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Jeffrey G Dickhout - One of the best experts on this subject based on the ideXlab platform.

  • Endoplasmic Reticulum Stress inhibition reduces hypertension through the preservation of resistance blood vessel structure and function
    Journal of Hypertension, 2016
    Co-Authors: Rachel E Carlisle, Kaitlyn E Werner, Muzammil Memon, Yejin No, Chao Lu, Jeffrey G Dickhout
    Abstract:

    OBJECTIVE: Our purpose was to determine if Endoplasmic Reticulum Stress inhibition lowers blood pressure (BP) in hypertension by correcting vascular dysfunction. METHODS: The spontaneously hypertensive rat (SHR) was used as a model of human essential hypertension with its normotensive control, the Wistar Kyoto rat. Animals were subjected to Endoplasmic Reticulum Stress inhibition with 4-phenylbutyric acid (4-PBA; 1 g/kg per day, orally) for 5 weeks from 12 weeks of age. BP was measured weekly noninvasively and at endpoint with carotid arterial cannulation. Small mesenteric arteries were removed for vascular studies. Function was assessed with a Mulvany-Halpern style myograph, and structure was assessed by measurement of medial-to-lumen ratio in perfusion fixed vessels as well as three-dimensional confocal reconstruction of vessel wall components. Endoplasmic Reticulum Stress was assessed by quantitative real time-PCR and western blotting; oxidative Stress was assessed by 3-nitrotyrosine and dihydroethidium staining. RESULTS: 4-PBA significantly lowered BP in SHR (vehicle 206.1 ± 4.3 vs. 4-PBA 178.9 ± 3.1, systolic) but not Wistar Kyoto. 4-PBA diminished contractility and augmented endothelial-dependent vasodilation in SHR small mesenteric arteries, as well as reducing media-to-lumen ratio. 4-PBA significantly reduced Endoplasmic Reticulum Stress in SHR resistance vessels. Normotensive resistance vessels, treated with the Endoplasmic Reticulum Stress-inducing agent, tunicamycin, show decreased endothelial-dependent vasodilation; this was improved with 4-PBA treatment. 3-Nitrotyrosine and dihydroethidium staining indicated that Endoplasmic Reticulum Stress leads to reactive oxygen species generation resolvable by 4-PBA treatment. CONCLUSION: Endoplasmic Reticulum Stress caused endothelial-mediated vascular dysfunction contributing to elevated BP in the SHR model of human essential hypertension.

  • Endoplasmic Reticulum Stress inhibition reduces hypertension through the preservation of resistance blood vessel structure and function
    Journal of Hypertension, 2016
    Co-Authors: Rachel E Carlisle, Kaitlyn E Werner, Muzammil Memon, Yejin No, Chao Lu, Jeffrey G Dickhout
    Abstract:

    OBJECTIVE: Our purpose was to determine if Endoplasmic Reticulum Stress inhibition lowers blood pressure (BP) in hypertension by correcting vascular dysfunction. METHODS: The spontaneously hypertensive rat (SHR) was used as a model of human essential hypertension with its normotensive control, the Wistar Kyoto rat. Animals were subjected to Endoplasmic Reticulum Stress inhibition with 4-phenylbutyric acid (4-PBA; 1 g/kg per day, orally) for 5 weeks from 12 weeks of age. BP was measured weekly noninvasively and at endpoint with carotid arterial cannulation. Small mesenteric arteries were removed for vascular studies. Function was assessed with a Mulvany-Halpern style myograph, and structure was assessed by measurement of medial-to-lumen ratio in perfusion fixed vessels as well as three-dimensional confocal reconstruction of vessel wall components. Endoplasmic Reticulum Stress was assessed by quantitative real time-PCR and western blotting; oxidative Stress was assessed by 3-nitrotyrosine and dihydroethidium staining. RESULTS: 4-PBA significantly lowered BP in SHR (vehicle 206.1 ± 4.3 vs. 4-PBA 178.9 ± 3.1, systolic) but not Wistar Kyoto. 4-PBA diminished contractility and augmented endothelial-dependent vasodilation in SHR small mesenteric arteries, as well as reducing media-to-lumen ratio. 4-PBA significantly reduced Endoplasmic Reticulum Stress in SHR resistance vessels. Normotensive resistance vessels, treated with the Endoplasmic Reticulum Stress-inducing agent, tunicamycin, show decreased endothelial-dependent vasodilation; this was improved with 4-PBA treatment. 3-Nitrotyrosine and dihydroethidium staining indicated that Endoplasmic Reticulum Stress leads to reactive oxygen species generation resolvable by 4-PBA treatment. CONCLUSION: Endoplasmic Reticulum Stress caused endothelial-mediated vascular dysfunction contributing to elevated BP in the SHR model of human essential hypertension.

