2,135 research outputs found
Calcium channel blockade blunts the renal effects of acute nitric oxide synthase inhibition in healthy humans
Montanari A, Lazzeroni D, Pelà G, Crocamo A, Lytvyn Y,
Musiari L, Cabassi A, Cherney DZ. Calcium channel blockade
blunts the renal effects of acute nitric oxide synthase inhibition in
healthy humans. Am J Physiol Renal Physiol 312: F870–F878, 2017.
First published February 8, 2017; doi:10.1152/ajprenal.00568.
2016.—Our aim was to investigate whether blockade of calcium
channels (CCs) or angiotensin II type 1 receptors (AT1R) modulates
renal responses to nitric oxide synthesis inhibition (NOSI) in humans.
Fourteen sodium-replete, healthy volunteers underwent 90-min infusions
of 3.0 g·kg1·min1 NG-nitro-L-arginine methyl ester
(L-NAME) on 3 occasions, preceded by 3 days of either placebo (PL),
10 mg of manidipine (MANI), or 50 mg of losartan (LOS). At each
phase, mean arterial pressure (MAP), glomerular filtration rate (GFR;
inulin), renal blood flow (RBF; p-aminohippurate), urinary sodium
(UNaV), and 8-isoprostane (U8-iso-PGF2V; an oxidative stress
marker) were measured. With PL L -NAME, the following changes
were observed: 6% MAP (P 0.005 vs. baseline), 10% GFR,
20% RBF, 49% UNaV (P 0.001), and 120% U8-iso-PGF2V
(P 0.01). In contrast, MAP did not increase during LOS
L-NAME or MANI L-NAME (P 0.05 vs. baseline), whereas renal
changes were the same during LOS L-NAME vs. PL L-NAME
(ANOVA, P 0.05). However, during MANI L-NAME, changes
vs. baseline in GFR (6%), RBF (12%), and UNaV (34%) were
blunted vs. PL L-NAME and LOS L-NAME (P 0.005), and the
rise in U8-iso-PGF2V was almost abolished (37%, P 0.05 vs.
baseline; P 0.01 vs. PL L-NAME or LOS L-NAME). We
conclude that, since MANI blunted L-NAME-induced renal hemodynamic
changes, CCs participate in the renal responses to NOSI in
healthy, sodium-replete humans independent of changes in MAP
and without the apparent contribution of the AT1R. Because the rise
in U8-iso-PGF2V was essentially prevented during MANI
L-NAME, CC blockade may oppose the renal effects of NOSI in part
by counteracting oxidative stress responses to acutely impaired renal
NO bioavailability
Half-integer Higher Spin Fields in (A)dS from Spinning Particle Models
We make use of O(2r+1) spinning particle models to construct linearized
higher-spin curvatures in (A)dS spaces for fields of arbitrary half-integer
spin propagating in a space of arbitrary (even) dimension: the field
potentials, whose curvatures are computed with the present models, are
spinor-tensors of mixed symmetry corresponding to Young tableaux with D/2 - 1
rows and r columns, thus reducing to totally symmetric spinor-tensors in four
dimensions. The paper generalizes similar results obtained in the context of
integer spins in (A)dS.Comment: 1+18 pages; minor changes in the notation, references updated.
Published versio
Maxwell-like Lagrangians for higher spins
We show how implementing invariance under divergence-free gauge
transformations leads to a remarkably simple Lagrangian description of massless
bosons of any spin. Our construction covers both flat and (A)dS backgrounds and
extends to tensors of arbitrary mixed-symmetry type. Irreducible and traceless
fields produce single-particle actions, while whenever trace constraints can be
dispensed with the resulting Lagrangians display the same reducible,
multi-particle spectra as those emerging from the tensionless limit of free
open-string field theory. For all explored options the corresponding kinetic
operators take essentially the same form as in the spin-one, Maxwell case.Comment: 77 pages, revised version. Erroneous interpretation and proof of the
gauge-fixing procedure for mixed-symmetry fields corrected. As a consequence,
the mixed-symmetry, one-particle Lagrangians are to be complemented with
conditions on the divergences of the fields; all other conclusions unchanged.
Additional minor changes including references added. To appear in JHE
The STAR Time Projection Chamber: A Unique Tool for Studying High Multiplicity Events at RHIC
The STAR Time Projection Chamber (TPC) is used to record collisions at the
Relativistic Heavy Ion Collider (RHIC). The TPC is the central element in a
suite of detectors that surrounds the interaction vertex. The TPC provides
complete coverage around the beam-line, and provides complete tracking for
charged particles within +- 1.8 units of pseudo-rapidity of the center-of-mass
frame. Charged particles with momenta greater than 100 MeV/c are recorded.
