These results suggest that a functioning nitric oxide system, especially through the nNOS, is important in mediating normal renal responses and that increased production of and/or sensitivity to nitric oxide during sustained VE plays an important role in the adaptive mechanism of the tubuloglomerular feedback.

TEB(Aesculon) overestimated CO compared to TD with ∼17% at rest and ∼34% during exercise, but the techniques showed similar results during NO inhalation. CO, furthermore, correlated poorly between TEB(Aesculon) and TD. TEB(Aesculon) may at present not replace TD for reliable CO measurements in humans.

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Immediately after unilateral nephrectomy, the glomerular filtration rate (GFR) and urinary excretion rate increase in the remaining transplanted rat kidney. In a previous study, we found that GFR in a transplanted kidney was reduced through an activation of the tubuloglomerular feedback control. Excision of the rat’s own remnant kidney then reduced feedback sensitivity and thereby allowed GFR to rise. The present study aimed at investigating whether prostaglandins are involved in this functional adaptation. Clearance and micropuncture experiments were performed before and after administration of indomethacin and after subsequent unilateral nephrectomy. GFR and the urinary excretion rate of electrolytes and water were measured. From proximal tubular stop-flow pressure (P_SF) measurements the feedback characteristics were determined as the maximal stop-flow pressure response (ΔP_SF) to an increase in distal flow and the turning point (TP), i.e. the end proximal flow rate that caused 50% reduction of ΔP_SF. The results showed that following nephrectomy the tubuloglomerular feedback sensitivity was decreased, with an increased TP and reduced ΔP_SF. Pretreatment with indomethacin (2 mg/kg BW) prevented not only the change in feedback sensitivity at nephrectomy but also the rise in GFR. These results suggest that the prostaglandins play a possible role as one link in the chain of adaptive events occurring immediately after nephron loss.

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Reduction of the functioning renal mass by unilateral nephrectomy or unilateral ureteral occlusion (UUO) leads to increased function of the remaining nephrons, an important factor being the glomerular filtration rate (GFR). GFR can be modified via the tubuloglomerular feedback control (TGF), which senses the distal delivery of fluid and alters the tonus of the glomerular arterioles. The aim of the present study was to investigate the TGF sensitivity in the intact left kidney of rats after 24 hours of right ureteral occlusion. Using a micropuncture technique, proximal tubular stop-flow pressure (Psf), as a relative index of glomerular capillary pressure, was measured upstream to the block, while late proximal segments were perfused with Ringer solution (rates 0-40 nl/min). The maximal drop in Psf and the tubular flow rate at which 50% of this response was achieved, the turning point (TP), were determined. Considerable decrease in the sensitivity of the TGF system in the contralateral kidney during UUO was indicated by a significantly higher TP as compared with control rats (sham operation), viz. 29 v. 19 nl/min. Maximal Psf drop after UUO was significantly less than in the controls (6 v. 12 mm Hg). Reduced TGF sensitivity in the contralateral kidney after protracted UUO is a prerequisite for that kidney's increased excretion of salt and water to compensate for the loss of functioning renal mass.

Renal blood flow was studied in rats 120 minutes after unilateral renal ablation. The influence of endogenous prostaglandin formation was evaluated by indomethacin treatment prior to the ablation. Radioactive microspheres were used for estimation of the total renal and cortical blood flow, and the renal medullary blood flow was determined with the 86-Rb chloride extraction method. The total blood flow in the remaining kidney was increased by 80% following contralateral ablation, with augmentation in all areas, particularly in the deep medullary region. Indomethacin treatment in intact rats evoked increased blood flow as compared with the indomethacin control group. The results indicated that the renal blood vessels respond to ablation of the contralateral kidney with dilation in all kidney regions, and that this vascular dilation may be prostaglandin-mediated.