Hypertension is a major risk factor leading to devastating cardiovascular events such as myocardial infarction, stroke, heart failure, and renal failure. Despite intensive research in this area, mechanisms underlying essential hypertension remain to be defined. Accumulating evidence indicates that neural components including both sympathetic and sensory nerves innervating the cardiovascular and renal tissues play a key role in regulating water and sodium homeostasis and blood pressure, and that abnormalities in these nervous systems contribute to increased salt sensitivity and development of hypertension. In contrast to relatively well-defined sympathetic nervous system, the role of sensory nerves in the control of cardiovascular homeostasis is largely unknown. Data from our laboratory show that degeneration of capsaicinsensitive sensory nerves renders a rat salt sensitive in terms of blood pressure regulation. Evidence is also available indicating that sensory nerves, in interacting with other neurohormonal systems including the sympathetic nervous system, the renin-angiotensin aldosterone system, the endothelin system, and superoxide, regulate cardiovascular and renal function in such that they play a counter-balancing role in preventing salt-induced increases in blood pressure under pathophysiological conditions. Altered activity of the sensory nervous system, a condition existed in both genetic and experimental models of hypertension, contributes to the development of hypertension. This article focuses on reviewing the current knowledge regarding the possible role of sensory nerves in regulating blood pressure homeostasis as well as the function and regulation of novel molecules expressed in sensory nerves.
Keywords: Capsaicin, vanilloid receptor, sympathetic nerve, angiotensin II, endothelin, oxidative stress, sodium, blood pressure
Rights & PermissionsPrintExport