Angiotensin II and the Renal Hemodynamic Response to an Isolated Increased Renal Venous Pressure in Rats

Elevated central venous pressure increases renal venous pressure (RVP) which can affect kidney function. We previously demonstrated that increased RVP reduces renal blood flow (RBF), glomerular filtration rate (GFR), and renal vascular conductance (RVC). We now investigate whether the RAS and RBF au...

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Autores principales:	Xiaohua Huang, Shereen M. Hamza, Wenqing Zhuang, William A. Cupples, Branko Braam
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	renal venous pressure cardiorenal syndrome renin – angiotensin – aldosterone system renal hemodynamics venous congestion Physiology QP1-981
Acceso en línea:	https://doaj.org/article/d255ba5cebed4d33837e5f1a651c514d
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spelling	oai:doaj.org-article:d255ba5cebed4d33837e5f1a651c514d2021-11-16T07:35:27ZAngiotensin II and the Renal Hemodynamic Response to an Isolated Increased Renal Venous Pressure in Rats1664-042X10.3389/fphys.2021.753355https://doaj.org/article/d255ba5cebed4d33837e5f1a651c514d2021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fphys.2021.753355/fullhttps://doaj.org/toc/1664-042XElevated central venous pressure increases renal venous pressure (RVP) which can affect kidney function. We previously demonstrated that increased RVP reduces renal blood flow (RBF), glomerular filtration rate (GFR), and renal vascular conductance (RVC). We now investigate whether the RAS and RBF autoregulation are involved in the renal hemodynamic response to increased RVP. Angiotensin II (ANG II) levels were clamped by infusion of ANG II after administration of an angiotensin-converting enzyme (ACE) inhibitor in male Lewis rats. This did not prevent the decrease in ipsilateral RBF (−1.9±0.4ml/min, p<0.05) and GFR (−0.77±0.18ml/min, p<0.05) upon increased RVP; however, it prevented the reduction in RVC entirely. Systemically, the RVP-induced decline in mean arterial pressure (MAP) was more pronounced in ANG II clamped animals vs. controls (−22.4±4.1 vs. −9.9±2.3mmHg, p<0.05), whereas the decrease in heart rate (HR) was less (−5±6bpm vs. −23±4bpm, p<0.05). In animals given vasopressin to maintain a comparable MAP after ACE inhibition (ACEi), increased RVP did not impact MAP and HR. RVC also did not change (0.018±0.008ml/minˑmmHg), and the reduction of GFR was no longer significant (−0.54±0.15ml/min). Furthermore, RBF autoregulation remained intact and was reset to a lower level when RVP was increased. In conclusion, RVP-induced renal vasoconstriction is attenuated when ANG II is clamped or inhibited. The systemic effect of increased RVP, a decrease in HR related to a mild decrease in blood pressure, is attenuated also during ANG II clamp. Last, RBF autoregulation remains intact when RVP is elevated and is reduced to lower levels of RBF. This suggests that in venous congestion, the intact RBF autoregulation could be partially responsible for the vasoconstriction.Xiaohua HuangXiaohua HuangShereen M. HamzaShereen M. HamzaWenqing ZhuangWilliam A. CupplesBranko BraamBranko BraamFrontiers Media S.A.articlerenal venous pressurecardiorenal syndromerenin – angiotensin – aldosterone systemrenal hemodynamicsvenous congestionPhysiologyQP1-981ENFrontiers in Physiology, Vol 12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	renal venous pressure cardiorenal syndrome renin – angiotensin – aldosterone system renal hemodynamics venous congestion Physiology QP1-981
spellingShingle	renal venous pressure cardiorenal syndrome renin – angiotensin – aldosterone system renal hemodynamics venous congestion Physiology QP1-981 Xiaohua Huang Xiaohua Huang Shereen M. Hamza Shereen M. Hamza Wenqing Zhuang William A. Cupples Branko Braam Branko Braam Angiotensin II and the Renal Hemodynamic Response to an Isolated Increased Renal Venous Pressure in Rats
description	Elevated central venous pressure increases renal venous pressure (RVP) which can affect kidney function. We previously demonstrated that increased RVP reduces renal blood flow (RBF), glomerular filtration rate (GFR), and renal vascular conductance (RVC). We now investigate whether the RAS and RBF autoregulation are involved in the renal hemodynamic response to increased RVP. Angiotensin II (ANG II) levels were clamped by infusion of ANG II after administration of an angiotensin-converting enzyme (ACE) inhibitor in male Lewis rats. This did not prevent the decrease in ipsilateral RBF (−1.9±0.4ml/min, p<0.05) and GFR (−0.77±0.18ml/min, p<0.05) upon increased RVP; however, it prevented the reduction in RVC entirely. Systemically, the RVP-induced decline in mean arterial pressure (MAP) was more pronounced in ANG II clamped animals vs. controls (−22.4±4.1 vs. −9.9±2.3mmHg, p<0.05), whereas the decrease in heart rate (HR) was less (−5±6bpm vs. −23±4bpm, p<0.05). In animals given vasopressin to maintain a comparable MAP after ACE inhibition (ACEi), increased RVP did not impact MAP and HR. RVC also did not change (0.018±0.008ml/minˑmmHg), and the reduction of GFR was no longer significant (−0.54±0.15ml/min). Furthermore, RBF autoregulation remained intact and was reset to a lower level when RVP was increased. In conclusion, RVP-induced renal vasoconstriction is attenuated when ANG II is clamped or inhibited. The systemic effect of increased RVP, a decrease in HR related to a mild decrease in blood pressure, is attenuated also during ANG II clamp. Last, RBF autoregulation remains intact when RVP is elevated and is reduced to lower levels of RBF. This suggests that in venous congestion, the intact RBF autoregulation could be partially responsible for the vasoconstriction.
format	article
author	Xiaohua Huang Xiaohua Huang Shereen M. Hamza Shereen M. Hamza Wenqing Zhuang William A. Cupples Branko Braam Branko Braam
author_facet	Xiaohua Huang Xiaohua Huang Shereen M. Hamza Shereen M. Hamza Wenqing Zhuang William A. Cupples Branko Braam Branko Braam
author_sort	Xiaohua Huang
title	Angiotensin II and the Renal Hemodynamic Response to an Isolated Increased Renal Venous Pressure in Rats
title_short	Angiotensin II and the Renal Hemodynamic Response to an Isolated Increased Renal Venous Pressure in Rats
title_full	Angiotensin II and the Renal Hemodynamic Response to an Isolated Increased Renal Venous Pressure in Rats
title_fullStr	Angiotensin II and the Renal Hemodynamic Response to an Isolated Increased Renal Venous Pressure in Rats
title_full_unstemmed	Angiotensin II and the Renal Hemodynamic Response to an Isolated Increased Renal Venous Pressure in Rats
title_sort	angiotensin ii and the renal hemodynamic response to an isolated increased renal venous pressure in rats
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/d255ba5cebed4d33837e5f1a651c514d
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Angiotensin II and the Renal Hemodynamic Response to an Isolated Increased Renal Venous Pressure in Rats

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