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  • 1
    Publication Date: 2024-01-06
    Description: The seasonal cycle is the dominant mode of variability in the air-sea CO2 flux in most regions of the global ocean, yet discrepancies between different seasonality estimates are rather large. As part of the Regional Carbon Cycle Assessment and Processes Phase 2 project (RECCAP2), we synthesize surface ocean pCO2 and air-sea CO2 flux seasonality from models and observation-based estimates, focusing on both a present-day climatology and decadal changes between the 1980s and 2010s. Four main findings emerge: First, global ocean biogeochemistry models (GOBMs) and observation-based estimates (pCO2 products) of surface pCO2 seasonality disagree in amplitude and phase, primarily due to discrepancies in the seasonal variability in surface DIC. Second, the seasonal cycle in pCO2 has increased in amplitude over the last three decades in both pCO2 products and GOBMs. Third, decadal increases in pCO2 seasonal cycle amplitudes in subtropical biomes for both pCO2 products and GOBMs are driven by increasing DIC concentrations stemming from the uptake of anthropogenic CO2 (Cant). In subpolar and Southern Ocean biomes, however, the seasonality change for GOBMs is dominated by Cant invasion, whereas for pCO2 products an indeterminate combination of Cant invasion and climate change modulates the changes. Fourth, biome-aggregated decadal changes in the amplitude of pCO2 seasonal variability are largely detectable against both mapping uncertainty (reducible) and natural variability uncertainty (irreducible), but not at the gridpoint scale over much of the northern subpolar oceans and over the Southern Ocean, underscoring the importance of sustained high-quality seasonally resolved measurements over these regions.
    Repository Name: EPIC Alfred Wegener Institut
    Type: Article , isiRev
    Format: application/pdf
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  • 2
    Electronic Resource
    Electronic Resource
    Melbourne, Australia : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 26 (1999), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The role of angiotensin (Ang)II in and the effects of angiotensin-converting enzyme (ACE) inhibitors on the regulation of sympathetic neural activity were examined in humans.2. We measured baseline values of muscle sympathetic nerve activity (MSNA) and its reflex inhibition in 28 patients with essential hypertension with elevated plasma renin activity (PRA; 〉1.0 ng/mL per h = 0.28 ng/L per s) before and after either acute or chronic oral administration of an ACE inhibitor or placebo and in 20 normotensive subjects before and after infusion of either AngII (5 ng/kg per min = 4.8 pmol/kg per min) or vehicle (5% dextrose). Muscle sympathetic nerve activity was recorded from the tibial nerve and its reflex inhibition was evaluated during pressor responses to bolus injection of phenylephrine (2 μg/kg, i.v.).3. Blood pressure was significantly decreased (P 〈 0.01) after the acute oral administration of captopril (25 mg), accompanied by a slight increase in MSNA in patients with essential hypertension compared with control patients who received placebo administration. Reflex changes in MSNA were significantly augmented after oral administration of captopril (–4.1±0.5 vs–6.2±0.6%/mmHg, respectively; P 〈 0.01), with a significant reduction of plasma AngII, while they were not affected by placebo administration.4. In contrast, acute AngII infusion was accompanied by decreases in both PRA and MSNA in normotensive subjects. Reflex changes in MSNA were significantly reduced after AngII infusion (–11.0±0.8 vs–7.4±1.0%/mmHg, respectively; P 〈 0.01) but not after vehicle alone.5. Chronic ACE inhibition by 12 week oral imidapril administration (5–10 mg/day) significantly (P 〈 0.05) decreased baseline values of MSNA, which were accompanied by a significant (P 〈 0.05) increase in the reflex inhibition of MSNA, while plasma concentrations of noradrenaline were unaffected.6. These results indicate that AngII blunts reflex inhibition of sympathetic neural activity and that inhibition of the renin–angiotensin system by an ACE inhibitor augments reflex regulation of sympathetic neural activity and reduces baseline values in patients with essential hypertension.
    Type of Medium: Electronic Resource
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