A differential response of diffuse brain injury on the concentrations of endothelin and nitric oxide in the plasma and brain regions in rats.

In the present study, we hypothesized that acute diffuse brain injury (DBI) in rats would produce an increase in endothelin-1 (ET-1), a potent vasoconstrictor, and/or nitric oxide (NO), a potent vasodilator, in plasma and brain areas in rats. DBI was induced in anesthetized male Sprague-Dawley rats (350-400 g) using a 350 g weight dropped from 1 meter height impact through a device designed by Marmarou et al., 1994.

Beating affects the posttranscriptional regulation of alpha-myosin mRNA in cardiac cultures.

Contractile arrest of cardiac myocytes results in increased abundance of alpha-myosin heavy chain (MHC) mRNA but decreased alpha-MHC protein content. Our aim is to determine the posttranscriptional mechanisms regulating alpha-MHC mRNA-protein uncoupling in cultured neonatal rat hearts during altered contractile activity. Spontaneously contracting myocytes were arrested by the use of verapamil (10 mumol/l; a Ca(2+)-channel blocker) or by 2,3-butanedione monoxime (5 mmol/l; a cross-bridge inhibitor).

Synthetic peptides as probes for G protein function. Carboxyl-terminal G alpha s peptides mimic Gs and evoke high affinity agonist binding to beta-adrenergic receptors.

The molecular interfaces between Gs and the beta-adrenergic receptor were investigated using synthetic peptides corresponding to various regions of its alpha subunit, alpha s. These experiments were carried out on saponin-permeable C6 glioma cells in which the beta-adrenergic receptor appears tightly coupled to Gs. Synthetic site-specific peptides from alpha s (corresponding to amino acids 15-29, 354-372, and 384-394) and alpha i (8-22, 315-324, and 345-455) were tested for their ability to interfere with coupling between the beta-adrenergic receptor and Gs.