Multiplicities in excess of 3,000 tracks per event are routinely reconstructed
in the software. The TPC measures 4 m in diameter by 4.2 m long, making it the
largest TPC in the world.Comment: 28 pages, 11 figure
Cardiovascular Effects of Canagliflozin in Relation to Renal Function and Albuminuria
Background: People with type 2 diabetes mellitus (T2DM) have elevated cardiovascular (CV) risk, including for hospitalization for heart failure (HHF). Canagliflozin reduced CV and kidney events in patients with T2DM and high CV risk or nephropathy in the CANVAS (CANagliflozin cardioVascular Assessment Study) Program and the CREDENCE (Canagliflozin and Renal Events in Diabetes with Established Nephropathy Clinical Evaluation) trial. Objectives: The aim of this study was to assess the effects of canagliflozin on CV outcomes according to baseline estimated glomerular filtration rate (eGFR) and urine albumin:creatinine ratio (UACR) in pooled patient-level data from the CANVAS Program and CREDENCE trial. Methods: Canagliflozin effects on CV death or HHF were assessed by baseline eGFR (60 mL/min/1.73 m2) and UACR (300 mg/g). HRs and 95% CIs were estimated by using Cox regression models overall and according to subgroups. Results: A total of 14,543 participants from the CANVAS Program (N = 10,142) and the CREDENCE (N = 4,401) trial were included, with a mean age of 63 years, 35% female, 75% White, 13.2% with baseline eGFR 300 mg/g. Rates of CV death or HHF increased as eGFR declined and/or UACR increased. Canagliflozin significantly reduced CV death or HHF compared with placebo (19.4 vs 28.0 events per 1,000 patient-years; HR: 0.70; 95% CI: 0.62-0.79), with consistent results across eGFR and UACR categories (all P interaction >0.40). Conclusions: Risk of CV death or HHF was higher in those with lower baseline eGFR and/or higher UACR. Canagliflozin consistently reduced CV death or HHF in participants with T2DM and high CV risk or nephropathy regardless of baseline renal function or level of albuminuria. (Canagliflozin Cardiovascular Assessment Study [CANVAS], NCT01032629; A Study of the Effects of Canagliflozin [JNJ-24831754] on Renal Endpoints in Adult Participants With Type 2 Diabetes Mellitus [CANVAS-R], NCT01989754; and Evaluation of the Effects of Canagliflozin on Renal and Cardiovascular Outcomes in Participants With Diabetic Nephropathy [CREDENCE], NCT02065791
Renal Hyperfiltration Is a Determinant of Endothelial Function Responses to Cyclooxygenase 2 Inhibition in Type 1 Diabetes
Effects of dapagliflozin on volume status and systemic haemodynamics in patients with chronic kidney disease without diabetes:Results from DAPASALT and DIAMOND
Aims To assess the effect of sodium-glucose cotransporter-2 inhibitor dapagliflozin on natriuresis, blood pressure (BP) and volume status in patients with chronic kidney disease (CKD) without diabetes. Materials and methods We performed a mechanistic open-label study (DAPASALT) to evaluate the effects of dapagliflozin on 24-hour sodium excretion, 24-hour BP, extracellular volume, and markers of volume status during a standardized sodium diet (150 mmol/d) in six patients with CKD. In parallel, in a placebo-controlled double-blind crossover trial (DIAMOND), we determined the effects of 6 weeks of dapagliflozin on markers of volume status in 53 patients with CKD. Results In DAPASALT (mean age 65 years, mean estimated glomerular filtration rate [eGFR] 39.4 mL/min/1.73 m(2), median urine albumin:creatinine ratio [UACR] 111 mg/g), dapagliflozin did not change 24-hour sodium and volume excretion during 2 weeks of treatment. Dapagliflozin was associated with a modest increase in 24-hour glucose excretion on Day 4, which persisted at Day 14 and reversed to baseline after discontinuation. Mean 24-hour systolic BP decreased by -9.3 (95% confidence interval [CI] -19.1, 0.4) mmHg after 4 days and was sustained at Day 14 and at wash-out. Renin, angiotensin II, urinary aldosterone and copeptin levels increased from baseline. In DIAMOND (mean age 51 years, mean eGFR 59.0 mL/min/1.73 m(2), median UACR 608 mg/g), compared to placebo, dapagliflozin increased plasma renin (38.5 [95% CI 7.4, 78.8]%), aldosterone (19.1 [95% CI -5.9, 50.8]%), and copeptin levels (7.3 [95% CI 0.1, 14.5] pmol/L). Conclusions During a standardized sodium diet, dapagliflozin decreased BP but did not increase 24-hour sodium and volume excretion. The lack of increased natriuresis and diuresis may be attributed to activation of intra-renal compensatory mechanisms to prevent excessive water loss
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Measurements of the transverse-momentum-dependent cross sections of J /ψ production at mid-rapidity in proton+proton collisions at s =510 and 500 GeV with the STAR detector
We present measurements of the differential cross sections of inclusive J/ψ meson production as a function of transverse momentum (pTJ/ψ) using the μ+μ- and e+e- decay channels in proton+proton collisions at center-of-mass energies of 510 and 500 GeV, respectively, recorded by the STAR detector at the Relativistic Heavy Ion Collider. The measurement from the μ+μ- channel is for
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