Rachel E Carlisle - One of the best experts on this subject based on the ideXlab platform.

  • Endoplasmic Reticulum Stress inhibition reduces hypertension through the preservation of resistance blood vessel structure and function
    Journal of Hypertension, 2016
    Co-Authors: Rachel E Carlisle, Kaitlyn E Werner, Muzammil Memon, Yejin No, Chao Lu, Jeffrey G Dickhout
    Abstract:

    OBJECTIVE: Our purpose was to determine if Endoplasmic Reticulum Stress inhibition lowers blood pressure (BP) in hypertension by correcting vascular dysfunction. METHODS: The spontaneously hypertensive rat (SHR) was used as a model of human essential hypertension with its normotensive control, the Wistar Kyoto rat. Animals were subjected to Endoplasmic Reticulum Stress inhibition with 4-phenylbutyric acid (4-PBA; 1 g/kg per day, orally) for 5 weeks from 12 weeks of age. BP was measured weekly noninvasively and at endpoint with carotid arterial cannulation. Small mesenteric arteries were removed for vascular studies. Function was assessed with a Mulvany-Halpern style myograph, and structure was assessed by measurement of medial-to-lumen ratio in perfusion fixed vessels as well as three-dimensional confocal reconstruction of vessel wall components. Endoplasmic Reticulum Stress was assessed by quantitative real time-PCR and western blotting; oxidative Stress was assessed by 3-nitrotyrosine and dihydroethidium staining. RESULTS: 4-PBA significantly lowered BP in SHR (vehicle 206.1 ± 4.3 vs. 4-PBA 178.9 ± 3.1, systolic) but not Wistar Kyoto. 4-PBA diminished contractility and augmented endothelial-dependent vasodilation in SHR small mesenteric arteries, as well as reducing media-to-lumen ratio. 4-PBA significantly reduced Endoplasmic Reticulum Stress in SHR resistance vessels. Normotensive resistance vessels, treated with the Endoplasmic Reticulum Stress-inducing agent, tunicamycin, show decreased endothelial-dependent vasodilation; this was improved with 4-PBA treatment. 3-Nitrotyrosine and dihydroethidium staining indicated that Endoplasmic Reticulum Stress leads to reactive oxygen species generation resolvable by 4-PBA treatment. CONCLUSION: Endoplasmic Reticulum Stress caused endothelial-mediated vascular dysfunction contributing to elevated BP in the SHR model of human essential hypertension.

  • Endoplasmic Reticulum Stress inhibition reduces hypertension through the preservation of resistance blood vessel structure and function
    Journal of Hypertension, 2016
    Co-Authors: Rachel E Carlisle, Kaitlyn E Werner, Muzammil Memon, Yejin No, Chao Lu, Jeffrey G Dickhout
    Abstract:

