Nitric oxide (NO), a modulator of several physiological processes, is involved in different human sperm functions. We have investigated whether NO may stimulate the motility of human spermatozoa via activation of the soluble guanylate cyclase (sGC)/cGMP pathway. Sperm samples obtained by masturbation from 70 normozoospermic patients were processed by the swim-up technique. The kinetic parameters of the motile sperm-rich fractions were assessed by computer-assisted sperm analysis. After a 30-90 min incubation, the NO donor S-nitrosoglutathione (GSNO) exerted a significant enhancing effect on progressive motility (77, 78, and 78% vs 66, 65, and 62% of the control at the corresponding time), straight linear velocity (44, 49, and 48 mm/s vs 34, 35, and 35.5 mm/s), curvilinear velocity (81, 83, and 84 mm/s vs 68 mm/s), and average path velocity (52, 57, and 54 mm/s vs 40, 42, and 42 mm/s) at 5 mM but not at lower concentrations, and in parallel increased the synthesis of cGMP. A similar effect was obtained with the NO donor spermine NONOate after 30 and 60 min. The GSNO-induced effects on sperm motility were abolished by 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (a specific sGC inhibitor) and mimicked by 8-bromo-cGMP (8-Br-cGMP; a cell-permeating cGMP analog); the treatment with Rp-8-Br-cGMPS (an inhibitor of cGMP-dependent protein kinases) prevented both the GSNO-and the 8-Br-cGMP-induced responses. On the contrary, we did not observe any effect of the cGMP/PRKG1 (PKG) pathway modulators on the onset of hyperactivated sperm motility. Our results suggest that NO stimulates human sperm motility via the activation of sGC, the subsequent synthesis of cGMP, and the activation of cGMP-dependent protein kinases.

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1. There are few studies on the effect of dietary protein content on pulmonary hypertension syndrome (PHS) in broiler chickens. Conflicting results from these studies prevent a clear conclusion on the effects of reduced-protein diets on development of the syndrome. 2. To obtain an understanding of the mechanisms involved, the current study, conducted at a high altitude (2100 m above sea level), evaluated the effect of three treatments that varied only according to dietary protein (CP) levels. One treatment with dietary CP advocated by National Research Council (1994) acted as a control. Two reduced-protein diets were also prepared with CP reduced 20 and 40 g/kg relative to the CP of the control, which were designated as LCPD2 and LCPD4, respectively. A total of 180 d-old male broilers (Ross 308) were randomised across 15 floor pens measuring 1.5 m(2) (12 birds per pen). Five such pens (replicates) were allotted to each dietary treatment. The protein treatments were applied from 1 to 42 d of age in which growth performance was measured and the mortality from PHS was monitored. At the end of trial (42 d), blood sampling was done and carcase characteristics were recorded. 3. Birds receiving LCPD4 gained more weight throughout the trial and had increased right ventricular weight ratio (RV:TV), relative liver weight, haematocrit, and heterophil: lymphocyte ratio at the end of the trial compared to the control. Plasma concentrations of nitric oxide (NO) and uric acid, however, were significantly lower in birds fed on LCPD4 than in those receiving the control diet. 4. Mortality from PHS was increased in birds fed the reduced-protein diets, which may have been associated with reduced concentration of plasma NO and increased haematocrit and RV:TV. In conclusion, feeding reduced-protein diets to broilers subjected to hypobaric hypoxia was associated with the development of PHS.

A total of 300 male broilers (Ross 308) were exposed to cool conditions at high altitudes to study the effects of dietary Arg supplementation on performance and physiological and zootechnical variables. A corn-soybean meal (SBM) and a corn-canola meal (CM) diet were formulated for the starting (1 to 3 wk of age) and growing (3 to 6 wk of age) stages according to NRC recommendations. Two additional diets were prepared by supplementing 0.2 and 0.4% l-Arg to the corn-CM diet. Substitution of CM for SBM caused a significant (P < 0.05) reduction in weight gain and feed intake and resulted in impaired feed:gain. Supplementing Arg in the CM diet restored the feed and weight losses to a significant extent so that a significant difference was found between CM diet and CM + 0.4% Arg in terms of weight gain for the growing (3 to 6 wk) stage and the entire study (1 to 6 wk; P < 0.05). Total plasma nitric oxide (NO) concentration analyzed by nitrate plus nitrite assay was measured in the treatment groups. A significant (P < 0.05) decrease in plasma NO level was observed by substituting CM for SBM in the diet. Supplementing the CM diet with Arg increased the plasma NO level above that of SBM group. Carcass and breast yields were significantly decreased (P < 0.05) as a result of substituting CM for SBM. The substitution of CM for SBM, however, significantly (P < 0.05) increased the proportions of thighs and heart. The right ventricular weight:total ventricular weight ratio and ascites mortality showed a significant (P < 0.05) increase when SBM was replaced by CM in the diet. Fortification of the CM diet with Arg eliminated the significant difference in the right-to-total ventricular weight ratios when compared with the SBM diet. In conclusion, feeding CM to broiler chickens raised at high altitude caused reduced growth performance and predisposed the birds to pulmonary hypertension and ascites, which were partly restored by Arg supplementation.