| The afferent renal nerves that contain both Aδ and C fibers are stemmed from intrarenal sensory receptors. Two classes of renal sensory receptors have been identified neurophysiologically: renal mechanoreceptors responding to increases in intrarenal hydrostatic pressure, and renal chemoreceptors responding to renal ischemia and changes in the chemical environment of the renal interstitium. The latter is further classified as R1 and R2 chemoreceptors. Some of the mechanoreceptors have a spontaneous discharge under control conditions. R1 chemoreceptors have no spontaneous activity and respond to renal ischemia. R2 chemoreceptors are spontaneously active. In addition to being activated by ischemia, it can be activated by alterations in the composition of the interstitial or pelvic fluid environment. Thus the afferent renal nerves have a basal discharge under normal physiological conditions and R2 chemoreceptors are the principal source of the ongoing activity observed in multiunit recordings. Although the afferent innervation is not directly involved in the regulation of vascular or tubular phenomena within the kidney, its potential role lies in the initiation of reflex effects that may participate in the reflex control system, such as renorenal reflex and cardiovascular activity regulating reflex ect. The changes in afferent renal nerve activity (ARNA) can also induce the release of vasopressin, cortisol and atrial natriuretic peptide. Adenosine, a metabolite of adenine nucleotides, is one of the major neuromodulators. It has been shown that adenosine exerts its actions to the kidney via high affinity to the adenosine receptors. For example, adenosine participates in the regulation of preglomerular and postglomerular vascular resistance, glomerular filtration rate, renin release, epithelial transport, intrarenal inflammation, and the growth of mesangial and vascular smooth muscle cells. Four adenosine receptor subtypes were found and cloned: A1, A2A, A2B, A3, which are all found in the kidney.Nitric oxide ( NO ) is an important signaling and effector molecule that plays critical roles in numerous essential physiological processes in virtually every organ. The three types of NO synthases ( NOS ), referred to as neuronal NOS ( nNOS ), inducible NOS ( iNOS), and endothelial NOS ( eNOS ), which have all been found in the kidney. At the same time, NO is known to function as an inhibitory neurotransmitter regulating the activity of renal afferent arteriole in rats. The present work was undertaken to study the effects of intrarenal artery injection of adenosine on spontaneous discharges of renal afferent nerve fibers, and further analyze the possible mechanisms. The results obtained are as follows: Sixty-five rabbits were used to determine the effects of intrarenal artery injection of adenosine on multi- and single-unit spontaneous discharges of renal afferent nerve fibers in anesthetized rabbits. The results obtained are as follows: (1) Intrarenal artery injection of adenosine ( 50, 100, and 200 nmol/kg ) increased the ARNA in a dose-dependent manner (from 100% to 138.06 ± 7.16 %, 201.09 ± 21.85 %, and 313.73 ± 23.81 % respectively, P < 0.001 ; lasted for 2 ~ 6 min) with arterial pressure unchanged; (2) Intrarenal adenosine ( 100 nmol/kg ) increased single-unit discharge of ARNA from 0.19 ± 0.03 to 0.42 ± 0.09 impulse/s ( P < 0.001 ), lasting 1~3 min; (3) Pretreatment with DPCPX ( 160 nmol/kg ) partly blocked the effects of adenosine on single-unit activity from 0.45 ± 0.04 to 0.29 ± 0.03 impulse/s ( P < 0.001 ) while MAP was unaltered. (4) Pretreatment with L-NAME ( 0.1 mmol/kg ) increased the effect of adenosine in single unit activity from 0.45 ± 0.10 to 0.64 ± 0.09 impulse/s ( P < 0.001 ), and the response of renal afferents to adenosine was also prolonged from 2 ~ 5 min to 3.5 ~ 7.5 min.
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