    OBJECTIVE: Our purpose was to determine if Endoplasmic Reticulum Stress inhibition lowers blood pressure (BP) in hypertension by correcting vascular dysfunction. METHODS: The spontaneously hypertensive rat (SHR) was used as a model of human essential hypertension with its normotensive control, the Wistar Kyoto rat. Animals were subjected to Endoplasmic Reticulum Stress inhibition with 4-phenylbutyric acid (4-PBA; 1 g/kg per day, orally) for 5 weeks from 12 weeks of age. BP was measured weekly noninvasively and at endpoint with carotid arterial cannulation. Small mesenteric arteries were removed for vascular studies. Function was assessed with a Mulvany-Halpern style myograph, and structure was assessed by measurement of medial-to-lumen ratio in perfusion fixed vessels as well as three-dimensional confocal reconstruction of vessel wall components. Endoplasmic Reticulum Stress was assessed by quantitative real time-PCR and western blotting; oxidative Stress was assessed by 3-nitrotyrosine and dihydroethidium staining. RESULTS: 4-PBA significantly lowered BP in SHR (vehicle 206.1 ± 4.3 vs. 4-PBA 178.9 ± 3.1, systolic) but not Wistar Kyoto. 4-PBA diminished contractility and augmented endothelial-dependent vasodilation in SHR small mesenteric arteries, as well as reducing media-to-lumen ratio. 4-PBA significantly reduced Endoplasmic Reticulum Stress in SHR resistance vessels. Normotensive resistance vessels, treated with the Endoplasmic Reticulum Stress-inducing agent, tunicamycin, show decreased endothelial-dependent vasodilation; this was improved with 4-PBA treatment. 3-Nitrotyrosine and dihydroethidium staining indicated that Endoplasmic Reticulum Stress leads to reactive oxygen species generation resolvable by 4-PBA treatment. CONCLUSION: Endoplasmic Reticulum Stress caused endothelial-mediated vascular dysfunction contributing to elevated BP in the SHR model of human essential hypertension.

Chao Lu - One of the best experts on this subject based on the ideXlab platform.

  • Endoplasmic Reticulum Stress inhibition reduces hypertension through the preservation of resistance blood vessel structure and function
    Journal of Hypertension, 2016
    Co-Authors: Rachel E Carlisle, Kaitlyn E Werner, Muzammil Memon, Yejin No, Chao Lu, Jeffrey G Dickhout
    Abstract:

    OBJECTIVE: Our purpose was to determine if Endoplasmic Reticulum Stress inhibition lowers blood pressure (BP) in hypertension by correcting vascular dysfunction. METHODS: The spontaneously hypertensive rat (SHR) was used as a model of human essential hypertension with its normotensive control, the Wistar Kyoto rat. Animals were subjected to Endoplasmic Reticulum Stress inhibition with 4-phenylbutyric acid (4-PBA; 1 g/kg per day, orally) for 5 weeks from 12 weeks of age. BP was measured weekly noninvasively and at endpoint with carotid arterial cannulation. Small mesenteric arteries were removed for vascular studies. Function was assessed with a Mulvany-Halpern style myograph, and structure was assessed by measurement of medial-to-lumen ratio in perfusion fixed vessels as well as three-dimensional confocal reconstruction of vessel wall components. Endoplasmic Reticulum Stress was assessed by quantitative real time-PCR and western blotting; oxidative Stress was assessed by 3-nitrotyrosine and dihydroethidium staining. RESULTS: 4-PBA significantly lowered BP in SHR (vehicle 206.1 ± 4.3 vs. 4-PBA 178.9 ± 3.1, systolic) but not Wistar Kyoto. 4-PBA diminished contractility and augmented endothelial-dependent vasodilation in SHR small mesenteric arteries, as well as reducing media-to-lumen ratio. 4-PBA significantly reduced Endoplasmic Reticulum Stress in SHR resistance vessels. Normotensive resistance vessels, treated with the Endoplasmic Reticulum Stress-inducing agent, tunicamycin, show decreased endothelial-dependent vasodilation; this was improved with 4-PBA treatment. 3-Nitrotyrosine and dihydroethidium staining indicated that Endoplasmic Reticulum Stress leads to reactive oxygen species generation resolvable by 4-PBA treatment. CONCLUSION: Endoplasmic Reticulum Stress caused endothelial-mediated vascular dysfunction contributing to elevated BP in the SHR model of human essential hypertension.

