Abstract
The immunohistochemical expression of neuronal nitric oxide synthase (nNOS) in the renal structure is predominantly described in macula densa - a structural component of the juxtaglomerular apparatus, represented by cells of the distal convoluted tubules. Under pathological conditions such as hypertension, the impaired nitric oxide (NO) bioactivity may be an important pathogenetic factor. In addition, the synthesized NO by nNOS is involved in the regulation of the afferent arteriole diameter, tubuloglomerular feedback mechanism, and the renin-angiotensin system. The aim of the present study was to make a detailed description of the nNOS expression in the renal corpuscles under hypertonic conditions in spontaneously hypertensive rats (SHRs). We used nine male SHRs and nine aged-matched male Wistar rats divided into the following groups: 4 months old, 6 months old and 12 months old, each group was represented by three SHRs and three Wistar rats. The immunohistochemical reaction was performed by specific monoclonal antibody for nNOS. In 4-month-old SHRs we observed heterogeneous expression of nNOS in the cells of parietal layer of Bowman`s capsule and glomerular capillary tuft (GCT), while the age-matched Wistar group was characterized by weak to missing immunoreactivity. During the period of target organ damage (6- and 12-month-old rats) we found intensified immunoreactivity of nNOS in the cells of the parietal layer of Bowman`s capsule and GCT compared to the control groups and noted differences in the distribution of the enzyme in the renal corpuscles of the cortical, midcortical and juxtamedullary nephrons. In conclusion, there are pronounced age-related differences of nNOS immunoreactivity in renal corpuscles of SHRs and Wistar rats. Most of the studies have discussed the role of macula densa nNOS-derived NO, but the information about the function and significance of this enzyme in the other renal structures is still limited. Future studies may reveal in details the importance of nNOS-derived NO in renal pathology.
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