Analytic properties of the Landau gauge gluon and quark propagators

We explore the analytic structure of the gluon and quark propagators of Landau gauge QCD from numerical solutions of the coupled system of renormalized Dyson--Schwinger equations and from fits to lattice data. We find sizable negative norm contributions in the transverse gluon propagator indicating the absence of the transverse gluon from the physical spectrum. A simple analytic structure for the gluon propagator is proposed. For the quark propagator we find evidence for a mass-like singularity on the real timelike momentum axis, with a mass of 350 to 500 MeV. Within the employed Green's functions approach we identify a crucial term in the quark-gluon vertex that leads to a positive definite Schwinger function for the quark propagator.Comment: 42 pages, 16 figures, revtex; version to be published in Phys Rev

Renal and hormonal responses to direct renin inhibition with aliskiren in healthy humans.

BACKGROUND: Pharmacological interruption of the renin-angiotensin system focuses on optimization of blockade. As a measure of intrarenal renin activity, we have examined renal plasma flow (RPF) responses in a standardized protocol. Compared with responses with angiotensin-converting enzyme inhibition (rise in RPF approximately 95 mL x min(-1) x 1.73 m(-2)), greater renal vasodilation with angiotensin receptor blockers (approximately 145 mL x min(-1) x 1.73 m(-2)) suggested more effective blockade. We predicted that blockade with the direct oral renin inhibitor aliskiren would produce renal vascular responses exceeding those induced by angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. METHODS AND RESULTS: Twenty healthy normotensive subjects were studied on a low-sodium (10 mmol/d) diet, receiving separate escalating doses of aliskiren. Six additional subjects received captopril 25 mg as a low-sodium comparison and also received aliskiren on a high-sodium (200 mmol/d) diet. RPF was measured by clearance of para-aminohippurate. Aliskiren induced a remarkable dose-related renal vasodilation in low-sodium balance. The RPF response was maximal at the 600-mg dose (197+/-27 mL x min(-1) x 1.73 m(-2)) and exceeded responses to captopril (92+/-20 mL x min(-1) x 1.73 m(-2); P<0.01). Furthermore, significant residual vasodilation was observed 48 hours after each dose (P<0.01). The RPF response on a high-sodium diet was also higher than expected (47+/-17 mL x min(-1) x 1.73 m(-2)). Plasma renin activity and angiotensin levels were reduced in a dose-related manner. As another functional index of the effect of aliskiren, we found significant natriuresis on both diets. CONCLUSIONS: Renal vasodilation in healthy people with the potent renin inhibitor aliskiren exceeded responses seen previously with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. The effects were longer lasting and were associated with significant natriuresis. These results indicate that aliskiren may provide more complete and thus more effective blockade of the renin-angiotensin system

Varying patterns of the antihypertensive and antialbuminuric response to higher doses of renin-angiotensin-aldosterone system blockade in albuminuric hypertensive type 2 diabetes mellitus patients

Objective: In patients with type 2 diabetes mellitus (T2DM), blocking of the renin-angiotensin-aldosterone system (RAAS) has demonstrated efficacy in lowering blood pressure (BP) and urinary albumin excretion rate (UAER). Nonetheless, not all patients successfully respond to RAAS blockade with a reduction in BP and UAER. Methods: This secondary analysis of a double-blind study of 391 patients with T2DM assessed the importance of using higher doses of the RAAS blocker valsartan to improve the BP and UAER response in patients initially identified as prompt or delayed responders. All patients received a starting dose of valsartan 160mg for a 4-week run-in period to classify them as either prompt responders (SBP<130mmHg or reduction in SBP 6510mmHg, 53%) or delayed responders (47%). All patients were then subsequently randomized to one of three valsartan doses: 160, 320, or 640 mg/day for 26 weeks. Results: Higher doses of valsartan (640 mg) demonstrated additional reductions in SBP among the prompt responders and led to greater SBP reductions from baseline (19.8mmHg) compared with valsartan 160 (14.4mmHg, P<0.05) and 320mg (16.5 mmHg). Among delayed responders, SBP reductions from baseline to end of study were similar (11-14mmHg, P 650.05) across all valsartan doses. For UAER, higher valsartan doses produced further reductions by week 30, regardless of initial response. Conclusion Higher doses of valsartan did not appear to recruit delayed responders, but enhanced the prompt responder effects in patients with T2DM. Not all patients successfully respond in concordance to RAAS blockade with both reductions in BP and UAER. Reduction in BP dominates the antialbuminuric effect in both valsartan prompt responders and delayed responders independent of dose