  • Endoplasmic Reticulum Stress inhibition reduces hypertension through the preservation of resistance blood vessel structure and function
    Journal of Hypertension, 2016
    Co-Authors: Rachel E Carlisle, Kaitlyn E Werner, Muzammil Memon, Yejin No, Chao Lu, Jeffrey G Dickhout
    Abstract:

    OBJECTIVE: Our purpose was to determine if Endoplasmic Reticulum Stress inhibition lowers blood pressure (BP) in hypertension by correcting vascular dysfunction. METHODS: The spontaneously hypertensive rat (SHR) was used as a model of human essential hypertension with its normotensive control, the Wistar Kyoto rat. Animals were subjected to Endoplasmic Reticulum Stress inhibition with 4-phenylbutyric acid (4-PBA; 1 g/kg per day, orally) for 5 weeks from 12 weeks of age. BP was measured weekly noninvasively and at endpoint with carotid arterial cannulation. Small mesenteric arteries were removed for vascular studies. Function was assessed with a Mulvany-Halpern style myograph, and structure was assessed by measurement of medial-to-lumen ratio in perfusion fixed vessels as well as three-dimensional confocal reconstruction of vessel wall components. Endoplasmic Reticulum Stress was assessed by quantitative real time-PCR and western blotting; oxidative Stress was assessed by 3-nitrotyrosine and dihydroethidium staining. RESULTS: 4-PBA significantly lowered BP in SHR (vehicle 206.1 ± 4.3 vs. 4-PBA 178.9 ± 3.1, systolic) but not Wistar Kyoto. 4-PBA diminished contractility and augmented endothelial-dependent vasodilation in SHR small mesenteric arteries, as well as reducing media-to-lumen ratio. 4-PBA significantly reduced Endoplasmic Reticulum Stress in SHR resistance vessels. Normotensive resistance vessels, treated with the Endoplasmic Reticulum Stress-inducing agent, tunicamycin, show decreased endothelial-dependent vasodilation; this was improved with 4-PBA treatment. 3-Nitrotyrosine and dihydroethidium staining indicated that Endoplasmic Reticulum Stress leads to reactive oxygen species generation resolvable by 4-PBA treatment. CONCLUSION: Endoplasmic Reticulum Stress caused endothelial-mediated vascular dysfunction contributing to elevated BP in the SHR model of human essential hypertension.

Yejin No - One of the best experts on this subject based on the ideXlab platform.

  • Endoplasmic Reticulum Stress inhibition reduces hypertension through the preservation of resistance blood vessel structure and function
    Journal of Hypertension, 2016
    Co-Authors: Rachel E Carlisle, Kaitlyn E Werner, Muzammil Memon, Yejin No, Chao Lu, Jeffrey G Dickhout
    Abstract:

    OBJECTIVE: Our purpose was to determine if Endoplasmic Reticulum Stress inhibition lowers blood pressure (BP) in hypertension by correcting vascular dysfunction. METHODS: The spontaneously hypertensive rat (SHR) was used as a model of human essential hypertension with its normotensive control, the Wistar Kyoto rat. Animals were subjected to Endoplasmic Reticulum Stress inhibition with 4-phenylbutyric acid (4-PBA; 1 g/kg per day, orally) for 5 weeks from 12 weeks of age. BP was measured weekly noninvasively and at endpoint with carotid arterial cannulation. Small mesenteric arteries were removed for vascular studies. Function was assessed with a Mulvany-Halpern style myograph, and structure was assessed by measurement of medial-to-lumen ratio in perfusion fixed vessels as well as three-dimensional confocal reconstruction of vessel wall components. Endoplasmic Reticulum Stress was assessed by quantitative real time-PCR and western blotting; oxidative Stress was assessed by 3-nitrotyrosine and dihydroethidium staining. RESULTS: 4-PBA significantly lowered BP in SHR (vehicle 206.1 ± 4.3 vs. 4-PBA 178.9 ± 3.1, systolic) but not Wistar Kyoto. 4-PBA diminished contractility and augmented endothelial-dependent vasodilation in SHR small mesenteric arteries, as well as reducing media-to-lumen ratio. 4-PBA significantly reduced Endoplasmic Reticulum Stress in SHR resistance vessels. Normotensive resistance vessels, treated with the Endoplasmic Reticulum Stress-inducing agent, tunicamycin, show decreased endothelial-dependent vasodilation; this was improved with 4-PBA treatment. 3-Nitrotyrosine and dihydroethidium staining indicated that Endoplasmic Reticulum Stress leads to reactive oxygen species generation resolvable by 4-PBA treatment. CONCLUSION: Endoplasmic Reticulum Stress caused endothelial-mediated vascular dysfunction contributing to elevated BP in the SHR model of human essential hypertension.

