Carotid Baroreceptor Stimulation
Baroreflex activation through electrical carotid sinus stimulation has been developed for resistant arterial hypertension and heart failure management. Electrical carotid sinus stimulation lowered blood pressure in various hypertensive animal models and i
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Jens Jordan, Jens Tank, and Hannes Reuter
23.1 Physiological Rational for Baroreflex Modulation Baroreceptors located in carotid artery and aortic walls sense changed vascular stretch elicited by blood pressure fluctuations. An increase in blood pressure raises baroreceptor output, while blood pressure reductions elicit the opposite response. The signal generated in baroreceptors is conveyed through afferent baroreflex fibers to cardiovascular control centers in the brain stem where it is integrated with information from other afferent inputs and brain regions. An example for the complex integration of afferent signals is the mutual inhibitory interaction between arterial baroreflex and peripheral chemoreflex responses [1]. Then, counter-regulatory adjustments in sympathetic and parasympathetic activity and, less recognized, vasopressin release help in stabilizing blood pressure. Indeed, vasopressin release appears to be an important backup mechanism when sympathetic nervous system and renin–angiotensin system fail to maintain blood pressure [2, 3]. Afferent baroreflex stimulation be it through electrical stimulation or mechanical means could attenuate sympathetic activity and vasopressin release while augmenting cardiac parasympathetic drive in patients with hypertension or with heart failure. Indeed, direct electrical stimulation of baroreflex afferents in patients acutely attenuated efferent sympathetic activity and blood pressure [4]. However, such treatment J. Jordan (*) · J. Tank Institute of Aerospace Medicine, German Aerospace Center (DLR) and Chair of Aerospace Medicine, University of Cologne, Cologne, Germany e-mail: [email protected]; [email protected] H. Reuter Department for Cardiology, Angiology, Pneumology and Intensive Care Medicine, University of Cologne, Cologne, Germany Department of Cardiology and Intensive Care Medicine, Ev. Krankenhaus Köln-Weyertal, Cologne, Germany e-mail: [email protected] © Springer Nature Switzerland AG 2019 M. Dorobantu et al. (eds.), Hypertension and Heart Failure, Updates in Hypertension and Cardiovascular Protection, https://doi.org/10.1007/978-3-319-93320-7_23
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would require that baroreflexes contribute to long-term cardiovascular control. No doubt, baroreflex mechanisms have a central role in short-term blood pressure maintenance. Loss of sympathetic efferents in autonomic failure patients is associated with profound orthostatic and postprandial hypotension [5]. Conversely, afferent baroreflex failure is associated with volatile hypertension [6, 7]. Yet, following experiments in dogs in whom baroreflex afferents were severed, leading physiologists argued that the baroreflex does not contribute to long-term blood pressure control [8]. These experiments were conducted in animals with minimal sensory input, which strongly affects autonomic tone and blood pressure in the absence of baroreflex restraint [6]. Others showed that interrupting afferent baroreflex input can induce sustained neurogenic arterial hypertension in rats [9
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