Abstract
Baroreceptors (BRs) are mechanosensitive nerve endings in carotid sinuses and aortic arch that function as arterial blood pressure (BP) sensors. Changes in BR activity evoke reflex circulatory adjustments that reduce BP variability and its adverse consequences. BR activation during increases in BP involves three processes: (1) vascular distension and deformation of BR nerve endings, (2) depolarization of the nerve terminals consequent to the opening of mechanosensitive ion channels (mechanoelectrical transduction), and (3) translation of mechanically induced depolarization into action potential discharge mediated by voltage-dependent Na(+) and K(+) channels. This chapter discusses the mechanism of mechanoelectrical transduction. A variety of physiological, pharmacological, and molecular approaches to this problem, including studies in animals and isolated BR neurons in culture is presented. The chapter provides an overview of the molecular basis of BR mechanoelectrical transduction. Emerging evidence points to the members of three evolutionarily conserved ion channel families in mediating BR activation: epithelial Na channels (ENaCs), acid-sensing ion channels (ASICs), and transient receptor potential (TRP) channels.
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