Open-loop static and dynamic characteristics of the arterial baroreflex system in rabbits and rats

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Abstract

The arterial baroreflex system is the most important negative feedback system for stabilizing arterial pressure (AP). This system serves as a key link between the autonomic nervous system and the cardiovascular system, and is thus essential for understanding the pathophysiology of cardiovascular diseases and accompanying autonomic abnormalities. This article focuses on an open-loop systems analysis using a baroreceptor isolation preparation to identify the characteristics of two principal subsystems of the arterial baroreflex system, namely, the neural arc from pressure input to efferent sympathetic nerve activity (SNA) and the peripheral arc from SNA to AP. Studies on the static and dynamic characteristics of the two arcs under normal physiological conditions and also under various interventions including diseased conditions are to be reviewed. Quantitative understanding of the arterial baroreflex function under diseased conditions would help develop new treatment strategies such as electrical activation of the carotid sinus baroreflex for drug-resistant hypertension.

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Vagal nerve stimulation markedly improves long-term survival after chronic heart failure in rats.

Meihua Li, Can Zheng, Takayuki Sato … (2004)

Diminished cardiac vagal activity and higher heart rate predict a high mortality rate of chronic heart failure (CHF) after myocardial infarction. We investigated the effects of chronic electrical stimulation of the vagus nerve on cardiac remodeling and long-term survival in an animal model of CHF after large myocardial infarction. Two weeks after the ligation of the left coronary artery, surviving rats were randomized to vagal- and sham-stimulated groups. Using an implantable miniature radio-controlled electrical stimulator, we stimulated the right vagal nerve of CHF rats for 6 weeks. The intensity of electrical stimulation was adjusted for each rat, so that the heart rate was lowered by 20 to 30 beats per minute. The treated rats had significantly lower left ventricular end-diastolic pressure (17.1+/-5.9 versus 23.5+/-4.2 mm Hg, P<0.05) and higher maximum dp/dt of left ventricular pressure (4152+/-237 versus 2987+/-192 mm Hg/s, P<0.05) than the untreated rats. Improvement of cardiac pumping function was accompanied by a decrease in normalized biventricular weight (2.75+/-0.25 versus 3.14+/-0.22 g/kg, P<0.01). Although the 140-day survival of the untreated group was only half, vagal stimulation markedly improved the survival rate (86% versus 50%, P=0.008). Vagal stimulation therapy achieved a 73% reduction in a relative risk ratio of death. Vagal nerve stimulation markedly improved the long-term survival of CHF rats through the prevention of pumping failure and cardiac remodeling.

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Interactions between ANG II, sympathetic nervous system, and baroreceptor reflexes in regulation of blood pressure.

I. D. Reid (1992)

The renin-angiotensin system plays an important role in the regulation of arterial blood pressure and in the development of some forms of clinical and experimental hypertension. It is an important blood pressure control system in its own right but also interacts extensively with other blood pressure control systems, including the sympathetic nervous system and the baroreceptor reflexes. Angiotensin (ANG) II exerts several actions on the sympathetic nervous system. These include a central action to increase sympathetic outflow, stimulatory effects on sympathetic ganglia and the adrenal medulla, and actions at sympathetic nerve endings that serve to facilitate sympathetic neurotransmission. ANG II also interacts with baroreceptor reflexes. For example, it acts centrally to modulate the baroreflex control of heart rate, and this accounts for its ability to increase blood pressure without causing a reflex bradycardia. The physiological significance of these actions of ANG II is not fully understood. Most evidence indicates that the actions of ANG to enhance sympathetic activity do not contribute significantly to the pressor response to exogenous ANG II. On the other hand, there is considerable evidence that the actions of endogenous ANG II on the sympathetic nervous system enhance the cardiovascular responses elicited by activation of the sympathetic nervous system.

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Increased reactive oxygen species in rostral ventrolateral medulla contribute to neural mechanisms of hypertension in stroke-prone spontaneously hypertensive rats.

Takuya Kishi, Yoshitaka Hirooka, Yoshikuni Kimura … (2004)

Oxidative stress increases in hypertension. The aim of this study was to determine whether reactive oxygen species (ROS) are increased in the rostral ventrolateral medulla (RVLM) in the brainstem, where the vasomotor center is located, in stroke-prone spontaneously hypertensive rats (SHRSP), and, if so, to determine whether the increased ROS contribute to neural mechanisms of hypertension in SHRSP. We measured ROS levels in the RVLM of SHRSP and compared them with those in Wistar-Kyoto rats (WKY). Thiobarbituric acid-reactive substances were increased in SHRSP compared with WKY. ROS were measured by electron spin resonance (ESR) spectroscopy. The ESR signal decay rate in the RVLM of SHRSP was significantly increased compared with that in WKY, and this increase was abolished by dimethylthiourea (a hydroxyl radical scavenger). The increased ESR signal decay rate was reduced to the same extent in the presence of desferrioxamine, catalase, and Tiron, indicating that hydroxyl radicals are derived from superoxide anions and hydrogen peroxide. In addition, total superoxide dismutase (SOD) activity in the RVLM was decreased in SHRSP compared with WKY. Furthermore, bilateral microinjection of tempol into the RVLM decreased blood pressure in SHRSP but not in WKY, and MnSOD overexpression in the RVLM of SHRSP decreased blood pressure and inhibited sympathetic nerve activity. These results suggest that superoxide anions in the RVLM, which generate hydroxyl radicals, are increased in SHRSP and contribute to the neural mechanisms of hypertension in SHRSP.

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Author and article information

Contributors

Toru Kawada: +81-6-6833-5012 , torukawa@ncvc.go.jp

Journal

Journal ID (nlm-ta): J Physiol Sci

Journal ID (iso-abbrev): J Physiol Sci

Title: The Journal of Physiological Sciences

Publisher: Springer Japan (Tokyo )

ISSN (Print): 1880-6546

ISSN (Electronic): 1880-6562

Publication date (Electronic): 5 November 2015

Publication date PMC-release: 5 November 2015

Publication date (Print): 2016

Volume: 66

Pages: 15-41

Affiliations

Department of Cardiovascular Dynamics, National Cerebral and Cardiovascular Center, 5-7-1 Fujishirodai, Suita, Osaka 565-8565 Japan

Article

Publisher ID: 412

DOI: 10.1007/s12576-015-0412-5

PMC ID: 4742515

PubMed ID: 26541155

SO-VID: 97689d22-283d-436a-b98d-2d7bbfeb2dca

History

Date received : 28 September 2015

Date accepted : 30 September 2015

Custom metadata

ScienceOpen disciplines: Anatomy & Physiology

Keywords: arterial pressure,sympathetic nerve activity,systems analysis,equilibrium diagram,white noise,transfer function

Data availability:

ScienceOpen disciplines: Anatomy & Physiology

Keywords: arterial pressure, sympathetic nerve activity, systems analysis, equilibrium diagram, white noise, transfer function

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