  • Endoplasmic Reticulum Stress inhibition reduces hypertension through the preservation of resistance blood vessel structure and function
    Journal of Hypertension, 2016
    Co-Authors: Rachel E Carlisle, Kaitlyn E Werner, Muzammil Memon, Yejin No, Chao Lu, Jeffrey G Dickhout
    Abstract:

    OBJECTIVE: Our purpose was to determine if Endoplasmic Reticulum Stress inhibition lowers blood pressure (BP) in hypertension by correcting vascular dysfunction. METHODS: The spontaneously hypertensive rat (SHR) was used as a model of human essential hypertension with its normotensive control, the Wistar Kyoto rat. Animals were subjected to Endoplasmic Reticulum Stress inhibition with 4-phenylbutyric acid (4-PBA; 1 g/kg per day, orally) for 5 weeks from 12 weeks of age. BP was measured weekly noninvasively and at endpoint with carotid arterial cannulation. Small mesenteric arteries were removed for vascular studies. Function was assessed with a Mulvany-Halpern style myograph, and structure was assessed by measurement of medial-to-lumen ratio in perfusion fixed vessels as well as three-dimensional confocal reconstruction of vessel wall components. Endoplasmic Reticulum Stress was assessed by quantitative real time-PCR and western blotting; oxidative Stress was assessed by 3-nitrotyrosine and dihydroethidium staining. RESULTS: 4-PBA significantly lowered BP in SHR (vehicle 206.1 ± 4.3 vs. 4-PBA 178.9 ± 3.1, systolic) but not Wistar Kyoto. 4-PBA diminished contractility and augmented endothelial-dependent vasodilation in SHR small mesenteric arteries, as well as reducing media-to-lumen ratio. 4-PBA significantly reduced Endoplasmic Reticulum Stress in SHR resistance vessels. Normotensive resistance vessels, treated with the Endoplasmic Reticulum Stress-inducing agent, tunicamycin, show decreased endothelial-dependent vasodilation; this was improved with 4-PBA treatment. 3-Nitrotyrosine and dihydroethidium staining indicated that Endoplasmic Reticulum Stress leads to reactive oxygen species generation resolvable by 4-PBA treatment. CONCLUSION: Endoplasmic Reticulum Stress caused endothelial-mediated vascular dysfunction contributing to elevated BP in the SHR model of human essential hypertension.

Muzammil Memon - One of the best experts on this subject based on the ideXlab platform.

  • Endoplasmic Reticulum Stress inhibition reduces hypertension through the preservation of resistance blood vessel structure and function
    Journal of Hypertension, 2016
    Co-Authors: Rachel E Carlisle, Kaitlyn E Werner, Muzammil Memon, Yejin No, Chao Lu, Jeffrey G Dickhout
    Abstract:

