Short-term Regulation Of Arterial Pressure Research Articles

Lowering of blood pressure by chronic suppression of central sympathetic outflow: insight from prolonged baroreflex activation

Device-based therapy for resistant hypertension by electrical activation of the carotid baroreflex is currently undergoing active clinical investigation, and initial findings from clinical trials have been published. The purpose of this mini-review is to summarize the experimental studies that have provided a conceptual understanding of the mechanisms that account for the long-term lowering of arterial pressure with baroreflex activation. The well established mechanisms mediating the role of the baroreflex in short-term regulation of arterial pressure by rapid changes in peripheral resistance and cardiac function are often extended to long-term pressure control, and the more sluggish actions of the baroreflex on renal excretory function are often not taken into consideration. However, because clinical, experimental, and theoretical evidence indicates that the kidneys play a dominant role in long-term control of arterial pressure, this review focuses on the mechanisms that link baroreflex-mediated reductions in central sympathetic outflow with increases in renal excretory function that lead to sustained reductions in arterial pressure.

Baroreflex Function: Determinants in Healthy Subjects and Disturbances in Diabetes, Obesity and Metabolic Syndrome

Arterial baroreceptors play an important role in the short-term regulation of arterial pressure, by reflex chronotropic effect on the heart and by reflex regulation of sympathetic outflow. Baroreflex sensitivity (BRS) represents an index of arterial baroreceptors function. Several methods of measuring BRS are available nowadays. Different factors influence BRS in the healthy population, including sex, age, blood pressure, heart rate, body fatness, arterial stiffness, blood glucose and insulin levels, as well as physical activity. Baroreceptors dysfunction is evident in diseases such as coronary artery disease, heart failure, arterial hypertension, diabetes mellitus and obesity. The underlying mechanism of BRS attenuation in diabetes or obesity is not yet well known; however, there is increasing evidence that it is at least partly related to autonomic nervous system dysfunction and particularly to sympathetic overactivity that accompanies these diseases. Blunted BRS provides prognostic information for cardiovascular diseases and possibly for diabetes, while its' prognostic information for obesity is not yet established. This review deals with the mechanisms affecting baroreflex function, the newer techniques of BRS estimation and the most recent insights of baroreflex function in the healthy population and in various diseases with emphasis on diabetes and obesity. In addition, the clinical implication of a reduced BRS in these disorders is discussed.

In vivo gene transfer to dissect neuronal mechanisms regulating cardiorespiratory function.

This lecture reviews recent information from our laboratory regarding brainstem mechanisms regulating the arterial baroreceptor reflex. Our long-term goal is to understand some of the mechanisms involved in the etiology of essential hypertension. Our hypothesis is that this problem may arise, in part, because of changes within brainstem circuits controlling arterial pressure, and in particular to occlusion of baroreceptive information at the level of the primary afferent relay within the brainstem. Although it is established that baroreceptors provide a mechanism for short-term regulation of arterial pressure, there is convincing evidence that they also play a role in its long-term control (see Thrasher 2002, for an example). It follows that dysfunction of this reflex circuit could contribute to high blood pressure levels. Here, we discuss the central actions of angiotensin II on the baroreceptor reflex circuitry within the nucleus of the solitary tract (NTS) for arterial pressure control. Our findings have led us to hypothesize a novel form of intercellular communication within the NTS, one of vascular-neuronal signaling.

Simulation study of the cardiovascular functional status in hypertensive situation

An extended cardiovascular model was established based on our previous work to study the consequences of physiological or pathological changes to the homeostatic functions of the cardiovascular system. To study hemodynamic changes in hypertensive situations, the impacts of cardiovascular parameter variations (peripheral vascular resistance, arterial vessel wall stiffness and baroreflex gain) upon hemodynamics and the short-term regulation of the cardiovascular system were investigated. For the purpose of analyzing baroregulation function, the short-term regulation of arterial pressure in response to moderate dynamic exercise for normotensive and hypertensive cases was studied through computer simulation and clinical experiments. The simulation results agree well with clinical data. The results of this work suggest that the model presented in this paper provides a useful tool to investigate the functional status of cardiovascular system in normal or pathological conditions.

