No abstract

Agriculture consumes more than two thirds of the total freshwater of the planet. This issue causes substantial conflict in freshwater allocation between agriculture and other economic sectors. Regulated deficit irrigation (RDI) is key technology because it helps to improve water use efficiency. Nonetheless, there is a lack of understanding of the mechanisms with which plants respond to RDI. In particular, little is known about how RDI might increase crop production while reducing the amount of irrigation water in real-world agriculture. In this review, we found that RDI is largely implemented through three approaches: (1) growth stage-based deficit irrigation, (2) partial root-zone irrigation, and (3) subsurface dripper irrigation. Among these, partial root-zone irrigation is the most popular and effective because many field crops and some woody crops can save irrigation water up to 20 to 30 % without or with a minimal impact on crop yield. Improved water use efficiency with RDI is mainly due to the following: (1) enhanced guard cell signal transduction network that decreases transpiration water loss, (2) optimized stomatal control that improves the photosynthesis to transpiration ratio, and (3) decreased evaporative surface areas with partial root-zone irrigation that reduces soil evaporation. The mechanisms involved in the plant response to RDI-induced water stress include the morphological traits, e.g., increased root to shoot ratio and improved nutrient uptake and recovery; physiological traits, e.g., stomatal closure, decreased leaf respiration, and maintained photosynthesis; and biochemical traits, e.g., increased signaling molecules and enhanced antioxidation enzymatic activity.

Abstract-We examined the hypothesis that ONOOϪ , a product of the interaction between superoxide (O 2 ·Ϫ ) and nitric oxide (NO), inhibits calcium-activated K ϩ (K Ca ) channel activity in vascular smooth muscle cells (VSMCs) of human coronary arterioles (HCAs), thereby reducing hyperpolarization-mediated vasodilation. HCAs were dissected from right atrial appendages. The interaction of ONOO Ϫ with microvessels was determined by immunohistochemistry using a nitrotyrosine antibody. Strong staining was observed in arteries exposed to authentic ONOO Ϫ or to sodium nitroprusside (SNP)ϩxanthine (XA)ϩxanthine oxidase (XO). Dilation to 10 Ϫ8 mol/L bradykinin (BK) was abolished in vessels exposed to ONOO Ϫ (Ϫ2.5Ϯ8%; PϽ0.05) but not DC-ONOO Ϫ (65Ϯ8%). Reduced dilation to BK was also observed after application of XO and SNP. Dilation to NS1619 (K Ca channel opener) was reduced in endothelial denuded arterioles treated with ONOO Ϫ . In isolated VSMCs, whole-cell peak K ϩ current density was reduced by ONOO