Separate development of nitric oxide synthase- and vasoactive intestinal polypeptide-immunoreactive nerves arising from the vertebral artery in the rat.

Development of nitric oxide synthase (NOS)-and vasoactive intestinal polypeptide (VIP)-immunoreactive (-IR) nerves supplying the basilar and vertebral arteries (BA and VA) was investigated in White Wistar rats, using double immunohistochemistry. NOS-IR and VIP-IR nerves via the anterior circulation (AC), which mostly expressed NO(+)/VIP(+), extended to the BA during the second postnatal week, and usually reached as far as the rostral two third of the BA on PND 20. NOS-IR nerves were completely lack in the cBA and the VA on PND10, and often absent from these arterial regions even at PND 20. Nevertheless, a small number of VIP(+)/NOS(-) nerves were localized in the walls from the caudal BA (cBA) to the VA on PND 5. On PND 20, they frequently met with the descending NOS-IR and VIP-IR nerves via the AC around the lower portion of the middle BA. Fiber bundles containing NOS(+)/VIP(+) axons were first visualized on the caudal VA at PND 30 and observed frequently at PND 80, with a distinct increase in number of NOS-IR and VIP-IR nerves supplying the cBA and the VA. Thus, NOS-IR nerves coming from the VA develop through its own characteristic sequence that lags markedly behind the time of appearance for VIP-IR nerves from the same vascular route and for NOS-IR and VIP-IR nerves via the AC.

Effects of gentamicin on the recovery of renal function after unilateral hydronephrosis.

BACKGROUND: Urinary tract infection is a complication of hydronephrosis and antibiotics such as gentamicin are indicated for treatment. However, gentamicin can cause drug-induced nephropathy in dehydrated patients. We used a rat kidney model to investigate the effects of gentamicin administration on functional recovery from unilateral hydronephrosis. MATERIALS AND METHODS: Gentamicin was intraperitoneally injected twice for 48 hours following the release of a unilateral ureteral obstruction. The function of both kidneys was separately quantified by Technetium-99mDMSA renoscintigraphy. We examined morphological changes in renal tubular cells by electron microscopy and by in situ DNA 3'-end labeling. RESULTS: Renal function in the contralateral, but not the obstructed, kidney was significantly damaged by gentamicin administration under our conditions and electron microscopy confirmed the presence of myeloid bodies in renal tubular cells. In situ DNA 3'-end labeling revealed characteristic damage to the renal tubules. CONCLUSION: These results suggest that damage to each kidney should be considered individually after gentamicin administration during recovery from hydronephrosis.