This study was designed to test the hypothesis that increased pressure itself could cause endothelial dysfunction and lead to decreased nitric oxide (NO) release, partly through effects on the tissue renin angiotensin system in hypertension. Cultured endothelial cells (ECs) isolated from the aortas of WKY rats were continuously exposed to a pressure of 150 mmHg in a CO2 incubator for 72 h using a pressure system, and the NOx (NO2 and NO3) and angiotensin II (Ang II) concentrations in the supernatant were measured. An Ang decreased in patients with secondary hypertension (3), and antihypertensive therapy can improve EDR (4, 5); moreover, we have demonstrated that lowering pressure improves NO release from the ECs of hypertensive rats (6). Thus high blood pressure itself may promote endothelial dysfunction.There are two very important modulators of endothelial NO release; one consists of direct hemodynamic changes and the other of humoral factors such as the renin-angiotensin system (RAS). Endothelial cells (ECs) lining the vessel lumen are exposed to various mechanical forces, including shear stress, stretch, and transmural pressure, which are produced by blood pressure and blood flow. These hemodynamic forces are known to elicit many important physio-

Stress elevates blood pressure (BP) by increased sympathetic nerve activity. Cilnidipine, a novel dihydropyridine calcium antagonist that has inhibitory actions on N-type as well as L-type voltage-dependent calcium channels, has been reported to attenuate the cold stress-induced increase in plasma norepinephrine and BP in rats. Because white coat effect is associated with an enhanced pressor response to mental stress, we postulated that cilnidipine would attenuate white coat effect in patients with essential hypertension. Sixty-one consecutive outpatients (50 men, 11 women) with essential hypertension were studied prospectively. Twenty-nine patients were treated with either cilnidipine (n = 15) or nifedipine, a representative L-type voltage-dependent calcium antagonist (n = 14). Gender, age, body mass index, duration of hypertension, target organ damage of hypertension, and BP and heart rate (HR) were not significantly different between cilnidipine and nifedipine groups, and both systolic (SBP) and diastolic BP (DBP) were significantly decreased after treatment in both groups. White coat effects on systolic and DBP and HR were not significantly different between groups before antihypertensive treatment. Cilnidipine, but not nifedipine, significantly reduced white coat effects on SBP and HR. Furthermore, white coat effects on systolic BP and HR were significantly lower after treatment in the cilnidipine group compared with the nifedipine group. These data suggest that cilnidipine may reduce white coat effect in hypertensive patients by N-type calcium channel antagonism.

SUMMARYPercutaneous interventional procedures in the renal arteries are usually performed employing a femoral or brachial vascular access. In contrast, the transradial approach has been established for coronary angiography and angioplasty. We encountered a patient with Leriche syndrome who had renovascular hypertension ascribed to a severe left renal artery stenosis. To stabilize his blood pressure, we made an attempt to relieve the renal artery stenosis with Leriche syndrome by transradial renal artery angioplasty and stenting, using devices for coronary intervention. The procedure was successful without complications or residual stenosis. His hypertension improved with less antihypertensive medications. This case suggests that the radial approach might become an alternative entry site for renal artery interventions. (Int Heart J 2005; 46: 557-562)

