Because endothelium-derived factors are known to have multiple actions throughout the body, the role of nitric oxide (NO) produced within the kidney in the regulation of renin release is still unclear. Therefore, the objectives of this study were to determine the effect of local NO synthesis inhibition within the kidney on renin secretion rate (RSR) and to determine whether the macula densa mechanism mediates the effect of NO on renin secretion rate in dogs. The NO synthesis inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) was administered via the renal artery at 5 microg x kg(-1) x min(-1) to dogs with normal kidney function and to dogs with the macula densa mechanism blocked, established by using the nonfiltering kidney model. In dogs with normal kidney function, renal arterial pressure (RAP) and glomerular filtration rate (GFR) remained constant throughout the experiment (131 +/- 5 mmHg and 22.6 +/- 3.0 ml/min, respectively). However, intrarenal NO synthesis inhibition decreased renal blood flow (RBF) by 16% (240 +/- 22 to 201 +/- 23 ml/min) and increased renal vascular resistance (RVR) by 24% (0.59 +/- 0.08 to 0.73 +/- 0.09 mmHg x ml(-1) x min). In addition, L-NAME decreased the fractional excretion of lithium by 27% (30.0 +/- 3.7 to 21.6 +/- 4.3%) and decreased the fractional excretion of sodium by 35% (0.86 +/- 0.29 to 0.56 +/- 0.21%). Associated with these changes in renal function, renin secretion rate increased by 194 and 235%. In marked contrast, renin secretion rate remained constant in dogs with the macula densa mechanism blocked. Intrarenal NO synthase blockade decreased RSR by 4 and 10% in dogs with the macula densa mechanism blocked. The RAP, RBF, and RVR responses to intrarenal NO synthesis inhibition in dogs with the macula densa mechanism blocked were similar to the renal hemodynamic response in dogs with normal kidney function. In summary, we have demonstrated that intrarenal NO synthesis blockade enhances renin secretion in dogs. The macula densa mechanism appears to play an important role in mediating the effect of intrarenal NO synthesis inhibition on renin release.

What's already known about this topic? Little is known about partial trisomy 16p as relatively few cases have been reported. An abnormal yolk sac and increased nuchal translucency are associated with aneuploidy and adverse pregnancy outcomes. What does this study add? We propose that congenital diaphragmatic hernia may be part of the phenotype of partial trisomy 16p. This case adds to other recent observations of congenital diaphragmatic hernia with chromosome imbalances in 16p. This report illustrates the natural progression of an abnormality, imaged by ultrasound during the first 17 weeks of pregnancy: abnormal yolk sac, increased nuchal translucency, and diaphragmatic hernia.

worse in out-of-hospital deliveries, though it was difficult to assess outcomes due to the small population in this group. Outcomes were similar between the GDM and DM group. In the GDM group, neonates were significantly more likely to have Apgars <7 at 5 minutes and transfusions (Apgar 0.13% hospital v 3.21% home, transport 0.87% v 2.71%, both p<0.001). Only Apgars <7 at 5 minutes reached statistical significance in the DM group (0.15% hospital v 3.70% home, p<0.001). As expected, CS was significantly higher in the hospital group (GDM 38.82% hospital v 0.17% home, DM 54.70% hospital v 0% home, both p<0.001). No other maternal outcomes reached statistical significance. CONCLUSION: Diabetic women delivering in hospital were significantly more likely to receive appropriate CS. Neonatal outcomes including Apgar <7 at 5 minutes and neonatal transfusion were improved in the hospital setting. No difference in neonatal or maternal outcomes was noted between GDM and DM groups. Further research is warranted to investigate improved education strategies for women about these high-risk deliveries at birth centers or at home.

No abstract

No abstract