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The expression of bone morphogenetic protein-7 (BMP-7) mRNA by in situ hybridization in rats with normal kidneys and those with acute renal failure has been studied cloning a rat BMP-7 cDNA and using it as a probe. BMP-7 is a member of the transforming growth factor-beta superfamily that are found abundantly in the fetal kidney. Results indicated that the BMP-7 mRNA has the highest expression in tubules of the outer medulla. Its expression is also localized to the adventitia of renal arteries, the epithelial cell layer of the renal pelvis and the ureter.

A study was conducted on the mechanism by which hepatic endothelin (ET) production is enhanced during endotoxin exposure. The findings suggest a model of paracrine signaling to describe the mechanism for the elevation of hepatic ET-1 levels following endotoxin exposure. This paracrine signaling mechanism operates between Kupffer cells that release transforming growth factor-Beta on endotoxin challenge and hepatic endothelial cells.

The characterization and partial purification of secretory platelet-activating factor (PAF)-acetylhydrolase of the rat hepatobiliary system were conducted. The objective is to show that both rat hepatocytes and Kupffer cells secrete constitutive pPAF-AH (plasma-type platelet-activating factor-acetylhydrolase) in cultured mediums. Results demonstrate that rat bile contains substantial amounts of PAF-AH exhibiting pPAF-AH properties.

The roles of endothelin A (ETA) and (ETB) B receptors on bone formation was analyzed in primary cultures of rat fetal calvarial cells to characterize osteoblast responsiveness to ET-1. Analysis of the effects of osteogenic protein (OP)-1 on ET-1 receptor expression indicated the presence of downregulated ETA gene expression in the presence of high levels of OP-1. Furthermore, ET-1 modulated osteoblastic function during discrete phases of osteoblast development.

The effects of endotoxemia on endothelin-1 synthesis by hepatic endothelial cells were analyzed in intact livers isolated from endotoxin-treated rats. Analysis of liver cells from endotoxemia-treated rats indicated the presence of elevated ET-1 hepatic messenger RNA expression. Analysis of liver cell types from endotoxin-treated rats also indicated high ET-1 concentrations in the hepatic endothelial cells. Furthermore, endotoxemia elevated the levels of circulating immunoreactive ET-1 in endotoxin-treated rats due to systemic trauma.

A study was conducted to examine the effects of osteogenic protein-1 (OP-1) on the proliferation and maturation of ROS 17/2.8 cells, which are associated with the growth and differentiation of bone osteoblasts. Treatment with OP-1 increased alkaline phosphatase activity, alkaline phosphatase mRNA, parathyroid hormone receptor mRNA and parathyroid hormone-stimulated adenosine 3',5'-cyclic monophosphate. However, OP-1 inhibited [3H]thymidine incorporation. These results suggest that potentiation of osteoblast by treatment with OP-1 affects bone morphogenesis.

The study of renal function using rats gives the same results as instruction using humans, with the added advantages of better diet and fluid intake control and urine and blood collection. The hemostatic control of plasma ion concentration and extracellular fluid volume by the nephrons along with the hypothalamus and the adrenal cortex can be easily studied. GFR, osmotic and Na+ and Cl- concentrations can also be studied using rats.

The DNA synthesis induced by epidermal growth factor (EGF) and platelet-derived growth factor (PGDF) is restricted by bradykinin. It restricts the DNA synthesis stimulated by EGF due to the release of prostaglandin E2 (PGE2). Bradykinin inhibition of the DNA synthesis stimulated by EGF was reduced in the presence of indomethacin. The generation of intracellular calcium fluxes and inositol phosphates did not evoke any interactions between EGF and bradykinin.

Research was conducted to find out whether calcium channel antagonists limit hepatic injury and inducible nitric oxide synthase (iNOS) expression in vivo following lipopolysaccharide (LPS) exposure and to examine their effects on the regulation of iNOS expression in cultured Kupffer cells (KC). Results showed that under endotoxemic conditions, calcium channel antagonists limit hepatocellular injury that is accompanied by an inhibition of LPS-mediated iNOS expression in rat liver KC.