المؤلفون: Kumagai, Eita, Adachi, Hisashi, Jacobs Jr, David R., Hirai, Yuji, Enomoto, Mika, Fukami, Ako, Otsuka, Maki, Kumagae, Shun-ichi, Nanjo, Yasuki, Yoshikawa, Kuniko, Esaki, Eishi, Yokoi, Kanako, Ogata, Kinuka, Kasahara, Akiko, Tsukagawa, Eri, Ohbu-Murayama, Kyoko, Imaizumi, Tsutomu, Jacobs, David R Jr

المصدر: Hypertension (0194911X); Dec2011, Vol. 58 Issue 6, p1043-1048, 6p

مستخلص: Aldosterone plays a role in hypertension, and hypertension is prevalent in patients with insulin resistance. Cross-sectional studies have reported that plasma aldosterone levels are higher in patients with insulin resistance. However, it is not known whether plasma aldosterone levels predict the development of insulin resistance. Subjects of the present study were 1235 local residents (490 men and 745 women) who participated in health screenings in Japan in 1999. Plasma aldosterone levels were measured by radioimmunoassay. We investigated the cross-sectional relationship between plasma aldosterone levels and insulin resistance (homeostasis model assessment index ≥1.73 according to the diagnostic criteria used in Japan) in 1088 nondiabetic participants. At the 10-year follow-up, 141 subjects had died, and 260 subjects refused re-examination. We performed a prospective analysis of 564 subjects to predict incident insulin resistance. We found a significant (P<0.001) cross-sectional relationship between plasma aldosterone and homeostasis model assessment index at baseline. In the prospective analysis, a significantly higher (P<0.05) relative risk (1.71 [95% CI: 1.03-2.84]) was observed in the highest tertile versus lowest tertile of plasma aldosterone for the development of insulin resistance, after adjustment for confounding factors. This 10-year prospective study demonstrated that plasma aldosterone levels predicted the development of insulin resistance in a general population. [ABSTRACT FROM AUTHOR]

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المؤلفون: Ogihara, Toshio, Saruta, Takao, Rakugi, Hiromi, Matsuoka, Hiroaki, Shimamoto, Kazuaki, Shimada, Kazuyuki, Imai, Yutaka, Kikuchi, Kenjiro, Ito, Sadayoshi, Eto, Tanenao, Kimura, Genjiro, Imaizumi, Tsutomu, Takishita, Shuichi, Ueshima, Hirotsugu, Valsartan in Elderly Isolated Systolic Hypertension Study Group

المصدر: Hypertension (0194911X); Aug2010, Vol. 56 Issue 2, p196-202, 7p, 1 Diagram, 4 Charts, 2 Graphs

مستخلص: In this prospective, randomized, open-label, blinded end point study, we aimed to establish whether strict blood pressure control (<140 mm Hg) is superior to moderate blood pressure control (> or =140 mm Hg to <150 mm Hg) in reducing cardiovascular mortality and morbidity in elderly patients with isolated systolic hypertension. We divided 3260 patients aged 70 to 84 years with isolated systolic hypertension (sitting blood pressure 160 to 199 mm Hg) into 2 groups, according to strict or moderate blood pressure treatment. A composite of cardiovascular events was evaluated for > or =2 years. The strict control (1545 patients) and moderate control (1534 patients) groups were well matched (mean age: 76.1 years; mean blood pressure: 169.5/81.5 mm Hg). Median follow-up was 3.07 years. At 3 years, blood pressure reached 136.6/74.8 mm Hg and 142.0/76.5 mm Hg, respectively. The blood pressure difference between the 2 groups was 5.4/1.7 mm Hg. The overall rate of the primary composite end point was 10.6 per 1000 patient-years in the strict control group and 12.0 per 1000 patient-years in the moderate control group (hazard ratio: 0.89; [95% CI: 0.60 to 1.34]; P=0.38). In summary, blood pressure targets of <140 mm Hg are safely achievable in relatively healthy patients > or = 70 years of age with isolated systolic hypertension, although our trial was underpowered to definitively determine whether strict control was superior to less stringent blood pressure targets. [ABSTRACT FROM AUTHOR]

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المؤلفون: Kudo, Hiroshi, Kai, Hisashi, Kajimoto, Hidemi, Koga, Mitsuhisa, Takayama, Narimasa, Mori, Takahiro, Ikeda, Ayami, Yasuoka, Suguru, Anegawa, Takahiro, Mifune, Hiroharu, Kato, Seiya, Hirooka, Yoshitaka, Imaizumi, Tsutomu

المصدر: Hypertension (0194911X); Oct2009, Vol. 54 Issue 4, p832-838, 7p, 2 Charts, 5 Graphs

