Absence of renin secretion in the portal venous system in rats

Zusammenfassung An 2–24h nephrektomierten männlichen und weiblichen Wistar-Ratten wurden Vergleichsbestimmungen der Renin-Aktivität im arteriellen und portalvenösen Plasma durchgeführt. Die Renin-Aktivität war in beiden Gefässystemen auf nicht messbare Werte abgefallen. Die infolge Blutentzug von 10–12 ml/kg erzielte hämorrhagische Hypotension führte im Zeitraum von 60–165 min nicht zu einem Renin-Aktivitätsanstieg. Die Versuchsresultate ergeben keine Bestätigung, dass Renin in der portalen Strombahn produziert oder freigesetzt wird.     

Activation of CD47 receptors causes histamine secretion from mast cells

Mast cells play pivotal roles in allergic and inflammatory processes via distinct activation pathways. Mucosal and serosal mast cells are activated by the IgE/FcɛRI pathway, while only serosal mast cells are activated by basic secretagogues. We show that CD47 receptors are expressed on rat peritoneal mast cells. 4N1K, a peptide agonist of CD47, rapidly caused exocytosis. Such exocytosis required increased intracellular calcium and was inhibited by pertussis toxin and an antibody against the βγ dimer of a G_i protein. Cooperation with integrins and glycosylphosphatidylinositol-anchored proteins was necessary, since anti-integrin antibodies and pretreatment with phosphatidylinositol-phospholipase C reduced exocytosis. Depletion of membrane cholesterol inhibited exocytosis and decreased CD47 in lipid rafts, consistent with a CD47/integrin/G_i protein complex being located in rafts. An anti-CD47 antibody inhibited exocytosis induced by 4N1K and by mastoparan and spermine, suggesting that basic secretagogues might target CD47. We propose that 4N1K-stimulated mast cell exocytosis involves a CD47/integrin/G_i protein complex. Received 8 December 2008; received after revision 12 January 2009; accepted 29 January 2009     

Corticosterone secretion after neurogenic stress in intact and hypophysectomized rats

Summary The time course of blood and adrenal corticosterone elevation after immobilization stress has been studied in intact and hypophysectomized male rats. The results suggest that the adrenal gland is able to respond to neurogenic stress, increasing the synthesis and release of corticosterone, in the absence of ACTH.     

In vivo conversion of corticosterone into aldosterone in rats treated with ACTH or submitted to stress

Zusammenfassung Es wurde die in vivo Konversion von Corticosteron zu Aldosteron in den Nebennieren der Ratte nachgewiesen. Wiederholte ACTH-Gaben verminderten die Konversion, während diese nach chronischer «Stress»-Einwirkung (Formol-Behandlung) unverändert blieb. Es wird angenommen, dass die Vergrösserung und Funktionsänderung der Nebennieren unter Stress-Einwirkung nicht nur durch vermehrte Abgabe von ACTH vermittelt wird.

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Supported by the Deutsche Forschungsgemeinschaft.     

Activation of complement by trypanosomes

Summary Factors exhibiting anti-complementary activity released from trypanosomes after incubation at 20°C were described. The active material was shown to consume the first component of bovine complement. While the anticomplementary factor(s) from T. lewisi could activate bovine, human and guinea pig complement, the factor(s) from T. congolense was observed to activate bovine complement, but not guinea pig and only slightly human complement. The roles of complement activating factor(s) of trypanosomes in the pathology of the disease are discussed.This project is supported by National Research Council of Canada grant A 0068 and a grant from the International Development Research Centre.     

Pressor and oxitocic-like effects of angiotensin affected by aldosterone pretreatment in guinea-pigs

Résumé Les auteurs examinent l'augmentation de l'action de l'angiotensine sur la pression carotidienne et sur la contraction utérine chez des animaux traités avec de l'aldostérone. Ils pensent aussi que le traitement conditionne le développement du phénomène taquiphylactique de l'angiotensine.     

Growth inhibition in mammalian cells exposed to thermal stress

Zusammenfassung Erhöhter Temperatur ausgesetzte Schweinenieren-Zellen produzieren, bei 37 °C kultiviert, Mikrokolonien. Eine Reduktion in der Wachstumsrate ist proportional zur Dauer und Intensität der Hitzebehandlung und verliert sich im Laufe der weitern Kultivierung.

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This work was supported by U.S. Public Health Service Research Grant No. GM-13692, and by an appointment as Research Professor in the Miller Institute for Basic Research in Science.     

Activation of subtilisin by luteotropic and luteinizing hormone

Zusammenfassung Die Katalysegeschwindigkeit der Hydrolyse vonN-l-Leucyl-2-naphthylamin durch Subtilisin war grösser in Gegenwart von luteotrophem Schafhormon und etwas geringer in Gegenwart von luteinisierendem Pferdehormon. Dieses Verhalten wird als kompetitive Aktivierung erklärt.     

Activation of stress signalling pathways enhances tolerance of fungi to chemical fungicides and antifungal proteins

Fungal disease is an increasing problem in both agriculture and human health. Treatment of human fungal disease involves the use of chemical fungicides, which generally target the integrity of the fungal plasma membrane or cell wall. Chemical fungicides used for the treatment of plant disease, have more diverse mechanisms of action including inhibition of sterol biosynthesis, microtubule assembly and the mitochondrial respiratory chain. However, these treatments have limitations, including toxicity and the emergence of resistance. This has led to increased interest in the use of antimicrobial peptides for the treatment of fungal disease in both plants and humans. Antimicrobial peptides are a diverse group of molecules with differing mechanisms of action, many of which remain poorly understood. Furthermore, it is becoming increasingly apparent that stress response pathways are involved in the tolerance of fungi to both chemical fungicides and antimicrobial peptides. These signalling pathways such as the cell wall integrity and high-osmolarity glycerol pathway are triggered by stimuli, such as cell wall instability, changes in osmolarity and production of reactive oxygen species. Here we review stress signalling induced by treatment of fungi with chemical fungicides and antifungal peptides. Study of these pathways gives insight into how these molecules exert their antifungal effect and also into the mechanisms used by fungi to tolerate sub-lethal treatment by these molecules. Inactivation of stress response pathways represents a potential method of increasing the efficacy of antifungal molecules.