Baroreflex Regulation of Blood Pressure

Jul 7, 2020, 08:49 AM by Sara Kruper

Baroreflex is the fastest mechanism to regulate acute blood pressure changes by controlling heart rate, contractility, and peripheral resistance.  Baroreceptors are mechanoreceptors located in the carotid sinus and aortic arch.  Their function is to sense pressure changes by responding to variations in tension of the arterial wall.  The baroreflex or baroreceptor sensitivity (BRS) index quantifies how much control the baroreflex has on the heart rate.  BRS can be valuable in assessing the development and progression of various diseases. Reduced BRS can indicate:

•   Neurological Disorders
•   Hypertension
•   Coronary Artery Disease
•   Myocardial Infarction (MI)
•   Heart Failure
•   End-organ Damage
•   Progression of Underlying Disease


BRS requires beat-to-beat information from both blood pressure and R-R interval. Systolic blood pressure is typically derived from systemic arterial pressure, whereas the R-R interval is derived from ECG.  The spectral analysis method to assess baroreceptor sensitivity outputs the gain and phase of the transfer function.  Gain corresponds to the effectiveness with which the baroreflex can maintain constant conditions.  Phase is the time lag between systolic blood pressure and R-R.


Publications Citing Use of DSI Technology To Study Baroreflex and Hypertension

Sleep-Related Changes in Cardiovascular Neural Regulation in Spontaneously Hypertensive Rats

This study examined variation in baroreflex sensitivity and sympathetic vasomotor activity related to spontaneous hypertension throughout sleep-wake cycles in rats.  The research team measured EEG, EMG, and ECG (R-R interval) using a tethered approach and mean arterial blood pressure using DSI implantable telemetry.  Spontaneous baroreflex sensitivity was evaluated by MAP-RR transfer function and MAP-RR linear regression.  This study confirmed previous animal and human studies, showing normotensive rats experience augmentation of baroreflex during sleep while spontaneously hypertensive rats do not.  Understanding why SHR rats are not able to augment baroreflex in sleep will require further studies.1

Resetting of the sympathetic baroreflex is associated with the onset of hypertension during chronic intermittent hypoxia

As chronic intermittent hypoxia (CIH) is associated with sleep apnea and increased resting arterial blood pressure, this research team studied the impact of exposing rats to CIH for seven days on arterial baroreflex control of renal sympathetic nerve activity and heart rate.  They used DSI implantable telemetry and software to collect and analyze mean arterial pressure, heart rate, and respiratory frequency before and after CIH exposure.  Spontaneous baroreflex sensitivity was calculated using an averaged slope of the linear regression between systolic AP and subsequent pulse interval pairs.  The study’s results indicate resetting of the sympathetic baroreflex control, rather impairing its sensitivity, may play a role in the onset of hypertension induced by CIH.2

Raised arterial blood pressure in neurokinin‐1 receptor‐deficient mice (NK1R −/−): evidence for a neural rather than a vascular mechanism

Ablation of the neurokinin‐1 receptor gene, Tacr1 , (NK1R −/−) is known to cause behavioral abnormalities as seen in attention deficit hyperactivity disorder (ADHD).  The spontaneously hypertensive rat is an established model for ADHD and has increased central sympathetic drive leading to high blood pressure.  This research team explored the effect of ablation on blood pressure levels.  They used DSI telemetry to measure systolic and diastolic blood pressure, heart rate, and locomotor activity.  They also calculated heart rate variability in the frequency and time domain using R-R intervals detected from the blood pressure signals.  The telemetry data was imported into a third-party analysis software to calculate baroreflex sensitivity.  As mice with ablation of Tacr1 experience increased mean arterial blood pressure, the study’s results indicate a role for neurokinin‐1 receptors in neural regulation of blood pressure.3


Solutions for Baroreflex and Hypertension Research

DSI offers a variety of solutions for measuring physiologic endpoints including blood pressure, ECG, EEG, EMG, blood glucose, temperature, activity, and more.  Implantable telemetry provides high quality data while reducing stress and the number of animals required in a study.  Researchers can collect continuous, chronic or acute, data from conscious freely moving animals.  DSI also offers non-invasive jacketed external telemetry (JET) which enables acute measurement of blood pressure, ECG, and respiration.  In addition, hardwired or tethered approaches are available for measurement of ECG, EEG, and EMG.

Ponemah is a high-powered acquisition and analysis software platform capable of collecting data from all the methods mentioned above.  It also enables calculation of more advanced biomarkers including heart rate variability.


For more information on how to calculate advanced cardiovascular biomarkers, download our free whitepaper or schedule a call with us at your convenience. Also, if you are attending the 2020 virtual AHA Hypertension meeting, make sure to visit our page!



1Kuo T, Yang C. (2005). “Sleep-Related Changes in Cardiovascular Neural Regulation in Spontaneously Hypertensive Rats”. Circulation. 112(6); 849-854.

2Yamamoto K, Eubank W, Franzke M, Mifflin S. (2012). “Resetting of the sympathetic baroreflex is associated with the onset of hypertension during chronic intermittent hypoxia”. Autonomic neuroscience : basic & clinical. 173(1-2); 22-7.

3Moyes AJ,  Stanford SC, Hosford PS, Hobbs AJ, Ramage AG. (2016). “Raised arterial blood pressure in neurokinin‐1 receptor‐deficient mice (NK1R −/−): evidence for a neural rather than a vascular mechanism”. Experimental Physiology, 588-598.


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