Distribution of nitric oxide synthase-containing ganglionic neuronal somata and postganglionic fibers in the rat kidney

Abstract

Nitric oxide synthase (NOS)-immunoreactive neurons were identified in the rat kidney by using an antibody against type Ia NOS and the avidin-biotin complex immunoperoxidase method in whole kidneys examined in 100 microns serial sections. The histochemical method for demonstration of the nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) was also used to characterize NOS-containing neurons. All somata showing NOS immunoreactivity also displayed NADPH-d activity. The greatest number of neuronal somata were observed in groups at the wall of the renal pelvis and in the angular space formed by the pole of the renal parenchyma and renal pelvic wall. They were also seen at the renal hilus close to the renal artery and along the interlobar vasculature. The size of the neuronal somata in the 35-day-old rat ranged from 13.6 to 34.8 microns, with a mean size of 21.52 +/- 4.81 microns. Seventy percent, however, ranged in size from 17.8 to 26.8 microns. The shape of the neuronal somata also varied, with the majority having an ovoid or round shape. The distribution of the postganglionic fibers was investigated by means of the camera lucida. Postganglionic fibers projected into the wall of the renal pelvis and/or to the interlobar arteries extending to the arcuate arteries and to the beginning of the afferent arterioles. The NOS-immunoreactive neurons may have a vasodilator and relaxing function on the renal pelvic wall and vasculature. In addition, the presence of NOS-containing nerve fibers in nerve bundles, which are known to have predominantly vasomotor and sensory fibers, suggest that they may have a possible modulatory role on renal neural function.

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

“…Unidentified transmitters were suggested. Neuronal NOS-or NADPH diaphorase-positive nerves were detected in arcuate and interlobar arteries and preglomerular afferent arterioles in the rat and human kidney (Bachmann et al, 1995;Liu et al, 1996b) and dog and monkey kidney (Okamura et al, 1995d). In isolated perfused rabbit renal afferent arterioles contracted with norepinephrine, nicotine induced vasodilatation, and treatment with L-NA reversed the response to vasoconstriction (T. Tamaki, S. Kimura, and Y. Abe, unpublished observations), suggesting a release of NO from periarterial nerves.…”

Interactions between nitric oxide and superoxide on the neural regulation of proximal fluid reabsorption in hypertensive rats

“…Immunohistochemical studies have revealed staining for the superoxide dismutase (SOD), which is a scavenger for O 2 − , in neuronal nitric oxide synthase (nNOS)-containing nerves, and would have the potential of protecting NO from destruction by O 2 − (Liu et al 1997). The observation by Liu et al (1996), that there are nitrergic nerve fibres in the kidney which colocalize with sympathetic fibres, has been taken to suggest that a relationship exists between O 2 − and NO at the neuroeffector junction. The oxidative and antioxidant systems are normally in balance but under pathophysiological conditions, for example in hypertensive states, there are often altered levels of NO or O 2 − generation giving rise to accelerated NO removal and a blunting of its physiological role.…”

Nitric Oxide Modulation of Neurally Induced Proximal Tubular Fluid Reabsorption in the Rat

“…However, the location of this nNOS was uncertain, although the nitrergic nerve fibers found in the kidney may be one of the important anatomical locations. 11 The aim of this study was to examine the potential influence of NO on the increased proximal tubular fluid reabsorption resulting from low level renal nerve stimulation and to elucidate which isoforms of NOS might be involved. This was performed by measuring the changes in proximal tubular fluid reabsorption in response to renal nerve stimulation following blockade of NOS using nonselective (L-NAME) and selective (7-NI and aminoguanidine) NOS inhibitors, as well as an NO donor (SNP) alone and together with L-NAME.…”