We examined the role of dietary electrolytes and humoral factors in causing seasonal changes in blood pressure. Normal subjects had no seasonal difference in blood pressure, although urinary sodium and norepinephrine were significantly higher in winter than in summer. In patients with essential hypertension blood pressure, urinary sodium and norepinephrine excretion and plasma norepinephrine concentration were significantly higher in winter. Plasma renin activity, plasma and urinary aldosterone and urinary kallikrein excretion were not significantly different between the two seasons in both normal subjects and hypertensive patients. In conclusions, the blood pressure of patients with essential hypertension has a seasonal variation with higher pressures in the winter than in the summer. Increased sympathetic nervous activity and an increased load of sodium presented to the kidney for excretion may be contributing factors in the rise in blood pressure in winter in patients with essential hypertension.

Endothehal function 1s known to be ImpaIred m essential hypertensive patients In this study, we examined whether antihypertensive drugs improve forearm vasochlatory response to reactive hyperenna m 26 patients with essential hypertension (6222 years) without dtabetes melhtus, hyperhpldemla, coronary heart disease, or cerebrovascular disease AntIhypertensive drugs were never given or were chscontmued for at least 4 weeks before the study Patients were treated with monotherapy of &her temocaprtl (2 or 4 mg, n= 15) or amlochpme (2 5 or 5 mg, n= 11) for 6 months Forearm blood flow was measured by strain-gauge plethysmography Vasodilator response to the release of upper arm compression at 300 mm Hg for 5 minutes and to sublingual admmistration of mtroglycenn (0 3 mg) were assessed Changes of forearm blood flow response to reactive hyperenna were sigmficantly less m hypertensive patients (99218%) than m age- E ndothehal cells play a pIvota role m the modulation of vascular tone by releasing vasoactive substances, such as endothelm, prostaglandm, and endothelium-derived relaxing factor (EDRF). 1~2 In the early stage of atherogenesis, endothehal cell function 1s known to be disturbed.3 This results in lmpairment of the vasochlator response to acetylcholme, which requires Intact endothehal function 4 There 1s considerable evidence that the endothehum-dependent vasodilation 1s impaired in human essential hypertenslon.5.10 The effects of various antlhypertenslve drugs on hypertension-induced endothehal dysfunction have been examined widely. In animal studies, angiotensmconverting enzyme (ACE) mhWors have been shown to improve endothehal function. II-14 However, m human hypertension, the results are not consistent, several investigators demonstrated that ACE mhibltors improved endothelial dysfunction m hypertensive patients,l5-17 while others failed to show an lmprovement 18,19 The effect of calcium antagonists has not been fully examined except m rats13 and an acute human study '6 CelermaJer et al*0 evaluated endothehal function by Doppler system m the brachlal and femoral arteries during reactive hyperemla and after sublmgual adnumstration of nitroglycerm. Both procedures induce vasochlation; however, the former 1s partly mediated by Hlgashlosaka 577 Japan E-mail nagano@ gerlat med Osaka-u ac JP 0 1997 American Heart Assoclatlon, Inc EDRF,2',22 while the latter acts directly on smooth muscle cells. In this study, we used CelermaJor's method with modlficatlon to evaluate the effects of an ACE mhlbitor, temocapnl, and a calcium antagonist, amlochpine, on forearm vasodllator response m patients with essential hypertension These drugs were given as monotherapy for 6 months in hypertensive patients without any overt chnlcal evidence of atherosclerosis Subjects MethodsThe SubJects were 26 panents with essential hypertension aged 52 to 80 years (mean+-SEM, 62?2 years) and another 37 age-and sexmatched normotensive mdividuals as control Hypertension was defined as systolic blood pressure at the outpatient department of ...

BackgroundPandemic influenza A(H1N1) virus infection quickly circulated worldwide in 2009. In Japan, the first case was reported in May 2009, one month after its outbreak in Mexico. Thereafter, A(H1N1) infection spread widely throughout the country. It is of great importance to profile and understand the situation regarding viral mutations and their circulation in Japan to accumulate a knowledge base and to prepare clinical response platforms before a second pandemic (pdm) wave emerges.MethodologyA total of 253 swab samples were collected from patients with influenza-like illness in the Osaka, Tokyo, and Chiba areas both in May 2009 and between October 2009 and January 2010. We analyzed partial sequences of the hemagglutinin (HA) and neuraminidase (NA) genes of the 2009 pdm influenza virus in the collected clinical samples. By phylogenetic analysis, we identified major variants of the 2009 pdm influenza virus and critical mutations associated with severe cases, including drug-resistance mutations.Results and ConclusionsOur sequence analysis has revealed that both HA-S220T and NA-N248D are major non-synonymous mutations that clearly discriminate the 2009 pdm influenza viruses identified in the very early phase (May 2009) from those found in the peak phase (October 2009 to January 2010) in Japan. By phylogenetic analysis, we found 14 micro-clades within the viruses collected during the peak phase. Among them, 12 were new micro-clades, while two were previously reported. Oseltamivir resistance-related mutations, i.e., NA-H275Y and NA-N295S, were also detected in sporadic cases in Osaka and Tokyo.

A 36-year-old female case of normotensive normoreninemic primary aldosteronism with persistent hypokalemia and nephrocalcinosis is reported. She was referred to us for episodes of sudden muscle weakness during 8 years prior to admission. On the first day of admission, her blood pressure was 174/104 mmHg. On the second day of admission blood pressure normalized to 120/80 mmHg. Both of her parents were hypertensive. Arterial blood gas analysis showed metabolic alkalosis. Except an impaired urine concentration ability, renal functions were normal. Intravenous pyelogram showed numerous granular calcifications. Basal plasma renin activity was 1.0 approximately 1.5 ng/ml/hr and increased by sodium depletion. Plasma aldosterone concentration was 70 approximately 80 ng/dl and did not respond to various stimulations. Blood pressure was dependent on sodium balance. It fell on salt restriction and rose on salt loading. Blood pressure responses to vasoactive hormones were normal. Circulating plasma volume was within normal range. After removal of an adrenal adenoma, there was mild fall of blood pressure, serum potassium returned to normal level and plasma renin activity increased slightly. Histologically, there was renal tubular calcifications, and juxtaglomerular apparatus was normal. Blood pressure was elevated to 160/100 mmHg when patient was followed at out-patient clinic after discharge. We concluded that she had essential hypertension associated with primary aldosteronism. Although sodium loss and an increase in urinary kallikrein were found, they did not seem to be the cause of normoreninemic normotensive state of this patient, and the pathogenesis remains to be elucidated.

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