Basal cardiomyopathy develops in rabbits with ventricular tachyarrhythmias induced by a single injection of adrenaline.

We have recently demonstrated that basal cardiomyopathy develops in rabbits with ventricular tachyarrhythmias that have been induced by electrical stimulation of the cervical vagus. This study investigated whether similar basal cardiomyopathy would develop in rabbits with ventricular tachyarrhythmias induced by a single injection of adrenaline. Adrenaline was intravenously infused for 10-360 seconds in anesthetized rabbits.

[An elderly woman with macrocytic anemia and acute high-output heart failure following acute bleeding due to a gastric ulcer].

Although macrocytic anemia can develop in patients with acute blood loss, such anemia in very old patients is uncommon. In this report, we describe the course of an 89-year-old woman who had a rapid recovery from macrocytic anemia by medication only after acute blood loss due to a gastric ulcer. She had been treated with antihypertensive drugs for the previous 28 years at our outpatient clinic, and was admitted because of acute anemia 6 days after she had experienced tarry stool.

Effects of the AT(1) receptor blocker losartan and the calcium channel blocker benidipine on the accumulation of lipids in the kidney of a rat model of metabolic syndrome.

Unfavorable lipid accumulation may occur in the kidneys in the presence of metabolic syndrome and diabetes. The aim of this study was to investigate whether excess lipids would accumulate in the kidneys of Otsuka Long-Evans Tokushima Fatty (OLETF) rats, an animal model of metabolic syndrome. From 34 weeks of age, OLETF rats were treated orally with a calcium channel blocker, benidipine (3 mg kg(-1) per day), or an AT1 receptor blocker, losartan (25 mg kg(-1) per day), for 8 weeks.

Administration of angiotensin II, but not catecholamines, induces accumulation of lipids in the rat heart.

Accumulation of lipids in the heart may cause cardiac dysfunction in various disorders, such as obesity and diabetes. In the current study, we have investigated whether administration of angiotensin II or norepinephrine induces accumulation of lipids and/or changes in the expression of genes related to lipid metabolism in the rat heart. Lipid deposition was found in myocardial, vascular wall, and perivascular cells of the angiotensin II-infused rat heart, and superoxide generation was increased in these lipid-positive cells.

Comparison of vasculoprotective effects of benidipine and losartan in a rat model of metabolic syndrome.

Although antihypertensive drugs confer improvement in endothelial dysfunction and protection from atherogenesis in hypertension, different classes of antihypertensive drugs may elicit different degrees of vasculoprotective effects. We have investigated the effects of a long-acting calcium antagonist, benidipine, and an angiotensin AT(1) receptor antagonist, losartan, on the vascular damage observed in OLETF rats, an animal model of metabolic syndrome. At 34 weeks of age, OLETF rats were treated with either benidipine (3 mg/kg/day, per os) or losartan (25 mg/kg/day, per os) for 8 weeks.

Angiotensin II-induced regulation of the expression and localization of iron metabolism-related genes in the rat kidney.

Due to recent discoveries of novel genes involved in iron metabolism, our understanding of the molecular mechanisms underlying iron metabolism has dramatically increased. We have previously shown that the administration of angiotensin II alters iron homeostasis in the rat kidney, which may in turn aggravate angiotensin II-induced renal damage. Here we have investigated the effect of angiotensin II administration on the localization and expression of transferrin receptor (TfR), divalent metal transporter 1 (DMT1), ferroportin 1 (FPN), and hepcidin mRNA in the rat kidney.

Expression and localization of PDGF-B, PDGF-D, and PDGF receptor in the kidney of angiotensin II-infused rat.

Lipid accumulation in the kidney is a marker of tissue damage and may play a role in the development of renal injury. We have previously shown that long-term administration of angiotensin II in rats causes increased expression of transforming growth factor-beta1, coupled with an accumulation of lipids in the tubular and vascular wall cells in the kidney. In this study, we examine the regulation of expression of platelet-derived growth factor (PDGF) and its receptor system and their co-localization with lipid deposits in the kidneys of angiotensin II-infused rats.

Lipid accumulation and transforming growth factor-beta upregulation in the kidneys of rats administered angiotensin II.

Abnormal lipid metabolism may play a role in progressive renal failure. We studied whether lipid accumulation occurs and whether lipid deposits are colocalized with transforming growth factor-beta1 (TGF-beta1) in the kidney of angiotensin II-infused animals. Oil red O staining showed marked lipid deposition in the tubular epithelial and vascular wall cells of angiotensin II-treated but not in norepinephrine-treated rats.

Iron chelation suppresses ferritin upregulation and attenuates vascular dysfunction in the aorta of angiotensin II-infused rats.

Objective: We have investigated whether long-term administration of angiotensin (Ang) II causes ferritin induction and iron accumulation in the rat aorta, and their possible relation to regulatory effects on gene expression and vascular function in Ang II-infused animals.

Methods And Results: Sprague-Dawley rats were given Ang II for 7 days via subcutaneously implanted osmotic minipumps. Ang II infusion caused a >20-fold increase in ferritin protein expression over control values.