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(Hypertension. 2007;50:6.)
© 2007 American Heart Association, Inc.

Brief Reviews

Arterial Chemoreceptors and Sympathetic Nerve Activity

Implications for Hypertension and Heart Failure

Harold D. Schultz; Yu L. Li; Yanfeng Ding

From the Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha.

Correspondence to Harold D. Schultz, Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, 985850 Nebraska Medical Center, Omaha, NE 68198-5850. E-mail hschultz@unmc.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Chronic elevation in sympathetic nerve activity (SNA) is associated with the development and maintenance of certain types of hypertension¹ and contributes to the progression of chronic heart failure (CHF).² The mechanisms involved in sympathetic dysfunction in these disorders appear to be complex and multifactorial. A unified hypothesis is likely to encompass alterations in multiple autonomic reflex pathways, central integratory sites, and chemical mediators that control sympathetic outflow. For example, tonic restraint of sympathetic outflow by arterial and cardiopulmonary baroreflexes is depressed in CHF² and depressed or reset in hypertension.³ Moreover, maladaptive changes also occur in the central nervous system at integrative sites for autonomic control in both disease processes.^4,5 It is also clear that sympathoexcitatory cardiac,⁶ somatic,⁷ and central/peripheral chemoreceptor reflexes⁸ are enhanced in CHF and hypertension.

Arterial chemoreceptors serve an important regulatory role in the control of alveolar ventilation, but they also exert a powerful influence on cardiovascular function.⁹ Activation of arterial chemoreceptors by hypoxemia increases sympathetic outflow to systemic vascular beds to compensate for the direct vasodilating effects of hypoxia on these vessels and to redistribute blood flow to essential organs. In this review, we highlight relevant information that implicates the arterial chemoreflex as a contributory mechanism for the sympathetic hyperactivity in CHF and hypertension and illustrate proposed mechanisms for this altered function.

	The Sympathetic Response to Arterial Chemoreceptor Activation

 
Arterial chemoreceptors located in the aortic and carotid bodies (CBs) respond to hypoxemia and hypercapnia. Because central chemoreceptors also respond to hypercapnia, hypoxia is typically used as a specific stimulus to arterial chemoreceptors. In some . . . [Full Text of this Article]

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