Impact of twospotted spider mite (Acari: Tetranychidae) duration of infestation on cotton seedlings.

The yield response of cotton, Gossypium hirsutum L., to twospotted spider mite, Tetranychus urticae Koch, duration of infestation during the seedling stage was measured at Starkville and Stoneville, MS, during 2010 and 2011. The treatments included a noninfested control, infestations lasting for 7, 14, 21, or 28 d, and a season long infested control. Twospotted spider mites from a greenhouse colony were inoculated on all of the infested cotton plots during the three-leaf stage. Applications of miticides were made to terminate infestations at the desired timings for each treatment. Twospotted spider mite densities and injury ratings were determined for each treatment at the end of the infestation period and yield was measured at the end of the season. Twospotted spider mite densities and injury rating significantly increased as duration of infestation increased. Significant differences in yield were observed between treatments. These data suggest infestations initiated at the three-leaf cotton growth stage with population densities at a minimum of 0.39 mites/cm2 existing > 14 d could result in reduction of cotton yields.

Sustained nitric oxide exposure decreases soluble guanylate cyclase mRNA and enzyme activity in pulmonary artery smooth muscle.

BACKGROUND: The soluble isoform of guanylate cyclase (sGC) is activated by nitric oxide (NO) to form guanoside 3':5'-cyclic monophosphate (cGMP). Cyclic GMP levels cause smooth muscle relaxation and regulate vascular tone to various vascular beds, including the lung. Under conditions of cytokine excess the inducible synthesis of NO may result in cGMP overproduction, generalized vasodilatation, and septic shock. In the pulmonary bed the opposite response, pulmonary hypertension, may occur. We hypothesized that sGC activity decreases in the face of sustained levels of NO. MATERIALS AND METHODS: We used the NO-donor S-nitroso-acetyl-D-L-penicillamine to study the effects of NO on sGC mRNA abundance and enzyme activity in cultured rat pulmonary artery smooth muscle cells. RESULTS: NO caused a prompt rise in extracellular cGMP production. Pretreating cells with NO for >/=45 min inhibited subsequent cGMP synthesis. NO-pretreated cells recovered the capacity for cGMP synthesis after removal of NO for 120 min. When actinomycin or cycloheximide was added to NO pretreatment, cells retained cGMP synthetic capacity. NO pretreatment decreased sGC mRNA abundance, but did not totally eliminate it. CONCLUSION: NO has important regulatory effects on cGMP synthesis at the level of enzyme activity and mRNA abundance. NO causes an immediate synthesis of large amounts of cGMP. With prolongation of exposure (>/=60 min) sGC enzyme activity decreases and cGMP production drops significantly. Soluble GC mRNA abundance also decreases and may result in decreased responsiveness of cells to NO with regard to cGMP production.

Escherichia coli lipopolysaccharide downregulates soluble guanylate cyclase in pulmonary artery smooth muscle.

The soluble isoform of guanylate cyclase (sGC) is activated by nitric oxide (NO) to form guanosine 3':5'-cyclic monophosphate (cGMP). Cyclic GMP levels cause smooth muscle relaxation and regulate vascular tone to various vascular beds, including the lung. Under conditions of cytokine excess the inducible synthesis of NO may result in cGMP overproduction, generalized vasodilation, and septic shock. In the pulmonary bed the opposite response may occur, pulmonary hypertension. We hypothesized that sGC activity becomes downregulated in the face of Escherichia coli lipopolysaccharide (LPS). We tested the effects of LPS on alpha1-subunit sGC mRNA abundance, Western analysis, and enzyme activity in cultured rat pulmonary artery smooth muscle cells. LPS increased extracellular cGMP production by pulmonary artery smooth muscle cells, with increased levels being first detectable at 3-6 h (10 microg/ml LPS) and exceeding 140 pmol/ml by 24 h (P < 0.05). The response was inhibited by 0.05 mM l-NG-monomethyl-l-arginine (l-NMA) and, in turn, restored by 1 mM l-arginine, indicating a NO synthase-dependent response. Pretreating cells with LPS for >/= 3 h inhibited subsequent cGMP synthesis in response to 10(-4) M SNAP for 60 min. Coincubating cells with 0.05 mM l-NMA also reversed this effect. Soluble GC enzyme activity in cells exposed to basal medium alone measured 0.74 pmol cGMP/ml per minute; activity in cells exposed to 10 microg/ml LPS for 24 h decreased to 0.04 pmol cGMP/ml per minute (P < 0.05). LPS pretreatment decreased sGC mRNA abundance and protein mass, but did not totally eliminate them. It is concluded that LPS affects cGMP synthesis at the level of enzyme activity, enzyme mass, and mRNA abundance. Over the short term (<24 h) LPS causes the synthesis of large amounts of cGMP. As the duration of exposure progresses (>/=3 h), mechanisms come into play that decrease cGMP production significantly and include decreases in mRNA abundance, enzyme mass, and enzyme activity.