Coronary vascular dysfunction promoted by oxidative‐nitrative stress in SHRSP.Z‐Lepr fa /IzmDmcr rats with metabolic syndrome
1. Metabolic syndrome is an independent risk factor for cardiovascular disease. SHRSP.Z‐Lepr fa /IzmDmcr (SHRSP fatty) rat, established as a new rat model of metabolic syndrome, spontaneously develops obesity, severe hypertension and shows hypertriglyceridaemia, hypercholesterolaemia and abnormal gl...
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| Published in: | Clinical and experimental pharmacology & physiology Vol. 37; no. 11; pp. 1035 - 1043 |
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| Language: | English |
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01-11-2010
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| Abstract | 1. Metabolic syndrome is an independent risk factor for cardiovascular disease. SHRSP.Z‐Lepr
fa
/IzmDmcr (SHRSP fatty) rat, established as a new rat model of metabolic syndrome, spontaneously develops obesity, severe hypertension and shows hypertriglyceridaemia, hypercholesterolaemia and abnormal glucose tolerance. Using SHRSP fatty rats, we examined whether or not oxidative stress was correlated with vascular dysfunction in small and large calibre coronary arteries in
ex vivo
beating hearts, isolated mesenteric arteries and aortas in comparison with normal rats, Wistar–Kyoto rats (WKY). Vasodilation of coronary arteries was determined by microangiography of the Langendorff heart.
2. Compared with WKY, acetylcholine (ACh) and sodium nitroprusside (SNP)‐induced relaxations were impaired in the coronary arteries of SHRSP fatty rats. The mesenteric arteries and aorta of SHRSP fatty rats showed impaired relaxation responses to ACh and SNP, decreased 3′,5′‐monophosphate (cGMP) production, and reduced soluble guanylyl cyclase protein expression. Superoxide release, angiotensin II and 3‐nitrotyrosine contents were increased.
3. SHRSP fatty rats were orally administered olmesartan, an angiotensin II receptor type 1 (AT
1
) antagonist, and amlodipine, a calcium channel blocker, at doses of 5 and 8 mg/kg per day, respectively, for 8 weeks. Both olmesartan and amlodipine reduced blood pressure, but only olmesartan prevented the development of abnormal vascular and biochemical parameters in the SHRSP fatty rats.
4. The results showed that in the SHRSP fatty rats, the impaired nitric oxide‐ and cGMP‐mediated relaxation of vascular smooth muscle cells were linked to AT
1
receptor‐induced oxidative‐nitrative stress, which occurred concurrently with severe hypertension and metabolic abnormalities
in vivo
. |
|---|---|
| AbstractList | 1. Metabolic syndrome is an independent risk factor for cardiovascular disease. SHRSP.Z‐Lepr
fa
/IzmDmcr (SHRSP fatty) rat, established as a new rat model of metabolic syndrome, spontaneously develops obesity, severe hypertension and shows hypertriglyceridaemia, hypercholesterolaemia and abnormal glucose tolerance. Using SHRSP fatty rats, we examined whether or not oxidative stress was correlated with vascular dysfunction in small and large calibre coronary arteries in
ex vivo
beating hearts, isolated mesenteric arteries and aortas in comparison with normal rats, Wistar–Kyoto rats (WKY). Vasodilation of coronary arteries was determined by microangiography of the Langendorff heart.
2. Compared with WKY, acetylcholine (ACh) and sodium nitroprusside (SNP)‐induced relaxations were impaired in the coronary arteries of SHRSP fatty rats. The mesenteric arteries and aorta of SHRSP fatty rats showed impaired relaxation responses to ACh and SNP, decreased 3′,5′‐monophosphate (cGMP) production, and reduced soluble guanylyl cyclase protein expression. Superoxide release, angiotensin II and 3‐nitrotyrosine contents were increased.
3. SHRSP fatty rats were orally administered olmesartan, an angiotensin II receptor type 1 (AT
1
) antagonist, and amlodipine, a calcium channel blocker, at doses of 5 and 8 mg/kg per day, respectively, for 8 weeks. Both olmesartan and amlodipine reduced blood pressure, but only olmesartan prevented the development of abnormal vascular and biochemical parameters in the SHRSP fatty rats.
4. The results showed that in the SHRSP fatty rats, the impaired nitric oxide‐ and cGMP‐mediated relaxation of vascular smooth muscle cells were linked to AT
1
receptor‐induced oxidative‐nitrative stress, which occurred concurrently with severe hypertension and metabolic abnormalities
in vivo
. |
| Author | Fukushima, Kazuhito Sugimura, Kazuro Shinozuka, Kazumasa Kagota, Satomi Nejime, Namie Mori, Hidezo Tada, Yukari Umetani, Keiji Nakamura, Kazuki Kunitomo, Masaru |
| Author_xml | – sequence: 1 givenname: Satomi surname: Kagota fullname: Kagota, Satomi – sequence: 2 givenname: Kazuhito surname: Fukushima fullname: Fukushima, Kazuhito – sequence: 3 givenname: Keiji surname: Umetani fullname: Umetani, Keiji – sequence: 4 givenname: Yukari surname: Tada fullname: Tada, Yukari – sequence: 5 givenname: Namie surname: Nejime fullname: Nejime, Namie – sequence: 6 givenname: Kazuki surname: Nakamura fullname: Nakamura, Kazuki – sequence: 7 givenname: Hidezo surname: Mori fullname: Mori, Hidezo – sequence: 8 givenname: Kazuro surname: Sugimura fullname: Sugimura, Kazuro – sequence: 9 givenname: Masaru surname: Kunitomo fullname: Kunitomo, Masaru – sequence: 10 givenname: Kazumasa surname: Shinozuka fullname: Shinozuka, Kazumasa |
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| References | e_1_2_6_31_2 Umetani K (e_1_2_6_20_2) 2008; 2008 e_1_2_6_30_2 e_1_2_6_18_2 e_1_2_6_19_2 e_1_2_6_12_2 e_1_2_6_35_2 e_1_2_6_13_2 e_1_2_6_34_2 e_1_2_6_10_2 e_1_2_6_33_2 e_1_2_6_11_2 e_1_2_6_32_2 e_1_2_6_16_2 e_1_2_6_39_2 e_1_2_6_17_2 e_1_2_6_38_2 e_1_2_6_14_2 e_1_2_6_37_2 e_1_2_6_15_2 e_1_2_6_36_2 e_1_2_6_42_2 e_1_2_6_41_2 e_1_2_6_40_2 e_1_2_6_8_2 e_1_2_6_7_2 e_1_2_6_9_2 e_1_2_6_29_2 e_1_2_6_4_2 e_1_2_6_3_2 e_1_2_6_6_2 e_1_2_6_5_2 e_1_2_6_24_2 Umetani K (e_1_2_6_21_2) 2009 e_1_2_6_23_2 e_1_2_6_2_2 e_1_2_6_22_2 e_1_2_6_28_2 e_1_2_6_43_2 e_1_2_6_27_2 e_1_2_6_44_2 e_1_2_6_26_2 e_1_2_6_45_2 e_1_2_6_25_2 e_1_2_6_46_2 |
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| Snippet | 1. Metabolic syndrome is an independent risk factor for cardiovascular disease. SHRSP.Z‐Lepr
fa
/IzmDmcr (SHRSP fatty) rat, established as a new rat model of... |
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| Title | Coronary vascular dysfunction promoted by oxidative‐nitrative stress in SHRSP.Z‐Lepr fa /IzmDmcr rats with metabolic syndrome |
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