Energy and Climate Implications for Agricultural Nutrient Use Efficiency

Energy and climate change are beginning to dominate the global political agenda and will drive policy formation that will shape the future of agriculture. Energy issues threaten national security and economic stability, as well as access to low-cost nutrient inputs for agriculture. Climate change has the potential to cause serious disruption to agricultural productivity. Paradoxically, nutrient use in agriculture to increase crop yields has the potential to negatively impact climate. This chapter will discuss recent and future energy and climate trends, the relationships between agricultural nutrient use efficiency and biofuels, and how global land limitations will shape agriculture in the future. Comparative gross energy yield and nitrogen use efficiency for ethanol production from crop residue, switchgrass, grain sorghum, sweet sorghum, and corn grain is presented, showing small differences in nitrogen use efficiency, but large differences in gross energy yields. In addition to considering the need to increase crop productivity to meet the demands of a growing population and bioenergy, agricultural nutrient use efficiency must be reconsidered with respect to the important energy and climate challenges shaping agriculture today

LPA(1) receptor-mediated thromboxane A(2) release is responsible for lysophosphatidic acid-induced vascular smooth muscle contraction

Lysophosphatidic acid (LPA) has been recognized recently as an endothelium-dependent vasodilator, but several lines of evidence indicate that it may also stimulate vascular smooth muscle cells (VSMCs), thereby contributing to vasoregulation and remodeling. In the present study, mRNA expression of all 6 LPA receptor genes was detected in murine aortic VSMCs, with the highest levels of LPA(1), LPA(2), LPA(4), and LPA(6). In endothelium-denuded thoracic aorta (TA) and abdominal aorta (AA) segments, 1-oleoyl-LPA and the LPA(1–3) agonist VPC31143 induced dose-dependent vasoconstriction. VPC31143-induced AA contraction was sensitive to pertussis toxin (PTX), the LPA(1&3) antagonist Ki16425, and genetic deletion of LPA(1) but not that of LPA(2) or inhibition of LPA(3), by diacylglycerol pyrophosphate. Surprisingly, vasoconstriction was also diminished in vessels lacking cyclooxygenase-1 [COX1 knockout (KO)] or the thromboxane prostanoid (TP) receptor (TP KO). VPC31143 increased thromboxane A(2) (TXA(2)) release from TA of wild-type, TP-KO, and LPA(2)-KO mice but not from LPA(1)-KO or COX1-KO mice, and PTX blocked this effect. Our findings indicate that LPA causes vasoconstriction in VSMCs, mediated by LPA(1)-, G(i)-, and COX1-dependent autocrine/paracrine TXA(2) release and consequent TP activation. We propose that this new-found interaction between the LPA/LPA(1) and TXA(2)/TP pathways plays significant roles in vasoregulation, hemostasis, thrombosis, and vascular remodeling.—Dancs, P. T., Ruisanchez, E., Balogh, A., Panta, C. R., Miklós, Z., Nüsing, R. M., Aoki, J., Chun, J., Offermanns, S., Tigyi, G., Benyó, Z. LPA(1) receptor-mediated thromboxane A(2) release is responsible for lysophosphatidic acid-induced vascular smooth muscle contraction