angiotensin/edema

Captopril (SQ14,225), an orally administered angiotensin converting enzyme inhibitor, was given to 8 patients with idiopathic edema, in order to study the role of the renin-angiotensin-aldosterone system in orthostatic sodium and water retention. Compared to 5 normal subjects, patients with

Recent studies have demonstrated that the renin-angiotensin system (RAS) participates in the processes of inflammation. An active component of this system, angiotensin II (Ang II), differentially regulates the production of oxyradicals, nitric oxide, prostaglandins, platelet-activating factors and

Plasma levels of renin activity, angiotensin II and aldosterone were determined in 16 patients with high altitude pulmonary edema (HAPE) with radioimmunoassay and compared with those in the controls including 9 patients with high altitude acute response (HAAR) and 14 health subjects. All of them

To test the hypothesis that angiotensin II could be a mediator of acute lung injury, we studied the effects of perindopril diacid, a new angiotensin-converting enzyme inhibitor, on hemodynamics, blood gases, lung mechanics, and extravascular lung water (EVLW). Twenty-four dogs were anesthetized,

BACKGROUND Peripheral edema is a common adverse effect of calcium channel blockers. The addition of a renin-angiotensin system blocker, either an angiotensin-converting enzyme inhibitor or an ARB, has been shown to reduce peripheral edema in a dose-dependent way. METHODS We performed a

This study was performed to demonstrate an experimental procedure of pulmonary edema induced by angiotensin I (AT I) in rats and to elucidate the mechanism of hemodynamic pulmonary edema. In the previous pilot study, 20 microg/kg of AT I was found to be an adequate dose for inducing pulmonary edema.

OBJECTIVE Angioneurotic edema is a well-documented complication of angiotensin-converting enzyme inhibitors (ACEI). We report a case of acute airway obstruction from a late-onset, probable ACEI-related angioneurotic edema and its subsequent management. METHODS A 48-yr-old obese man presented for

This study examined the hypothesis that the development of hydrops fetalis after asphyxia in the 0.6 gestation sheep fetus would be associated with activation of the fetal renin-angiotensin system (RAS). Fetuses were randomly assigned to either sham occlusion (n = 7) or to 30 min of asphyxia induced

OBJECTIVE Neurogenic pulmonary edema (NPE ) was indicative of poor prognosis in the epidemic of enterovirus 71 infections. The pathogenesis of NPE remains poorly understood. The objectives of this experimental study were to explore whether RAS is activated during NPE in rabbit models induced by

We conducted the present study to propose a rabbit model of pulmonary edema (PE) induced by angiotensin II (AII) and to test the preventive effect of losartan on this form of PE. AII was administered to rabbits intravenously at 50, 100, 150 or 300 microg/kg, either by continuous infusion (10 min) or

Either flash pulmonary edema or hyponatremic hypertensive syndrome has been described in renal artery stenosis. However, coexistence of these two disorders has never been previously reported. We describe a patient who presented with flash pulmonary edema and hyponatremic hypertensive syndrome

Carrageenan-induced edema of rat paw was greatly potentiated by orally or locally administered angiotensin converting enzyme (CE, identical with kininase II) inhibitor, (4R)-3-[(2S)-3-mercapto-2-methylpropanoyl]-4-thiazolidinecarboxylic acid (YS980). The potentiative effect of YS980 was observed by

Elevated levels of angiotensin-converting enzyme activity (ACE) in bronchoalveolar lavage fluid (BAL) have been used as a specific marker for pulmonary endothelial cell injury associated with high permeability lung edema. Alternatively, however, BAL-ACE elevations might reflect a nonspecific leak of