author_facet Vari, R C
Zinn, S
Verburg, K M
Freeman, R H
Vari, R C
Zinn, S
Verburg, K M
Freeman, R H
author Vari, R C
Zinn, S
Verburg, K M
Freeman, R H
spellingShingle Vari, R C
Zinn, S
Verburg, K M
Freeman, R H
Hypertension
Renal nerves and the pathogenesis of angiotensin-induced hypertension.
Internal Medicine
author_sort vari, r c
spelling Vari, R C Zinn, S Verburg, K M Freeman, R H 0194-911X 1524-4563 Ovid Technologies (Wolters Kluwer Health) Internal Medicine http://dx.doi.org/10.1161/01.hyp.9.4.345 <jats:p>The present study examined the role of the renal nerves in the development of hypertension produced by chronic infusion of angiotensin II in the conscious rat. The animals were divided into four groups, and a unilateral nephrectomy was performed. The remaining kidney was denervated in two groups, whereas in the other two groups of animals the nerves were left intact. Four days later either angiotensin II (83 ng/min) or saline infusions were begun through subcutaneously implanted osmotic minipumps. The rats were subsequently studied for 14 days. The results indicate that renal denervation significantly attenuated the pressor response to angiotensin II for approximately 6 days. Following this period, there was no difference in blood pressure between the innervated and denervated rats infused with angiotensin II, as both groups attained a hypertensive level of 170 to 180 mm Hg, which was 60 to 70 mm Hg above the blood pressure of the control rats infused with saline. Kidney norepinephrine content was reduced 95% by the denervation procedure and by 40% following infusion of angiotensin II into rats with intact renal nerves. These data demonstrate that, while the renal nerves appear to play a modulatory role in the development of the hypertension, they are not essential for the pathogenesis to occur nor do they determine the final level of hypertension achieved following chronic infusion of angiotensin II in the rat.</jats:p> Renal nerves and the pathogenesis of angiotensin-induced hypertension. Hypertension
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title Renal nerves and the pathogenesis of angiotensin-induced hypertension.
title_unstemmed Renal nerves and the pathogenesis of angiotensin-induced hypertension.
title_full Renal nerves and the pathogenesis of angiotensin-induced hypertension.
title_fullStr Renal nerves and the pathogenesis of angiotensin-induced hypertension.
title_full_unstemmed Renal nerves and the pathogenesis of angiotensin-induced hypertension.
title_short Renal nerves and the pathogenesis of angiotensin-induced hypertension.
title_sort renal nerves and the pathogenesis of angiotensin-induced hypertension.
topic Internal Medicine
url http://dx.doi.org/10.1161/01.hyp.9.4.345
publishDate 1987
physical 345-349
description <jats:p>The present study examined the role of the renal nerves in the development of hypertension produced by chronic infusion of angiotensin II in the conscious rat. The animals were divided into four groups, and a unilateral nephrectomy was performed. The remaining kidney was denervated in two groups, whereas in the other two groups of animals the nerves were left intact. Four days later either angiotensin II (83 ng/min) or saline infusions were begun through subcutaneously implanted osmotic minipumps. The rats were subsequently studied for 14 days. The results indicate that renal denervation significantly attenuated the pressor response to angiotensin II for approximately 6 days. Following this period, there was no difference in blood pressure between the innervated and denervated rats infused with angiotensin II, as both groups attained a hypertensive level of 170 to 180 mm Hg, which was 60 to 70 mm Hg above the blood pressure of the control rats infused with saline. Kidney norepinephrine content was reduced 95% by the denervation procedure and by 40% following infusion of angiotensin II into rats with intact renal nerves. These data demonstrate that, while the renal nerves appear to play a modulatory role in the development of the hypertension, they are not essential for the pathogenesis to occur nor do they determine the final level of hypertension achieved following chronic infusion of angiotensin II in the rat.</jats:p>
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author Vari, R C, Zinn, S, Verburg, K M, Freeman, R H
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description <jats:p>The present study examined the role of the renal nerves in the development of hypertension produced by chronic infusion of angiotensin II in the conscious rat. The animals were divided into four groups, and a unilateral nephrectomy was performed. The remaining kidney was denervated in two groups, whereas in the other two groups of animals the nerves were left intact. Four days later either angiotensin II (83 ng/min) or saline infusions were begun through subcutaneously implanted osmotic minipumps. The rats were subsequently studied for 14 days. The results indicate that renal denervation significantly attenuated the pressor response to angiotensin II for approximately 6 days. Following this period, there was no difference in blood pressure between the innervated and denervated rats infused with angiotensin II, as both groups attained a hypertensive level of 170 to 180 mm Hg, which was 60 to 70 mm Hg above the blood pressure of the control rats infused with saline. Kidney norepinephrine content was reduced 95% by the denervation procedure and by 40% following infusion of angiotensin II into rats with intact renal nerves. These data demonstrate that, while the renal nerves appear to play a modulatory role in the development of the hypertension, they are not essential for the pathogenesis to occur nor do they determine the final level of hypertension achieved following chronic infusion of angiotensin II in the rat.</jats:p>
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spelling Vari, R C Zinn, S Verburg, K M Freeman, R H 0194-911X 1524-4563 Ovid Technologies (Wolters Kluwer Health) Internal Medicine http://dx.doi.org/10.1161/01.hyp.9.4.345 <jats:p>The present study examined the role of the renal nerves in the development of hypertension produced by chronic infusion of angiotensin II in the conscious rat. The animals were divided into four groups, and a unilateral nephrectomy was performed. The remaining kidney was denervated in two groups, whereas in the other two groups of animals the nerves were left intact. Four days later either angiotensin II (83 ng/min) or saline infusions were begun through subcutaneously implanted osmotic minipumps. The rats were subsequently studied for 14 days. The results indicate that renal denervation significantly attenuated the pressor response to angiotensin II for approximately 6 days. Following this period, there was no difference in blood pressure between the innervated and denervated rats infused with angiotensin II, as both groups attained a hypertensive level of 170 to 180 mm Hg, which was 60 to 70 mm Hg above the blood pressure of the control rats infused with saline. Kidney norepinephrine content was reduced 95% by the denervation procedure and by 40% following infusion of angiotensin II into rats with intact renal nerves. These data demonstrate that, while the renal nerves appear to play a modulatory role in the development of the hypertension, they are not essential for the pathogenesis to occur nor do they determine the final level of hypertension achieved following chronic infusion of angiotensin II in the rat.</jats:p> Renal nerves and the pathogenesis of angiotensin-induced hypertension. Hypertension
spellingShingle Vari, R C, Zinn, S, Verburg, K M, Freeman, R H, Hypertension, Renal nerves and the pathogenesis of angiotensin-induced hypertension., Internal Medicine
title Renal nerves and the pathogenesis of angiotensin-induced hypertension.
title_full Renal nerves and the pathogenesis of angiotensin-induced hypertension.
title_fullStr Renal nerves and the pathogenesis of angiotensin-induced hypertension.
title_full_unstemmed Renal nerves and the pathogenesis of angiotensin-induced hypertension.
title_short Renal nerves and the pathogenesis of angiotensin-induced hypertension.
title_sort renal nerves and the pathogenesis of angiotensin-induced hypertension.
title_unstemmed Renal nerves and the pathogenesis of angiotensin-induced hypertension.
topic Internal Medicine
url http://dx.doi.org/10.1161/01.hyp.9.4.345