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Angiotensin II (ANG II) infusion increases renal superoxide (O(2)(-)) and enhances renal vasoconstriction via macula densa (MD) regulation of tubuloglomerular feedback, but the mechanism is unclear. We targeted the p22(phox) subunit of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) with small-interfering RNA (siRNA) to reduce NADPH oxidase activity and blood pressure response to ANG II in rats. We compared single nephron glomerular filtration rate (SNGFR) in samples collected from the proximal tubule (PT), which interrupts delivery to the MD, and from the distal tubule (DT), which maintains delivery to the MD, to assess MD regulation of GFR. SNGFR was measured in control and ANG II-infused rats (200 ng.kg(-1).min(-1) for 7 days) 2 days after intravenous injection of vehicle or siRNA directed to p22(phox) to test the hypothesis that p22(phox) mediates MD regulation of SNGFR during ANG II. The regulation of SNGFR by MD, determined by PT SNGFR-DT SNGFR, was not altered by siRNA in control rats (control + vehicle, 13 +/- 1, n = 8; control + siRNA, 12 +/- 2 nl/min, n = 8; not significant) but was reduced by siRNA in ANG II-treated rats (ANG II + vehicle, 13 +/- 2, n = 7; ANG II + siRNA, 7 +/- 1 nl/min, n = 8; P < 0.05). We conclude that p22(phox) and NADPH oxidase regulate the SNGFR during ANG II infusion via MD-dependent mechanisms.

In this study, 160 73-week-old laying hens (HyLine W-36) were used to investigate the changes in production performance and egg quality parameters of aged laying hens after injection of different doses of growth hormone (GH) and a fixed dose of testosterone (Ts). The hens were weighed individually, placed in laying cages and then randomly assigned to four treatments with four replicates of 10 birds each, in a completely randomised design. The experiment was started at the 75th week and lasted until the 82nd week of age. The treatments were: 1: injection of 100 µL distilled water (control group), 2: injection of 500 µg Ts/kg liveweight + 50 µg GH/kg liveweight, 3: injection of 500 µg Ts/kg liveweight + 100 µg GH/kg liveweight and 4: injection of 500 µg Ts/kg liveweight + 150 µg GH/kg liveweight. In this study, ovulation rate (egg production percent), egg mass and feed intake were significantly higher in Treatment 3 than the control group (P < 0.05), and in Treatment 4, feed conversion ratio was significantly higher than for the other experimental groups (P < 0.05). In addition, the birds in Treatment 3 showed greater egg weight, albumen height, eggshell weight, eggshell density and eggshell weight per surface area than the control group (P < 0.05). In Treatment 3, egg length significantly increased compared with Treatments 1 and 4 (P < 0.05), and in Treatments 2 and 4, shell breaking strength was significantly lower than for the control group (P < 0.05). In conclusion, our results showed positive effects of GH and Ts administration on egg quality parameters and production performance in aged laying hens. Taken together, in the present study Treatment 3 was found more effective in improving egg quality and production performance of the old laying hens.

Abstract. Potassium deficiency (KD) is associated with severe growth failure, in part caused by growth hormone (GH) resistance. This study set out to determine whether the resistance could be caused by a defect in GH-mediated janus associated kinasesignal transducers and activators of transcription (STAT) signaling as occurs in uremia. To this end, rats were fed a K-deficient diet for 8 d and pair-fed controls received a K-replete diet. Animals from each group received GH or vehicle, and during this period, KD rats were GH resistant; GH induced body and liver weight gain and linear body growth were severely attenuated in these rats. In addition, signal transduction was studied in the liver of rats that were killed 10 or 15 min after an intravenous GH bolus or vehicle. When the rats were killed, GH receptor mRNA and protein levels were similar in the two groups. The abundance of STAT5, STAT3, and STAT1, proteins that mediate GH signaling, was significantly increased by 40 to 130% in KD. Furthermore, GH induced a far greater increase in STAT5 and STAT3 phosphorylation in this group. STAT5 phosphorylation was enhanced fourfold even when normalized for total STAT5 content. Phosphorylated STAT5 and STAT3 proteins were also increased in nuclear extracts, suggesting normal nuclear translocation of the activated signaling proteins. DNA binding of nuclear STAT5 was unaltered. Thus, in KD, there is resistance to the growth-promoting action of GH despite hyperactivation of the janus associated kinase-STAT signaling pathway. This suggests the presence of a defect distal to the nuclear binding of STAT or, alternatively, a defect in a STAT-independent GH-activated signaling pathway.