To learn more about controlling renal interstitial hydrostatic pressure (RIHP), we assessed its response to renal medullary direct interstitial volume expansion (rmDIVE = 100 μL bolus infusion/30 sec). Three experimental series (S) were performed in hydropenic, anesthetized, right‐nephrectomized, acute left renal‐denervated and renal perfusion pressure‐controlled rats randomly assigned to groups in each S. S1: Rats without hormonal clamp were contrasted before and after rmDIVE induced via 0.9% saline solution bolus (SS group) or 2% albumin in SS bolus (2% ALB + SS group). Subcapsular ΔRIHP rose slowly, progressively and similarly in both groups by ~3 mmHg. S2: Rats under hormonal clamp were contrasted before and after sham rmDIVE (time CTR group) and real rmDIVE induced via either SS bolus (SS group) or SS bolus containing the subcutaneous tissue fibroblast relaxant dibutyryl‐cAMP (SS + db‐cAMP group). ΔRIHP showed time, group, and time*group interaction effects with a biphasic response (early: ~1 mmHg; late: ~4 mmHg) in the SS group that was absent in the SS + db‐cAMP group. S3: Two groups of rats (SS and SS + db‐cAMP) under hormonal clamp were contrasted as in S2, producing similar ΔRIHP results to those of S2 but showing a slow, progressive, and indistinct decrease in renal outer medullary blood flow in both groups. These results provide highly suggestive preliminary evidence that the renal interstitium is capable of contracting reactively in vivo in response to rmDIVE with SS and demonstrate that such a response is abolished when db‐cAMP is interstitially and concomitantly infused.

This paper presents the design, experimental modeling, and control of a pump-driven renal perfusion pressure (RPP)-regulatory system to implement precise and relatively fast RPP regulation in rats. The mechatronic system is a simple, low-cost, and reliable device to automate the RPP regulation process based on flow-mediated occlusion. Hence, the regulated signal is the RPP measured in the left femoral artery of the rat, and the manipulated variable is the voltage applied to a dc motor that controls the occlusion of the aorta. The control system is implemented in a PC through the LabView software, and a data acquisition board NI USB-6210. A simple first-order linear system is proposed to approximate the dynamics in the experiment. The parameters of the model are chosen to minimize the error between the predicted and experimental output averaged from eight input/output datasets at different RPP operating conditions. A closed-loop servocontrol system based on a pole-placement PD controller plus dead-zone compensation was proposed for this purpose. First, the feedback structure was validated in simulation by considering parameter uncertainty, and constant and time-varying references. Several experimental tests were also conducted to validate in real time the closed-loop performance for stepwise and fast switching references, and the results show the effectiveness of the proposed automatic system to regulate the RPP in the rat, in a precise, accurate (mean error less than 2 mmHg) and relatively fast mode (10-15 s of response time).

Despite the morphological and physiological differences between male and female kidneys., and the differences in the pathophysiological response to ischemia‐reperfusion injury at different experimental models (genetic, subcellular, cellular, animals and humans), they're still controversies between if these responses are depended to nitric oxide ‐ nitrosative stress vía, and the site in the renal parenchyma which are predominant. METHODS We analyzed (Image G program and Wilcoxon test in JMP software) the level of nitrosylated protein (fluorescent microscopy, DHPEF‐filter, 20x objective, 0.5 slight exposure, antibodies AB61392, revealed with antibody‐CF488A, diluted 1:1000) in 10‐µm slices of left‐kidney subjected to 45 min ischemia and 24 h reperfusion, both male (n=5 w= 120‐150g) and female Wistar adult rats (n=9, w=120‐150g). The right kidney of the same animals was the control kidney (no ischemia). RESULTS The level of nitrosylated protein were similar between groups for the internal medulla (ischemic kidney male= 115.24±10.73, ischemic kidney female= 130.97 ± 2.54, control kidney male= 107.72 ± 3.41, control kidney female= 112.53 ± 3.31, p=ns) and the glomeruli (ischemic kidney male= 122.88 ± 16.13, ischemic kidney female= 117.79 ± 9.26, control kidney male= 101.58 ± 13.75, control kidney female= 98.26 ± 5.75, p=ns). For the external medulla, there was an increase in the level of nitrosylated protein after the treatment (45 min ischemia, 24 h reperfusion), in both male and females (ischemic kidney male= 121.81 ± 10.97, ischemic kidney female= 125.96 ± 3.19) compared with control kidney (male= 93.75 ± 4.94, female= 99.78 ± 2.29, p=0.0004 ischemic vs control female kidney, p=0.0069 ischemic vs controlled male kidney, p=0.01 ischemic male vs control female kidney), but without differences between sexes. CONCLUSION The level of nitrosative protein was similar in control kidney (without ischemia) in both sexes, which represents a nitrosative basal level necessary for physiological responses and independent of the protein level sex‐differences reported in the literature (SOD, eNOS and iNOS, among others). Also, the level of nitrosative protein was increased in 29% in males and 26% in females only in the external medulla, without differences in the other sections of renal parenchyma. The results of this work showed similarities in epigenetic changes secondary to flow interruption of the whole renal pedicle in female and male rats only in the external medulla, but not a behavior pattern in the papilla or cortex. In‐situ study of this phenomenon, in contrast to other techniques that require tissue homogenization (like flow cytometry or western blot), allowed for a precise quantitative signal measurement in each region.

The effects of an acute renal medullary interstitial infusion (RMII) of 100 μl of either 0.9% saline (Sal) or 2% albumin in saline (Alb) on the time course (30 min) of renal interstitial hydrostatic pressure (RIHP, subcapsular), renal medullary blood flow (RMBF, L‐D), urinary nitrogen oxides excretion (UNOxV, Griess) and urinary flow rate (V) were assessed in the left denervated kidney of anesthetized male Wistar rats under control of renal perfusion pressure at 100 mmHg. After a 10 min control period (CP) and a 15s RMII period, three 10 min post‐infusion periods (P‐IP) of urinary collections were generated. The results are mean ± SEM; ^ p<0.05 vs. CP. Group CP RMII P‐IP 10min 20 min 30 min RIHP (mmmHg) Sal 3.0 3.8 3.9 5.3 6.8 n=17 ± 0.4 ± 0.5 ±0.5^ ± 0.7^ ± 0.8^ Alb 3.0 3.2 3.5 4.0 4.8 n=17 ± 0.3 ± 0.3^ ± 0.3^ ± 0.5^ ± 0.7^ RMBF (%Δ) Sal 0.0 2.0 10.7 12.5 8.2 n=17 ± 3.4 ± 3.3^ ± 4.0 ± 4.3 Alb 0.0 2.2 9.1 6.6 8.7 n=17 ± 5.0 ± 4.5^ ± 4.7 ± 5.2 There were no differences between groups in UNOxV nor in V through time.ConclusionsAcute RMII of either 0.9% saline or 2% albumin indistinctly rises RIHP and RMBF in the anesthetized rat, without affecting UNOxV nor urinary flow rate at all. Supported by IPL's financial resources.