腎臟藉由精密的排泄構造是體內主要調控體液的器官。隨著感覺神經的存在，腎臟主動性扮演成一個感應器而不再是循環系統中被動調控的標的器官。存在於腎傳入神經末梢上的機械性和化學性受體兩種不同的腎受體可即時監控腎臟內的靜水壓和間質環境組成的變化。而在疾病狀態下，腎受體主要功能是可透過神經軸和痛感覺不同層次的連結，而誘發一反射性的感覺反應。這些感覺不僅可藉由交感神經的放電和特定內分泌系統的變化反射性地影響心血管功能，以及腎臟自我的功能，即所謂的腎臟腎臟反射。神經胜肽物質P 的釋放可活化辣椒素敏感型腎傳入神經，此機制可反射性地降低腎交感神經而導致利鈉利尿反應。目前研究結果顯示，感覺神經胜肽功能的低下在腎排泄功能變差和體液滯留中扮演極其重要的角色。許多分子，例如前列腺素、一氧化氮、緩肽素和內皮素已經知道可調控腎感覺中物質P 的釋放，然而，可偵測腎臟內機械性和化學性刺激的正確受體並不清楚。近來研究已清楚的揭示第一普遍型瞬時受體電位通道和甲基天門冬胺酸受體是腎臟中機械性受體，並且在腎盂中透過物質P 誘發感覺訊息。因為任何在物質P 系統的組成缺失會導致腎臟腎臟反射功能不全和促成不正常體液滯留，所以了解腎感覺調控的潛在機制是非常重要的。

The kidneys are the main organ which regulates body fluids via the delicate excretory structure. With the presence of sensory nerves, the kidney is not just a passive target organ in the circulation, but actively acts as a sensor. Changes in intrarenal hydrostatic pressure and the composition of the interstitial environment are instantly detected by 2 types of renal receptors, mechanoreceptors and chemoreceptors, both of which are present on renal afferent fibers. Renal receptors appear to havemajor functions in evoking a reflex response through their connections at different levels of the neuraxis and pain sensation in diseased states. These sensations are able to reflexively influence not only cardiovascular function by changes in sympathetic discharge and certain portions of the endocrine system, but also the function of the kidneys themselves in term of the renorenal reflex. The release of substance P (SP), which is responsible for activation of capsaicin-sensitive renal afferents, leads to a reflexive decrease in efferent renal sympathetic nerve activity and causes diuresis and natriuresis. The retarded function of sensory neuropeptides was shown to play a vital role in kidney diseases associated with poor renal excretion and body fluid retention. Several molecules, such as prostaglandin, nitric oxide, bradykinin, and endothelin, are known to regulate the release of SP in renal sensory activation. However, the exact receptors in response to sensing intrarenal mechanical or chemical stimulation are still unclear. Recent studies clearly revealed that transient receptor potential vanilloid type 1 (TRPV1) channels and N-methyl- D-aspartate (NMDA)receptors act asmechanoreceptors in the renal pelvis for SP-induced sensory activation. Understanding the underlying mechanisms of renal sensory regulation is important because defects in any component of the SP system causes renorenal reflex impairment and contributes to abnormal fluid retention.