Researchers tested the hypothesis that Protein Kinase C-beta is a key modulator of atherogenesis in a hyperlipidemic environment. They found that mice lacking both apolipoprotein E (ApoE) and PKC beta II displayed significantly decreased atherosclerosis. To test if this was due to deletion of PKC beta they tested an inhibitor of this enzyme. The fed ApoE null mice with chow containing the PCK beta inhibitor ruboxistaurin, or vehicle chow. Compared to mice receiving vehicle chows, mice fed ruboxistaurin displayed significantly decreased atherosclerosis. Taken together the findings highlight key roles for PKC beta in atherosclerosis development. The studies suggest that atherosclerosis may be affected by the inhibitor of the protein, ruboxistaurin, which is in clinical trials.
"Chronic secondary hypertension during pregnancy: impact on maternal renal function."
Devaki Maduwegedera, Rebecca L Flower, Kate M Denton, Monash University, Department of Physiology, Melbourne, Australia. Physiology 703.6.
Researchers wanted to study whether inadequate maternal kidney function in pregnancy might contribute to the fetal programming of adult hypertension. To start, they determined kidney function before and after nitric oxide blockade. The found that renal function was not different between normotensive pregnant and nulliparious (never pregnant) groups. However, after pregnancy in hypertensive rabbits, renal function was reduced by 25% in a damaged kidney, but increased 25% in the non-damaged kidney. So there was no change in total kidney function, but during pregnancy plasma creatinine levels were significantly increased, suggesting that kidney function may have been further compromised. They also found that the damaged kidney didn't appear to produce nitric oxide; if so, this may account for the further reducti
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4-Apr-2005