Quantification of Mechanical and Neural Components of Vagal Baroreflex in Humans

Abstract

Abstract-Traditionally, arterial baroreflex control of vagal neural outflow is quantified by heart period responses to falling and/or rising arterial pressures (ms/mm Hg). However, it is arterial pressure-dependent stretch of barosensory vessels that determines afferent baroreceptor responses, which, in turn, generate appropriate efferent cardiac vagal outflow. Thus, mechanical transduction of pressure into barosensory vessel stretch and neural transduction of stretch into vagal outflow are key steps in baroreflex regulation that determine the conventional integrated input-output relation. We developed a novel technique for direct estimation of gain in both mechanical and neural components of integrated cardiac vagal baroreflex control. Concurrent, beat-by-beat measures of arterial pressures (Finapres), carotid diameters (B-mode ultrasonography), and R-R intervals (ECG lead II) were made during bolus vasoactive drug infusions (modified Oxford technique) in 16 healthy humans. The systolic carotid diameter/pressure relationship (r 2 ϭ0.79Ϯ0.008, meanϮSEM) provided a gain estimate of dynamic mechanical transduction of pressure into a baroreflex stimulus. The R-R interval/systolic diameter relationship (r 2 ϭ0.77Ϯ0.009) provided a gain estimate of afferent-efferent neural transduction of baroreflex stimulus into a vagal response. Variance between repeated measures for both estimates was no different than that for standard gain (PϾ0.40). Moreover, in these subjects, the simple product of the 2 estimates almost equaled standard baroreflex gain (ms/mm Hgϭ0.98xϩ2.27; r 2 ϭ0.93, Pϭ0.001). This technique provides reliable information on key baroreflex components not distinguished by standard assessments and gives insight to dynamic mechanical and neural events during acute changes in arterial pressure. Key Words: arterial pressure Ⅲ carotid arteries Ⅲ ultrasonography D epressed baroreflex sensitivity is associated with hypertension, 1 heart disease, 2 diabetes, and other pathophysiological states, 3 attesting that appropriate baroreflex regulation of autonomic outflow is crucial to maintenance of cardiovascular health and homeostasis. Traditionally, cardiac-vagal baroreflex sensitivity or gain has been quantified by the magnitude of heart period responses to falling and/or rising arterial pressure (ie, ⌬ R-R interval/⌬ systolic pressure). 4 This estimate represents an integrated input-output relation and provides broad insight to baroreflex function. However, it has long been recognized that baroreceptors respond to deformation not pressure per se. Early in the last century, Sollman and Brown 5 reported that stretch of the carotid artery produces bradycardia and hypotension in dogs. Similar reflex responses in humans derive from proportionalities between changes in carotid diameter and carotid nerve firing 6 and between the R-R interval and the frequency of afferent carotid sinus nerve activation. 7 Thus, mechanical transduction of arterial pressure into carotid stretch and neural transduction of carotid stretch into vaga...

Does Reduced Vascular Stiffening Fully Explain Preserved Cardiovagal Baroreflex Function in Older, Physically Active Men?

“…11 This technique, when properly applied, provides robust linear gain estimates of the mechanical and neural baroreflex components. Importantly, our estimates are unaffected by set-point differences that can produce erroneous differences in gain.…”

“…3 This allows an estimation of the mechanical transduction of pressure into barosensory stretch (⌬diameter/⌬pressure), the neural transduction of stretch into vagal outflow (⌬R-R interval/⌬diameter), and conventional integrated cardiovagal baroreflex gain (⌬R-R interval/⌬pressure). 11 To compare our dynamic mechanical transduction with the static index previously reported, 1 we calculated pulsatile carotid vascular stiffness. From 1 minute of beat-by-beat data before each of 3 cardiovagal baroreflex tests, we derived stiffness [log (systolic pressure/ diastolic pressure)/(pulsatile diameter/diastolic diameter)].…”

“…10 We determined the impact of altered carotid stiffness with age and habitual physical activity on baroreflex function using our recently developed, novel approach to quantify vascular and neural components during dynamic baroreflex engagement. 11 Concurrent beat-by-beat arterial pressures, carotid diameters, and R-R intervals during vasoactive drug infusions provide insight into key steps of cardiovagal baroreflex regulation: mechanical transduction of pressure into barosensory vessel stretch and neural transduction of stretch into vagal outflow. On the basis of previous observations, 1 we hypothesized that lower cardiovagal baroreflex gain in older untrained men would most strongly relate to reduced mechanical transduction.…”

Maturation of Cardiovagal Autonomic Function From Childhood to Young Adult Age

“…11 Baroreceptors are stretch-sensitive receptors embedded in the barosensory vessel wall, and their response to pressure-induced stretch is importantly determined by the compliance of the vessel wall. 12 A relation between BRS and carotid distensibility has been shown in healthy subjects and in hypertensive patients.…”

The Role of Ultrasonography in the Assessment of Arterial Baroreflex Function

“…Therefore, the transduction of blood pressure into barosensory stretch, and the consequent transduction of barosensory stretch into efferent parasympathetic and sympathetic neural outflow are critical steps that determine the integrated baroreflex response. The major contribution of vascular ultrasound imaging to baroreflex research has been the enabling of these critical components of the integrated baroreflex arc to be studied separately and noninvasively in humans through the use of B and M-mode imaging processes 15 .…”