotid declamping were analyzed. Mean ± SD time signals, power spectra, and transfer and coherence functions before and after declamping were calculated. Immediately after carotid declamping, both heart rate (HR) and BP declined in an exponential-like manner lasting 10.3 ± 5.9 min, and their power spectra increased in the entire frequency range. Transfer function magnitude and coherence functions between BP and HR increased predominantly in the midfrequency region (∼0.1 Hz), with no change in phase function. Thus, in carotid endarterectomy patients, step increase in baroreceptor gain elicits a prolonged decline in HR and BP. Frequency analyses support the notion that the baroreflex control mechanism generates the midfrequency HR and BP variability, although other frequency regions are also affected.

scholarly journals Computational Modelling of the Role of Atrial Fibrillation on Cerebral Blood Perfusion.

2021 ◽  
Author(s):  
Timothy Hunter ◽  
Jermiah Joseph ◽  
Sanjay R Kharche ◽  
Daniel Goldman
Keyword(s):  
Atrial Fibrillation ◽  
Cerebral Perfusion ◽  
Control Mechanism ◽  
Computational Modelling ◽  
Blood Perfusion ◽  
Whole Body ◽  
Baroreflex Control ◽  
Computational Work ◽  
The Impact

Atrial fibrillation is a prevalent cardiac arrhythmia, and may reduce cerebral blood perfusion augmenting the risk of dementia. It is thought that cer- ebral arterial geometry variants play an important role in cerebral perfusion. This computational work investigated the role of geometric variants on cerebral blood flow in the presence of cardiac atrial fibrillation.A model consisting of a detailed cerebral and whole-body circulation, along with baroreflex control mechanism was developed. Cerebral perfusion based on vasculature geometry variations, represented by Circle of Willis variants, was simulated in the presence of atrial fibrillation conditions. Perfusion and its heter- ogeneity were quantified using segment-wise hypoperfusion events and mean perfusion at terminals.It was found that cerebral perfusion and the rate of hypoperfusion events strongly depends geometry variation as well as atrial fibrillation induced stochas- tic heart rates. The hypoperfusion events were specific to particular arteries in each variant. Our results, based on biophysical principles, suggest that cerebral vascular geometries modulate the impact of atrial fibrillation in cerebral perfu- sion. Further, our findings suggest potential clinical assessment sites.

scholarly journals Integration of the baroreflex control mechanism in a heterogeneous model of the cardiovascular system

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Luciano Gonçalves Fernandes ◽  
Paulo Roberto Trenhago ◽  
Pablo Javier Blanco ◽  
Raúl A Feijóo
Keyword(s):  
Cardiovascular System ◽  
Control Mechanism ◽  
Baroreflex Control ◽  
Heterogeneous Model

Baroreflex Setting and Sensitivity after Acute and Chronic Nicardipine Therapy

1984 ◽  
Vol 66 (2) ◽  
pp. 233-235 ◽  
Author(s):  
M. A. Young ◽  
R. D. S. Watson ◽  
W. A. Littler
Keyword(s):  
Heart Rate ◽  
Acute Treatment ◽  
Baroreflex Sensitivity ◽  
Chronic Treatment ◽  
Control Mechanism ◽  
Control Period ◽  
Significant Shift ◽  
Baroreflex Control ◽  
Set Point ◽  
Arterial Blood

1. Intra-arterial pressure, baroreflex sensitivity and the baroreflex set point were measured in eight patients with essential hypertension during a control period and then after acute treatment (2 h after a 30 mg oral dose) and after chronic treatment (at least 2 months) with nicardipine hydrochloride, a calcium channel antagonist. 2. Mean intra-arterial blood pressure fell after the acute treatment from 130 ± 14 (sd) control to 118 ± 11 mmHg, P<0.05, and after chronic treatment to 112 ± 19 mmHg, P<0.05. Heart rate increased from 72 ± 11 control to 81 ± 16 beats/min, P<0.05, during acute treatment indicating activation of the baroreflex control mechanism, but returned to control values with chronic treatment (72 ± 11 control vs 69 ± 9 beats/min chronic), indicating a significant shift to the left of the baroreflex set point. There was no change in baroreflex sensitivity after either acute or chronic treatment (control 4.7, acute 4.3, chronic 5.1 ms/mmHg, P not significant for all values). 3. Nicardipine significantly reduces mean intraarterial pressure both acutely and chronically; the latter is associated with a return of the heart rate to control values due to resetting of the baroreflex control mechanism.

Role of the Cilia Membrane in Control of Microtubule Sliding

1980 ◽  
Vol 38 ◽  
pp. 612-615
Author(s):  
Edna S. Kaneshiro
Keyword(s):  
Control Mechanism ◽  
Beat Frequency ◽  
Surface Membrane ◽  
Ciliary Membrane ◽  
Ciliary Beating ◽  
Ciliary Reversal ◽  
Voltage Dependent ◽  
Reversal Mechanism ◽  
And Function

It is currently believed that ciliary beating results from microtubule sliding which is restricted in regions to cause bending. Cilia beat can be modified to bring about changes in beat frequency, cessation of beat and reversal in beat direction. In ciliated protozoans these modifications which determine swimming behavior have been shown to be related to intracellular (intraciliary) Ca2+ concentrations. The Ca2+ levels are in turn governed by the surface ciliary membrane which exhibits increased Ca2+ conductance (permeability) in response to depolarization. Mutants with altered behaviors have been isolated. Pawn mutants fail to exhibit reversal of the effective stroke of ciliary beat and therefore cannot swim backward. They lack the increased inward Ca2+ current in response to depolarizing stimuli. Both normal and pawn Paramecium made leaky to Ca2+ by Triton extrac¬tion of the surface membrane exhibit backward swimming only in reactivating solutions containing greater than IO-6 M Ca2+ Thus in pawns the ciliary reversal mechanism itself is left operational and only the control mechanism at the membrane is affected. The topographic location of voltage-dependent Ca2+ channels has been identified as a component of the ciliary mem¬brane since the inward Ca2+ conductance response is eliminated by deciliation and the return of the response occurs during cilia regeneration. Since the ciliary membrane has been impli¬cated in the control of Ca2+ levels in the cilium and therefore is the site of at least one kind of control of microtubule sliding, we have focused our attention on understanding the structure and function of the membrane.

Self-Damping Mechanism in Blood Coagulation

1974 ◽  
Vol 32 (01) ◽  
pp. 057-064 ◽  
Author(s):  
Y Nemerson ◽  
S.A Silverberg ◽  
J Jesty
Keyword(s):  
Tissue Factor ◽  
Blood Coagulation ◽  
Calcium Ions ◽  
Control Mechanism ◽  
Factor Vii ◽  
Damping Factor ◽  
Factor V ◽  
Factor X ◽  
Extrinsic Pathway ◽  
Two Systems

SummaryTwo reactions of the extrinsic pathway of coagulation, the activations of Factor X and prothrombin, have been studied in purified systems and shown to be self-damping. Factor X was activated by the tissue factor - Factor VII complex, and prothrombin by two systems: the coagulant protein of Taipan venom, and the physiological complex of activated Factor X, Factor V, lipid, and calcium ions. In each case the yield of enzyme, activated Factor X or thrombin, is a function of the concentration of activator. These and other observations are considered as a basis for a control mechanism in coagulation.

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