مستخلص: Hypertensive patients with large blood pressure variability (BPV) have aggravated end-organ damage. However, the pathogenesis remains unknown. We investigated whether exaggerated BPV aggravates hypertensive cardiac remodeling and function by activating inflammation and angiotensin II-mediated mechanisms. A model of exaggerated BPV superimposed on chronic hypertension was created by performing bilateral sinoaortic denervation (SAD) in spontaneously hypertensive rats (SHRs). SAD increased BPV to a similar extent in Wistar Kyoto rats and SHRs without significant changes in mean blood pressure. SAD aggravated left ventricular and myocyte hypertrophy and myocardial fibrosis to a greater extent and impaired left ventricular systolic function in SHRs. SAD induced monocyte chemoattractant protein-1, transforming growth factor-beta, and angiotensinogen mRNA upregulations and macrophage infiltration of the heart in SHRs. The effects of SAD on cardiac remodeling and inflammation were much smaller in Wistar Kyoto rats compared with SHRs. Circulating levels of norepinephrine, the active form of renin, and inflammatory cytokines were not affected by SAD in Wistar Kyoto rats and SHRs. A subdepressor dose of candesartan abolished the SAD-induced left ventricular/myocyte hypertrophy, myocardial fibrosis, macrophage infiltration, and inductions of monocyte chemoattractant protein-1, transforming growth factor-beta, and angiotensinogen and subsequently prevented systolic dysfunction in SHRs with SAD. These findings suggest that exaggerated BPV induces chronic myocardial inflammation and thereby aggravates cardiac remodeling and systolic function in hypertensive hearts. The cardiac angiotensin II system may play a role in the pathogenesis of cardiac remodeling and dysfunction induced by a combination of hypertension and exaggerated BPV. [ABSTRACT FROM AUTHOR]

: Copyright of Hypertension (0194911X) is the property of Lippincott Williams & Wilkins and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Kusaba, Ken, Kai, Hisashi, Koga, Mitsuhisa, Takayam, Narimasa, Ikeda, Ayami, Yasukawa, Hideo, Seki, Yukihiko, Egashira, Kensuke, Imaizumi, Tsutomu

المصدر: Hypertension (0194911X); Apr2007, Vol. 49 Issue 4, p909-915, 7p, 1 Chart, 5 Graphs

مستخلص: The article presents the results of a study on whether inhibition of intrinsic interferon-γ (IFN-γ) can prevent neointima formation after balloon injury. Muscle degeneration, tissue necrosis and inflammation were not observed at the injection site of IFN-γ receptor α-subunit (sIFNγR) plasmid. sIFNγR treatment prevented neointima formation after the injury in rats. sIFNγR treatment also prevented gene expression in the carotid artery.

المؤلفون: TAKESHITA, AKIRA, IMAIZUMI, TSUTOMU, ASHIHARA, TOSHIAKI, NAKAMURA, MOTOOMI, Takeshita, A, Imaizumi, T, Ashihara, T, Nakamura, M

المصدر: Hypertension (0194911X); Mar/Apr1982, Vol. 4 Issue 2, p288-293, 6p

المؤلفون: Egashira, Kensuke, Suzuki, Satoshi, Hirooka, Yoshitaka, Kai, Hisashi, Sugimachi, Masaru, Imaizumi, Tsutomu, Takeshita, Akira, Egashira, K, Suzuki, S, Hirooka, Y, Kai, H, Sugimachi, M, Imaizumi, T, Takeshita, A

المصدر: Hypertension (0194911X); Feb1995, Vol. 25 Issue 2, p201-206, 6p

المؤلفون: Sakai, Kazuhiro, Imaizumi, Tsutomu, Maeda, Hirotaka, Nagata, Hideaki, Tsukimori, Kiyomi, Takeshita, Akira, Nakano, Hitoo

المصدر: Hypertension (0194911X); Oct1994, Vol. 24 Issue 4, p461-467, 7p

المؤلفون: Sakai, Kikuo, Imaizumi, Tsutomu, Masaki, Hiroyuki, Takeshita, Akira, Sakai, K, Imaizumi, T, Masaki, H, Takeshita, A

المصدر: Hypertension (0194911X); Jul1993, Vol. 22 Issue 1, p67-73, 7p

المؤلفون: Imaizumi, Tsutomu, Hirooka, Yoshitaka, Masaki, Hiroyuki, Harada, Seiki, Momohara, Michiko, Tagawa, Tatsuya, Takeshita, Akira, Imaizumi, T, Hirooka, Y, Masaki, H, Harada, S, Momohara, M, Tagawa, T, Takeshita, A

المصدر: Hypertension (0194911X); Oct1992, Vol. 20 Issue 4, p511-517, 7p

المؤلفون: Hirooka, Yoshitaka, Imaizumi, Tsutomu, Masaki, Hiroyuki, Ando, Shin-Ichi, Harada, Seiki, Momohara, Michiko, Takeshita, Akira, Hirooka, Y, Imaizumi, T, Masaki, H, Ando, S, Harada, S, Momohara, M, Takeshita, A

المصدر: Hypertension (0194911X); Aug1992, Vol. 20 Issue 2, p175-180, 6p