No abstract available.
Angiotensin II ; Angiotensin Receptor Antagonists ; Angiotensins ; Hyperkalemia ; Receptors, Angiotensin

Angiotensin Receptor Antagonists ; Heart Failure ; Humans ; Neprilysin ; Receptors, Angiotensin

Angiotensin Receptor Antagonists ; Atrial Fibrillation ; physiopathology ; Heart Atria ; cytology ; physiopathology ; Humans ; Membrane Potentials ; Receptors, Angiotensin ; agonists

Whether immunosuppressive therapy may have beneficial effects in the treatment of IgA nephropathy remains controversial. ACE inhibitor or angiotensin II receptor antagonist(AIIA) are suggested to reduce urinary protein excretion(Up) in patients with renal diseases. We therefore investigated the effects of the angiotensin II receptor antagonist losartan on the proteinuria and renal function in patients with IgA nephropathy. AIIA reduced blood pressure in patients with hypertension, but there were no significant differences statistically before and after therapy. AIIA reduced Up after 1-4 months(2.8+/-1.1 to 1.1+/-1.0g/24h, p=0.001) and 7-13 months(2.8+/-1.1 to 1.7+/-0.6g/24h, p=0.017). There were no significant changes of serum creatinine levels after AIIA treatment. Cough or angioedema were not observed during AIIA treatment. In conclusion, AIIA may be useful in the treatment of patients with IgA nephropathy and proteinuria.
Angioedema ; Angiotensin II* ; Angiotensin Receptor Antagonists* ; Angiotensins* ; Blood Pressure ; Cough ; Creatinine ; Glomerulonephritis, IGA ; Humans ; Hypertension ; Losartan ; Proteinuria ; Receptors, Angiotensin*

Pharmacotherapy for the treatment of heart failure has advanced considerably in recent years, and clinical trials have demonstrated the favorable long-term effects of angiotensin-converting enzyme inhibitors (ACEI) and beta-blockers on the morbidity and mortality. Although the current guidelines recommend ACEI and beta-blockers as standard therapy for heart failure, as they have demonstrated benefits in terms of mortality, only one third of patients with heart failure are receiving both classes of drug due to concern over their adverse effects. The benefit of ACEI has been attributed largely to blockade of angiotensin II production, but also to the accumulation of bradykinin. The accumulation of bradykinin however, has been implicated as contributing to adverse effects, such as a dry cough, associated with ACEI treatment, and has also been suggested to result in prejunctional norepinephine release. Recently, many clinical trials have shown that angiotensin receptor blockers (ARBs) had similar effect on the mortality and morbidity of patients with heart failure. The side effects, notably the cough, are significantly less than with ACE inhibitors. ARBs could also be recommended for patients who can not tolerate ACE inhibitors for symptomatic treatment. In combination with ACEI, ARBs may improve the symptoms of heart failure, and reduce hospitalizations due to heart failure deterioration. Whether concomitant beta-blockade negatively affects the effect of ARB will require further evaluation. In this paper, recent large clinical trials of ARBs therapy in heart failure, and the ongoing clinical trials, were reviewed for the recommendation of the optimal conditions for ARBs treatment in heart failures.
Angiotensin II* ; Angiotensin Receptor Antagonists* ; Angiotensin-Converting Enzyme Inhibitors ; Angiotensins* ; Bradykinin ; Cough ; Drug Therapy ; Estrogens, Conjugated (USP)* ; Heart ; Heart Failure* ; Hospitalization ; Humans ; Mortality ; Receptors, Angiotensin*

BACKGROUND: To compare the parameters of local carotid stiffness with those of global arterial stiffness and to investigate the effects of angiotensin II receptor blocker (ARB) on the parameters of local carotid arterial stiffness as well as global arterial stiffness. METHODS: The correlations of the parameters between local carotid and global arterial stiffness were compared at baseline, and the changes of these parameters were evaluated after 6 months of valsartan therapy in 50 patients with newly diagnosed hypertension. Diameter change, strain, and 2-dimensional circumferential strain (2D CS) of the carotid artery measured by speckle tracking method were used as parameters of local arterial stiffness, and the parameters of pulse wave velocity (PWV) and pulse wave analysis (PWA) were used as standard parameters of global arterial stiffness. RESULTS: Carotid 2D CS, not conventional strain or diameter change, showed significant correlation with age (r = -0.592, p < 0.01), brachial-ankle PWV (r = -0.338, p < 0.05), and augmentation index (r = -0.298, p < 0.05). After 6 months of medical therapy, systolic blood pressure (SBP) and diastolic blood pressure (DBP) were decreased significantly (SBP: 155.9 +/- 14.2 to 137.6 +/- 10.5 mm Hg, p < 0.01; DBP: 90.1 +/- 11.8 to 81.6 +/- 8.0 mm Hg, p < 0.01). The parameters of PWV and PWA were significantly improved, but the parameters of carotid arterial stiffness were not changed significantly. CONCLUSIONS: In hypertensives, carotid 2D CS showed better correlation with ageing and the parameters of global arterial stiffness than conventional strain or diameter change of the carotid artery. Global arterial stiffness was improved by 6 months of medical treatment with ARB, but the local carotid arterial stiffness was not changed.
Angiotensin Receptor Antagonists ; Blood Pressure ; Carotid Arteries ; Humans ; Hypertension* ; Pulse Wave Analysis ; Receptors, Angiotensin ; Vascular Stiffness* ; Valsartan

