Neurohormonal consequences of diuretics in different cardiovascular syndromes

Diuretics have long been used to lower blood pressure in hypertensive patients or to control body fluid and electrolyte homeostasis in diseases such as congestive heart failure, chronic renal failure or cirrhosis. The initial response to diuretics is negative sodium and fluid balance. The diuretic-induced loss of salt and water activates several hormonal systems such as vasopressin, the renin-angiotensin-aldosterone system or the sympathetic nervous system which tend to compensate for the changes in sodium and water balance. This neurohormonal response may have important clinical implications. Thus, the activation of the renin-angiotensin-aldosterone cascade appears to be partially responsible for the flat dose-blood pressure response curve of thiazides in hypertensive patients. It may also be responsible for the difference between responders and non-responders to diuretic therapy and for the development of side-effects such as hypokalaemia, metabolic alkalosis or hyponatraemia. There are several ways to prevent the undesirable consequences of the neurohormonal responses to diuretics. The first is to use low doses of these agents. It is also possible to combine them with agents that block the activity of the renin-angiotensin-aldosterone system such as ACE inhibitors or in combination with drugs that reduce aldosterone secretion such as calcium antagonists. The development of drugs able to enhance urinary sodium excretion and to reduce simultaneously the activity of the renin-angiotensin-aldosterone system may offer a new interesting alternative. This might perhaps be achieved in the future with the administration of neutral endopeptidase inhibitors which interfere with the enzymatic degradation of atrial natriuretic peptid

Measuring the equation of state of a hard-disc fluid

We use video microscopy to study a two-dimensional (2D) model fluid of charged colloidal particles suspended in water and compute the pressure from the measured particle configurations. Direct experimental control over the particle density by means of optical tweezers allows the precise measurement of pressure as a function of density. We compare our data with theoretical predictions for the equation of state, the pair-correlation function and the compressibility of a hard-disc fluid and find good agreement, both for the fluid and the solid phase. In particular the location of the transition point agrees well with results from Monte Carlo simulations.Comment: 7 pages, to appear in EPL, slightly corrected versio

Electronic properties of very thin native SiO2/a-Si:H interfaces and their comparison with those prepared by both dielectric barrier discharge oxidation at atmospheric pressure and by chemical oxidation

The contribution deals with electronic properties of thin oxide/amorphous hydrogenated silicon (a-Si:H) measured by capacitance-voltage (C-V) and charge version of deep level transient spectroscopy (Q-DLTS). The interest was focused on the studies of the interface properties of very thin dielectrics formed by dielectric barrier discharge (DBD) or natively on the a-Si:H layer. These properties were compared with those of oxide layers prepared by chemical oxidation in HNO3. The DBD was used for the preparation of a very thin SiO2 layer on a-Si:H for the first time to our knowledge. Preliminary electrical measurements confirmed that a very low interface states density was detected in the case of the native oxide/a-Si:H and DBD oxide/a-Si:H

Plasma Angiotensin II and the Antihypertensive Action of Angiotensin-Converting Enzyme Inhibition

The measurement of immunoreactive "angiotensin II” in plasma cannot provide an accurate reflection of the efficacy of angiotensin-converting enzyme (ACE) inhibition because different angiotensin fragments interfere in all radioimmunoassays available so far. More complex methods are necessary in order to measure specifically angiotensin-(1-8)octapeptide. With such methodology it can be shown that no tolerance develops to the angiotensin II-reducing effect of ACE inhibitors after prolonged administration. Marked reduction of angiotensin II levels can be shown even in patients with primary aldosteronism. At peak blockade, the level of plasma angiotensin II is still related to circulating active renin and angiotensin I. Accordingly, because ACE inhibitors raise circulating angiotensin I in a dose-dependent fashion, this should be taken into account when dosing ACE inhibitors. The hypothesis that tissue renin-angiotensin systems play an important independent role in determining vasomotor tone is very interesting. However, any discussion on whether tissue or plasma renin determines the pharmacological effect of ACE inhibitors should be based on the simultaneous measurement of true angiotensin II in tissue and plasma under steady-state conditions. Am J Hypertens 1989;2:286-29

Dose-Response Relationships of ACE Inhibitors and Angiotensin II Blockers

It is difficult to establish dose-response relationships for ACE inhibitors in patients with hyperternion or congestive heart failure. This has led to the widely held opinion that the effects of ACE inhibitors are hardly dose dependent. The purpose of this short discussion is to demonstrate that this class of compounds, as well as the more recent angiotemin II receptor antagonists, exhibit some very clear dose-response relationships when these are evaluated in normal volunteers based on the mechanisms for which they were designed. Characterization of these dose-response curves is important in order to use these drugs at their optimol dose and to obtain the maximal therapeutic benefi

D-brane superpotentials and RG flows on the quintic

The behaviour of D2-branes on the quintic under complex structure deformations is analysed by combining Landau-Ginzburg techniques with methods from conformal field theory. It is shown that the boundary renormalisation group flow induced by the bulk deformations is realised as a gradient flow of the effective space time superpotential which is calculated explicitly to all orders in the boundary coupling constant.Comment: 24 pages, 1 figure, v2:Typo in (3.14) correcte

Hybrid diffractive-refractive optics: opportunities and technologies to realize complex optical imaging Systems

[no abstract available

Effect of many-body interactions on the solid-liquid phase-behavior of charge-stabilized colloidal suspensions

The solid-liquid phase-diagram of charge-stabilized colloidal suspensions is calculated using a technique that combines a continuous Poisson-Boltzmann description for the microscopic electrolyte ions with a molecular-dynamics simulation for the macroionic colloidal spheres. While correlations between the microions are neglected in this approach, many-body interactions between the colloids are fully included. The solid-liquid transition is determined at a high colloid volume fraction where many-body interactions are expected to be strong. With a view to the Derjaguin-Landau-Verwey-Overbeek theory predicting that colloids interact via Yukawa pair-potentials, we compare our results with the phase diagram of a simple Yukawa liquid. Good agreement is found at high salt conditions, while at low ionic strength considerable deviations are observed. By calculating effective colloid-colloid pair-interactions it is demonstrated that these differences are due to many-body interactions. We suggest a density-dependent pair-potential in the form of a truncated Yukawa potential, and show that it offers a considerably improved description of the solid-liquid phase-behavior of concentrated colloidal suspensions

The renin—angiotensin system in refractory heart failure: clinical, hemodynamic and hormonal effects of captopril and enalapril

Studies using a competitive inhibitor of angiotensin II (saralasin) or converting enzyme inhibitors (teprotide, captopril, enalapril) have established that the renin-angiotensin system participates in the control of vascular tone in congestive heart failure both in experimental settings and in patients. In man, the marked decrease in left ventricular filling pressure and the variable increase in stroke volume induced by renin-angiotensin blockade suggests that angiotensin II actively constricts venous as well as arteriolar vascular beds. Captopril, in doses of 25 to 150 mg p.o. TID, maintains its efficacy during chronic administration with persistent clinical and hemodynamic improvement as well as increased exercise tolerance. In our experience, enalapril, 10 mg p.o., improves cardiac function within 4 to 6 h as reflected by a 30% decrease in left ventricular filling pressure, a 28% increase in stroke volume in the face of unchanged heart rate. Clinical improvement, enhanced exercise tolerance and characteristic hormonal responses suggest that enalapril also maintains its efficacy during long-term treatment. Chronic angiotensin II converting enzyme inhibition appears to be a major advance in the treatment of patients with severe congestive heart failure, refractory to digitalis and diuretic