Computer simulation of the baroregulation in response to moderate dynamic exercise.

A baroregulation model, based on a previous pulsatile non-linear multielement cardiovascular model, is extended and used to study short-term regulation mechanisms. Using this model, the responses of several cardiovascular variables to different exercise levels are simulated and compared with the experimental data reported in the literature. The impact of physiological or pathological changes on the short-term regulation of arterial pressure under the stimulus of moderate dynamic exercise is then studied. The simulation results indicate that baroreflex feedback plays a critical role in the short-term regulation of arterial pressure. When the baroreflex gain decreases to one-third of the normal value, the response of the mean arterial pressure to moderate dynamic exercise and post-exercise recovery time increases by factors of 1.7 and 2.3, respectively. Clinical data from 36 subjects (two groups: normal and hypertensive) are collected to validate the model. Computer simulations for the hypertensive group show that the elastic modulus of the arterial vessel wall is increased by 1.5 times, and peripheral resistance is increased by 1.3 times the normal value, and the baroreflex gain decreases from 0.55 (for the normal group) to 0.40. The simulation results for normal and hypertensive groups agree well with the clinical data.

Mechanisms of heart rate and arterial blood pressure control: implications for the pathophysiology of neurocardiogenic syncope.

Neurocardiogenic syncope is a general term that describes syncope resulting from altered autonomic activity, as manifested by abnormal regulation of peripheral vascular resistance and heart rate. Although there has been great interest in the contribution of heart rate to this form of syncope, the peripheral circulation plays the dominant role in the induction of neurocardiogenic syncope in most patients. We review in this brief article the physiology of cardiovascular reflexes, which are important for short-term arterial pressure control, and their potential contribution to the pathophysiology of neurocardiogenic syncope. This type of syncope represents a profound failure of the normal mechanisms for short-term regulation of arterial pressure. Any therapeutic strategies for the management of neurocardiogenic syncope must deal with alterations in vascular control, which contribute to its pathogenesis.

Hormonal-sympathetic interactions in long-term regulation of arterial pressure: an hypothesis.

The importance of the sympathetic nervous system in short-term regulation of arterial pressure is well accepted. However, the question of whether neural systems participate in long-term control of pressure has been debated for decades and remains unresolved. The principal argument against such a control system is that arterial baroreceptors adapt to sustained changes in arterial pressure. In addition, denervation of baroreceptors has minimal to no effect on basal levels of arterial pressure chronically. This argument assumes, however, that baroreceptors provide the primary chronic feedback signal to the central nervous system. An alternate model is proposed in which circulating hormones, primarily arginine vasopressin and angiotensin II, provide a long-term afferent signal to the central nervous system via binding to specific receptors in central sites lacking a blood-brain barrier (circumventricular organs). Studies suggest that the release of the hormones and the sympathetic response to alterations in their plasma concentrations are nonadaptive but may be gated by baroreceptor input. Evidence that this "hormonal-sympathetic reflex" model may explain the long-term alterations in sympathetic activity in response to chronic salt depletion and salt loading as well as congestive heart failure is presented. Finally, the role of an impaired hormonal sympathetic reflex in hypertension, specifically salt-dependent hypertension, is discussed.

Short-term regulation of arterial pressure and the calculation of open-loop gain in the intact anesthetized dog.

Open-loop gain of the short-term systemic pressure regulation was determined under closed-loop conditions in the closed chest anesthetized dog (n = 5). For this purpose, cardiac output and mean systemic pressure were varied by ventricular pacing after the production of complete heart block. From the pressure-flow data resistance gain (the ratio of peripheral resistance change to pressure change in the steady state) was obtained by means of a simple model. The value of this gain was automatically estimated by fitting the pressure-flow relation described by the model to the experimental data. The model allows the pressure-flow relation to be straight or curved with or without a zero-flow pressure intercept. The best fit was obtained when the pressure-flow curve was convex to the pressure axis and had no intercept. When the model was linearized about the control values of pressure and flow (operating point), open-loop gain could be calculated from resistance gain. Its averaged value in the control condition, 1.63 +/- 0.45, is in agreement with values found by other investigators in open-loop conditions. During vasoconstriction open-loop gain, at the (new) operating point, increased to 2.51 +/- 0.51; during vasodilation it decreased to 1.17 +/- 0.27. Open-loop gain about an operating point thus can be determined in the intact animal from measurements of mean pressure and mean flow in the steady state.