BACKGROUND: Weight reduction is a lifestyle intervention that has been introduced for prevention and management of chronic kidney disease (CKD). We investigate the additive anti-proteinuric effect of weight reduction on the usage of angiotensin II receptor blockers (ARBs) and its potential mechanisms in hypertensive CKD patients. METHODS: This study is a subanalysis of data from an open-label, randomized, controlled clinical trial. Among the 235 participants, 227 were assigned to subgroups according to changes in body weight. RESULTS: Fifty-eight participants (25.6%) were assigned to group 1 (≥1.5% decrease in body weight after 16 weeks), 32 participants (14.1%) were assigned to group 2 (1.5–0.1% decrease in body weight), and 136 participants (59.9%) were assigned to group 3 (≥ 0.0% increase in body weight). Characteristics at enrollment were not different among the three groups, but mean differences in weight and percent changes in urinary sodium excretion over the period were statistically different (P < 0.001 and P = 0.017). Over the study period, unintentional weight loss independently increased the probability of reduced albuminuria (group 1, relative risk 6.234, 95% confidence interval 1.913–20.315, P = 0.002). Among urinary cytokines, only podocalyxin level decreased significantly in participants who lost weight (P = 0.013). CONCLUSION: We observed that weight loss had an additive effect on the anti-proteinuric effects of ARBs in nondiabetic hypertensive CKD patients, although it was minimal. An additive effect was shown in both obese and non-obese participants, and its possible mechanism is related to reduction of podocyte damage.
Albuminuria ; Angiotensin II* ; Angiotensin Receptor Antagonists* ; Angiotensins* ; Body Weight ; Cytokines ; Humans ; Hypertension ; Life Style ; Podocytes ; Proteinuria* ; Receptors, Angiotensin* ; Renal Insufficiency, Chronic* ; Sodium ; Weight Loss*

The renin-angiotensin system (RAS) is an important regulator of cirrhosis and portal hypertension. As hepatic fibrosis progresses, levels of the RAS components angiotensin (Ang) II, Ang-(1–7), angiotensin-converting enzyme (ACE), and Ang II type 1 receptor (AT1R) are increased. The primary effector Ang II regulates vasoconstriction, sodium homoeostasis, fibrosis, cell proliferation, and inflammation in various diseases, including liver cirrhosis, through the ACE/Ang II/AT1R axis in the classical RAS. The ACE2/Ang-(1–7)/Mas receptor and ACE2/Ang-(1–9)/AT2R axes make up the alternative RAS and promote vasodilation, antigrowth, proapoptotic, and anti-inflammatory effects; thus, countering the effects of the classical RAS axis to reduce hepatic fibrogenesis and portal hypertension. Patients with portal hypertension have been treated with RAS antagonists such as ACE inhibitors, Ang receptor blockers, and aldosterone antagonists, with very promising hemodynamic results. In this review, we examine the RAS, its roles in hepatic fibrosis and portal hypertension, and current therapeutic approaches based on the use of RAS antagonists in patients with portal hypertension.
Angiotensin-Converting Enzyme Inhibitors ; Angiotensins ; Cell Proliferation ; Fibrosis* ; Hemodynamics ; Humans ; Hypertension, Portal* ; Inflammation ; Liver Cirrhosis ; Mineralocorticoid Receptor Antagonists ; Receptors, Angiotensin ; Renin-Angiotensin System* ; Sodium ; Vasoconstriction ; Vasodilation

The physiological roles of brain angiotensin II in mediating water deprivation-induced drinking and in regulating renal renin release were assessed in male Sprague-Dawley rats. Specific AT1 receptor antagonists, losartan and SK 1080, and antisense oligonucleotide (AS-ODN) directed to AT1 receptor mRNA were intracerebroventricularly (i.c.v.) administered in conscious unrestrained rats. When water was given 20 min after i.c.v. injection of AT1 receptor antagonists in 48-h water-deprived rats, losartan and SK 1080 produced approximatly 20% and 50% decrease in 1-h water intake, respectively. In contrast, i.c.v. treatment of the AS-ODN to AT1 receptor mRNA for 24-h did not alter 1-h water intake in 24-h water-deprived rats, but prevented the increase in overnight water intake after 24-h water-deprivation. Six-day i.c.v. treatment of AS-ODN did not alter either the basal plasma renin concentration or renal cortical levels of renin and renin mRNA. The present results suggest that endogenous brain Ang II plays an important role in thirst and water intake through AT1 receptors, but further studies are required to elucidate its regulatory role in renal renin synthesis.
Angiotensin II* ; Angiotensin Receptor Antagonists* ; Angiotensins* ; Animals ; Brain* ; Drinking* ; Humans ; Losartan ; Male ; Negotiating ; Plasma ; Rats* ; Rats, Sprague-Dawley ; Receptors, Angiotensin* ; Renin* ; RNA, Messenger ; Thirst ; Water

Recently several kinds of new antihypertensive agents were introduced. Diuretics such as indapamide, metyrazone and eprelerone have less side effects compared to thiazide, and have an effect in renal insufficiency. Carvedilol, combined alpha- and beta- adrenergic blocker, has a vasodilating property and an effect on heart failure. The lipid soluble third generation calcium antagonists such as amlodipine, lacidipine and lercardipine are slow onset and long acting and have less side effects, which provide continued effect even if daily doses are missed. Multiple angiotensin converting inhibitors and angiotensin receptor blockers, and the specific aldosterone antagonist eprenolone to block renin-angiotensin-aldosterone system are now available. Additionally new class antihypertensive drugs such as the vasopeptidase inhibitor, the endothelin receptor blocker and the renin inhibitor have been under investigation and shown favorable clinical results, and will be available for clinical use soon.
Adrenergic Antagonists ; Aldosterone ; Amlodipine ; Angiotensin Receptor Antagonists ; Angiotensins ; Antihypertensive Agents ; Calcium ; Diuretics ; Heart Failure ; Hypertension* ; Indapamide ; Receptors, Endothelin ; Renal Insufficiency ; Renin ; Renin-Angiotensin System