RESUMO
The aim of this study was to use multivariate methods and Pearson and partial correlations to disregard phenotypic characteristics that contribute little to differentiation between Brachiaria ruziziensis genotypes. Eighty-one genotypes of B. ruziziensis were assessed in completely randomized blocks with three replications. Ten phenotypic characteristics were assessed: plant height, leaf length, leaf width, sheath length, length of the flower stem, length of the inflorescence axis, number of racemes per inflorescence, length of the basal raceme, number of spikelets per basal raceme, and width of the rachis. The best traits for differentiation between genotypes were determined by assessing relative contribution to diversity, canonical variables, as well as Pearson and partial correlations. Four canonical variables were found to account for 57% of the overall variation, while plant height, sheath length, and number of racemes per inflorescence were considered traits that could potentially be disregarded in future assessments.
Assuntos
Brachiaria/genética , Variação Genética , Genótipo , Fenótipo , Brachiaria/crescimento & desenvolvimento , Melhoramento Vegetal , Característica Quantitativa HerdávelRESUMO
Members of the spider genus Lasiodora are widely distributed in Brazil, where they are commonly known as caranguejeiras. Lasiodora spider venom is slightly harmful to humans. The bite of this spider causes local pain, edema and erythema. However, Lasiodora sp. spider venom may be a source of important pharmacological tools. Our research group has described previously that Lasiodora sp. venom produces bradycardia in the isolated rat heart. In the present work, we sought to evaluate the vascular effect of Lasiodora sp. venom and to isolate the vasoactive compounds from the venom. The results showed that Lasiodora spider venom induced a concentration-dependent vasodilation in rat aortic rings, which was dependent on the presence of a functional endothelium and abolished by the nitric oxide synthase (NOS) inhibitor L-NAME. Western blot experiments revealed that the venom also increased endothelial NOS function by increasing phosphorylation of the Ser¹¹77 residue. Assay-directed fractionation isolated a vasoactive fraction from Lasiodora sp. venom. Mass spectrometry (MS) and nuclear magnetic resonance (NMR) assays identified a mixture of two compounds: adenosine diphosphate (ADP, approximately 90%) and adenosine monophosphate (AMP, approximately 10%). The vasodilator effects of Lasiodora sp. whole venom, as well as ADP, were significantly inhibited by suramin, which is a purinergic P2-receptor antagonist. Therefore, the results of the present work indicate that ADP is a main vasodilator component of Lasiodora sp. spider venom.
Assuntos
Difosfato de Adenosina/farmacologia , Venenos de Aranha/química , Aranhas/química , Vasodilatadores/farmacologia , Difosfato de Adenosina/química , Monofosfato de Adenosina/química , Animais , Western Blotting , Fracionamento Químico , Endotélio/efeitos dos fármacos , Técnicas In Vitro , Espectrometria de Massas , NG-Nitroarginina Metil Éster/metabolismo , Óxido Nítrico Sintase/metabolismo , Ressonância Magnética Nuclear Biomolecular , Fosforilação/efeitos dos fármacos , Ratos , Suramina/química , Vasodilatação/efeitos dos fármacos , Vasodilatadores/químicaRESUMO
BACKGROUND AND PURPOSE: Vasculopathies represent the main cause of morbidity and mortality in diabetes. Vascular malfunctioning in diabetes is associated with abnormal vasoconstriction and Ca(2+) handling by smooth muscle cells (SMC). Phosphatidylinositol 3-kinases (PI3K) are key mediators of insulin action and have been shown to modulate the function of voltage-dependent L-type Ca(2+) channels (Ca(V) 1.2). In the present work, we investigated the involvement of PI3K signalling in regulating Ca(2+) current through Ca(V) 1.2 (I(Ca,L) ) and vascular dysfunction in a mouse model of type I diabetes. EXPERIMENTAL APPROACH: Changes in isometric tension were recorded on myograph. Ca(2+) currents in freshly dissociated mice aortic SMCs were measured using the whole-cell patch-clamp technique. Antisense techniques were used to knock-down the PI3Kδ isoform. KEY RESULTS Contractile responses to phenylephrine and KCl were strongly enhanced in diabetic aorta independent of a functional endothelium. The magnitude of phenylephrine-induced I(Ca,L) was also greatly augmented. PI3Kδ expression, but not PI3Kα, PI3Kß, PI3Kγ, was increased in diabetic aortas and treatment of vessels with a selective PI3Kδ inhibitor normalized I(Ca,L) and contractile response of diabetic vessels. Moreover, knock-down of PI3Kδin vivo decreased PI3Kδ expression and normalized I(Ca,L) and contractile response of diabetic vessels ex vivo. CONCLUSIONS AND IMPLICATIONS: Phosphatidylinositol 3-kinase δ was essential to the increased vascular contractile response in our model of type I diabetes. PI3Kδ signalling was up-regulated and most likely accounted for the increased I(Ca,L,) leading to increased vascular contractility. Blockade of PI3Kδ may represent a novel therapeutic approach to treat vascular dysfunction in diabetic patients.