We examined the role of the central nervous system, and particularly the renin-angiotensin (RA) system, in the development of hypertension produced by chronic inhibition of NO synthesis. In experiment 1, Wistar rats drank either nitro-L-arginine-methyl ester (L-NAME) or tap water. Before L-NAME treatment rats were divided into 6 groups. Four of them were administered either losartan or artificial cerebroventricular fluid (a-CSF) intracerebroventricularly (i.c.v.) for 1 week using an osmotic mini pump. The other two groups were administered the same amount of losartan intravenously (i.v.). In experiment 2, cardiovascular responses to acute i.c.v. losartan and muscimol, a GABA(A) agonist, were examined in conscious L-NAME-treated rats. Finally, in experiment 3, effects of ablation of the AV3V (anteroventral third ventricle) area, known to be one of the centers of cardiovascular control, were tested in the development of L-NAME hypertension. The development of hypertension by L-NAME treatment was attenuated with chronic i.c.v. losartan in a dose-dependent manner, while i.v. losartan had no effect. One week after cessation of i.c.v. losartan, blood pressure was elevated to the same level as in a-CSF-infused, L-NAME-treated rats. Acute i.c.v. losartan produced no cardiovascular changes in either L-NAME-treated or control rats. On the other hand, although i.c.v. muscimol elicited depressor effects in both groups, these responses were significantly larger in L-NAME-treated rats. Cardiovascular responses to i.v. hexamethonium were similar in both groups. The existence of prior lesions in the AV3V area significantly attenuated the development of L-NAME-induced hypertension. These results indicate that the central RA system plays an important role in the development of hypertension produced by chronic inhibition of NO synthase. Moreover, disorder of the central GABA system, rather than that of the RA system, might be important in the maintenance of hypertension in this model.

Acute necrotizing eosinophilic myocarditis is characterized by acute onset, fulminant congestive heart failure, and extensive necrosis of myocytes with striking eosinophilic infiltration. However, multinucleated giant cells sometimes appear in the fulminant phase of severe myocarditis. This is the first case of a patient with a 1 year previous history of idiopathic thrombocytopenic purpura, whopresented with acute necrotizing eosinophilic myocarditis with giant cell infiltration. (Internal Medicine 36: 894-897, 1997) Key words: eosinophils, hypereosinophilic syndrome, giant cell myocarditis Case ReportA 41-year-old manwas referred to our hospital for evaluation of cardiac failure on May 31, 1995. He had a past history of idiopathic thrombocytopenic purpura (ITP) in April 1994 when he complained of purpura at his extremities and bleeding in his oral cavity. At that time, his platelet count was markedly reduced to 2.0xl09//. The white blood cell (WBC)count was 6.2x109//with 5% eosinophils. He was diagnosed as having ITP at another hospital on the basis of an elevated level of platelet- (25 g/day for 5 days) effectively and rapidly improved his platelet count to 308x109// nine days later. Then, the dosage of prednisolone was reduced by 5 mg per week and discontinued 1 month later. In September 1994, his platelet count was 359xl09//andWBC countwas 9.0xl09//with 16% eosinophils. Thereafter, he did not consult a doctor because he recovered from ITP without recurrence. On May 26, 1995, he began to complain of dyspnea and general fatigue without any preceding clinical symptomsof infection. He consulted a doctor again and was noted to have an electrocardiogram (ECG) abnormality, elevated levels of myocardial enzymes, and pericardial effusion. Because of sustained hypotension in spite of treatment with catecholamines, he was transferred to our hospital for further evaluation. On admission, he had a body temperature of 37.5 degrees centigrade, blood pressure of 94/70 mmHg, heart rate of 1 10 beats/min, and a respiratory rate of 24/min. His jugular veins were markedly dilated. Heart auscultation revealed the presence of a gallop rhythm, but no crackles were audible. There was no peripheral edema. Neither Osier' s painful spot nor splinter hemorrhagewas noted. The ECGshowed sinus tachycardia, complete right bundle branch block, left posterior hemiblock, and a low voltage in peripheral leads (Fig. 1). The chest radiograph showed cardiomegaly and moderate pulmonary congestion (Fig. 2). The 2-dimensional echocardiography showed diffuse hypokinesis of the left ventricle (LV) and an apparent pericardial effusion. LV wall thickness was increased to 20 mmat the interventricular septum and to 14 mmat the posterior wall. The LVejection fraction was 28%. Laboratory data on admission were as follows: WBCcount of 8.3xl09// with an increased eosinophils (21%). Red blood cell (RBC) count of 4,700x109//, hemoglobin of 150 g/Z, and a platelet count of 209x109//. The erythrocyte sedimentation rate was 26 mm/h. The lactate dehydrogenase (L...