Endogenous Angiotensin II‐induced p44/42 Mitogen‐Activated Protein Kinase Activation Mediates Sodium Appetite but not Thirst or Neurohypophysial Secretion in Male Rats

The renin–angiotensin–aldosterone system makes a critical contribution to body fluid homeostasis, and abnormalities in this endocrine system have been implicated in certain forms of hypertension. The peptide hormone angiotensin II (AngII) regulates hydromineral homeostasis and blood pressure by acting on both peripheral and brain targets. In the brain, AngII binds to the angiotensin type 1 receptor (AT1R) to stimulate thirst, sodium appetite and both arginine vasopressin (AVP) and oxytocin (OT) secretion. The present study used an experimental model of endogenous AngII to examine the role of p44/42 mitogen‐activated protein kinase (MAPK) as a signalling mechanism to mediate these responses. Animals were given a combined treatment of furosemide and a low dose of captopril (furo/cap), comprising a diuretic and an angiotensin‐converting enzyme inhibitor, respectively, to elevate endogenous AngII levels in the brain. Furo/cap induced p44/42 MAPK activation in key brain areas that express AT1R, and this effect was reduced with either a centrally administered AT1R antagonist (irbesartan) or a p44/42 MAPK inhibitor (U0126). Additionally, furo/cap treatment elicited water and sodium intake, and irbesartan markedly reduced both of these behaviours. Central injection of U0126 markedly attenuated furo/cap‐induced sodium intake but not water intake. Furthermore, p44/42 MAPK signalling was not necessary for either furo/cap‐ or exogenous AngII‐induced AVP or OT release. Taken together, these results indicate that p44/42 MAPK is required for AngII‐induced sodium appetite but not thirst or neurohypophysial secretion. This result may allow for the discovery of more specific downstream targets of p44/42 MAPK to curb sodium appetite, known to exacerbate hypertension, at the same time as leaving thirst and neurohypophysial hormone secretion undisturbed

Endogenous Angiotensin II‐induced p44/42 Mitogen‐Activated Protein Kinase Activation Mediates Sodium Appetite but not Thirst or Neurohypophysial Secretion in Male Rats

The renin–angiotensin–aldosterone system makes a critical contribution to body fluid homeostasis, and abnormalities in this endocrine system have been implicated in certain forms of hypertension. The peptide hormone angiotensin II (AngII) regulates hydromineral homeostasis and blood pressure by acting on both peripheral and brain targets. In the brain, AngII binds to the angiotensin type 1 receptor (AT1R) to stimulate thirst, sodium appetite and both arginine vasopressin (AVP) and oxytocin (OT) secretion. The present study used an experimental model of endogenous AngII to examine the role of p44/42 mitogen‐activated protein kinase (MAPK) as a signalling mechanism to mediate these responses. Animals were given a combined treatment of furosemide and a low dose of captopril (furo/cap), comprising a diuretic and an angiotensin‐converting enzyme inhibitor, respectively, to elevate endogenous AngII levels in the brain. Furo/cap induced p44/42 MAPK activation in key brain areas that express AT1R, and this effect was reduced with either a centrally administered AT1R antagonist (irbesartan) or a p44/42 MAPK inhibitor (U0126). Additionally, furo/cap treatment elicited water and sodium intake, and irbesartan markedly reduced both of these behaviours. Central injection of U0126 markedly attenuated furo/cap‐induced sodium intake but not water intake. Furthermore, p44/42 MAPK signalling was not necessary for either furo/cap‐ or exogenous AngII‐induced AVP or OT release. Taken together, these results indicate that p44/42 MAPK is required for AngII‐induced sodium appetite but not thirst or neurohypophysial secretion. This result may allow for the discovery of more specific downstream targets of p44/42 MAPK to curb sodium appetite, known to exacerbate hypertension, at the same time as leaving thirst and neurohypophysial hormone secretion undisturbed

Integrated Ecosystem Assessments: Developing the Scientific Basis for Ecosystem-Based Management of the Ocean

Integrated ecosystem assessments challenge the broader scientific community to move beyond the important task of tallying insults to marine ecosystems to developing quantitative tools that can support the decisions national and regional resource managers must make

Non-Standard Errors

In statistics, samples are drawn from a population in a data-generating process (DGP). Standard errors measure the uncertainty in estimates of population parameters. In science, evidence is generated to test hypotheses in an evidence-generating process (EGP). We claim that EGP variation across researchers adds uncertainty: Non-standard errors (NSEs). We study NSEs by letting 164 teams test the same hypotheses on the same data. NSEs turn out to be sizable, but smaller for better reproducible or higher rated research. Adding peer-review stages reduces NSEs. We further find that this type of uncertainty is underestimated by participants

The Five-Step Process of Integrated Ecosystem Assessment

<p>An IEA begins with a scoping process to identify key management objectives and constraints, identifies appropriate indicators and management thresholds, determines the risk that indicators will fall below management targets, and combines risk assessments of individual indicators into a determination of overall ecosystem status. The potential of different management strategies to alter ecosystem status is evaluated, and then management actions are implemented and their effectiveness monitored. The cycle is repeated in an adaptive manner.</p

The Origin of NOAA’s Integrated Ecosystem Assessment Program: A Retrospective and Prospective

In response to calls for marine ecosystem-based management (EBM), the U.S. National Oceanic and Atmospheric Administration (NOAA) developed a multidisciplinary science support framework called integrated ecosystem assessment (IEA). The IEA framework and a national NOAA program for implementing that framework were the culmination of many efforts in the 2000s. At a recent workshop, five leaders from the early days of NOAA IEA development participated in a panel to discuss the history of the framework and program, and to provide recommendations for future work. Panelists intended IEA to be a call to action for scientists and agencies to support EBM, and they designed the framework to be adaptable, scalable, and non-prescriptive so that it could be applied to a range of issues. Panelists emphasized the complementary nature of the processes, tools, and products that make up IEA efforts, and also stressed the need to adapt the IEA approach to shifting management and governance structures. Finally, panelists offered a range of recommendations for future development of the IEA approach, including: (1) broadening the stakeholder base; (2) developing objectives and reference points in partnership with end-users; (3) increasing diversity of IEA practitioners to better reflect the communities that IEA serves; (4) increasing development of readily updatable, real-time products; (5) carefully assessing and prioritizing the demands placed on IEA practitioners; (6) increasing collaboration across disciplines and resource sectors; (7) seeking opportunities to engage with emerging governance structures; and (8) strengthening support for IEA by effectively communicating its stories