Dynamic model of the short-term regulation of arterial pressure in the cat

Dynamic model of the short-term regulation of arterial pressure in the cat

Dynamics of the short-term regulation of arterial pressure: frequency dependence and role of arterial compliance.

The purpose of this study was to investigate the role of the interaction between peripheral resistance regulation and arterial compliance in the overall short-term regulation of mean arterial pressure. A nonlinear model previously proposed was linearised about control values of mean arterial pressure and cardiac output so that it could be reformulated in terms of transfer functions. The resulting pressure to pressure open-loop transfer function H(s) consists of a complex conjugate pair of poles (pertaining to the resistance regulating system) and a real pole (pertaining to the arterial system, 1/(R0 C), R0=control resistance). Such a structure suggests an interaction between the resistance regulation and the arterial compliance (C). Quantitative evaluation of this interaction was obtained by estimating the model parameters during partial vena cava occlusions in four cats. Using these parameters the time response of the open-loop control system to a pressure step was found to be underdamped and oscillatory in all four cats (damping factor ξ ranged from 0·20 to 0·66), the amplitude of oscillations depending on the value of ξ and on the relative amplitude of the arterial time constant (compliance and peripheral resistance) with respect to the time constant 1/(ξωn). Bode diagrams of H(jω) showed that the resonance peak due to the resistance regulating system may not be detectable, either because of the relatively high value of ξ or because it is masked by the pole of the arterial system.

Dynamic model of the short-term regulation of arterial pressure in the cat.

The purpose of this study was to characterise the dynamics of the short-term control of arterial pressure in the cat with the aid of a model consisting of a nonlinear negative-feedback control system. The arterial system was described by a three element windkessel model (peripheral resistance, R, aortic characteristic impedance, Rc, and total arterial compliance, C). The resistance regulation was represented by a second-order system with static gain GR, a damping factor σ and an undamped natural frequency ωn. The resistance gain, GR, and the windkessel parameters were obtained from measurements of aortic and venous pressures and cardiac output in two steady states. The parameters σ and ωn were estimated from mean pressure and mean flow during the transient from control to the new steady state. Pressure reductions averaged 10 per cent and resistance changes averaged 12 per cent. Average windkessel model parameters in the control condition were: C=(25·9±6·1) 10−6 g−1 cm4 s2, Rc=(2·51±0·53) 103 g cm−4 s−1, R=(40·9±9·8) 103 g cm−4 s−1. Average estimates of parameters of the resistance regulator were: GR=(4·14±2·38) 10−3 min ml−1, ωn = 1·0 ± 1·0 rad s−1, σ=0·41±0·19. A satisfactory fit was found between model predicted and measured pressure. The results suggest that the dynamic short-term control of pressure is underdamped and oscillatory. The amplitude of these oscillations is affected by arterial compliance, suggesting an interaction between the arterial system and short-term resistance regulation.

Vasopressin Vascular and Reflex Effects–A Theoretical Analysis

Publisher Summary This chapter describes the role of vasopressin (AVP) in cardiovascular function and presents evidence for the (1) participation of AVP in the short-term regulation of arterial pressure by its direct vascular actions and (2) AVP interaction with the central nervous system baroreceptor reflex pathways. The chapter suggests that most of the arterial pressure regulation with AVP infusion can be explained by reflex control of venous compliance or unstressed volume. The extent to which cardiac output is altered by AVP is dependent on the relative degree of arterial vasoconstriction between the compliant and non-compliant parallel flow beds. However, not all of the observed actions of AVP are accounted for, particularly, the predicted rise in total peripheral resistance (TPR) is less than that seen in normal animals with comparable AVP concentrations. It appears that some mechanism exists, whereby the reflex buffering of arterial resistance with AVP infusion is attenuated so that TPR rises to a higher level than would be predicted if the baroreceptors are attempting to offset the rise in resistance. While, equations are found, which could predict such behavior, they differ significantly from the classical single set point control theory and go beyond the present understanding of the autonomic nervous system.