    OBJECTIVE: Our purpose was to determine if Endoplasmic Reticulum Stress inhibition lowers blood pressure (BP) in hypertension by correcting vascular dysfunction. METHODS: The spontaneously hypertensive rat (SHR) was used as a model of human essential hypertension with its normotensive control, the Wistar Kyoto rat. Animals were subjected to Endoplasmic Reticulum Stress inhibition with 4-phenylbutyric acid (4-PBA; 1 g/kg per day, orally) for 5 weeks from 12 weeks of age. BP was measured weekly noninvasively and at endpoint with carotid arterial cannulation. Small mesenteric arteries were removed for vascular studies. Function was assessed with a Mulvany-Halpern style myograph, and structure was assessed by measurement of medial-to-lumen ratio in perfusion fixed vessels as well as three-dimensional confocal reconstruction of vessel wall components. Endoplasmic Reticulum Stress was assessed by quantitative real time-PCR and western blotting; oxidative Stress was assessed by 3-nitrotyrosine and dihydroethidium staining. RESULTS: 4-PBA significantly lowered BP in SHR (vehicle 206.1 ± 4.3 vs. 4-PBA 178.9 ± 3.1, systolic) but not Wistar Kyoto. 4-PBA diminished contractility and augmented endothelial-dependent vasodilation in SHR small mesenteric arteries, as well as reducing media-to-lumen ratio. 4-PBA significantly reduced Endoplasmic Reticulum Stress in SHR resistance vessels. Normotensive resistance vessels, treated with the Endoplasmic Reticulum Stress-inducing agent, tunicamycin, show decreased endothelial-dependent vasodilation; this was improved with 4-PBA treatment. 3-Nitrotyrosine and dihydroethidium staining indicated that Endoplasmic Reticulum Stress leads to reactive oxygen species generation resolvable by 4-PBA treatment. CONCLUSION: Endoplasmic Reticulum Stress caused endothelial-mediated vascular dysfunction contributing to elevated BP in the SHR model of human essential hypertension.

  • Endoplasmic Reticulum Stress inhibition reduces hypertension through the preservation of resistance blood vessel structure and function
    Journal of Hypertension, 2016
    Co-Authors: Rachel E Carlisle, Kaitlyn E Werner, Muzammil Memon, Yejin No, Chao Lu, Jeffrey G Dickhout
    Abstract:

    OBJECTIVE: Our purpose was to determine if Endoplasmic Reticulum Stress inhibition lowers blood pressure (BP) in hypertension by correcting vascular dysfunction. METHODS: The spontaneously hypertensive rat (SHR) was used as a model of human essential hypertension with its normotensive control, the Wistar Kyoto rat. Animals were subjected to Endoplasmic Reticulum Stress inhibition with 4-phenylbutyric acid (4-PBA; 1 g/kg per day, orally) for 5 weeks from 12 weeks of age. BP was measured weekly noninvasively and at endpoint with carotid arterial cannulation. Small mesenteric arteries were removed for vascular studies. Function was assessed with a Mulvany-Halpern style myograph, and structure was assessed by measurement of medial-to-lumen ratio in perfusion fixed vessels as well as three-dimensional confocal reconstruction of vessel wall components. Endoplasmic Reticulum Stress was assessed by quantitative real time-PCR and western blotting; oxidative Stress was assessed by 3-nitrotyrosine and dihydroethidium staining. RESULTS: 4-PBA significantly lowered BP in SHR (vehicle 206.1 ± 4.3 vs. 4-PBA 178.9 ± 3.1, systolic) but not Wistar Kyoto. 4-PBA diminished contractility and augmented endothelial-dependent vasodilation in SHR small mesenteric arteries, as well as reducing media-to-lumen ratio. 4-PBA significantly reduced Endoplasmic Reticulum Stress in SHR resistance vessels. Normotensive resistance vessels, treated with the Endoplasmic Reticulum Stress-inducing agent, tunicamycin, show decreased endothelial-dependent vasodilation; this was improved with 4-PBA treatment. 3-Nitrotyrosine and dihydroethidium staining indicated that Endoplasmic Reticulum Stress leads to reactive oxygen species generation resolvable by 4-PBA treatment. CONCLUSION: Endoplasmic Reticulum Stress caused endothelial-mediated vascular dysfunction contributing to elevated BP in the SHR model of human essential hypertension.