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Christopher S Wilcox – One of the best experts on this subject based on the ideXlab platform.

  • high salt enhances reactive oxygen species and angiotensin ii contractions of glomerular Afferent Arterioles from mice with reduced renal mass
    Hypertension, 2018
    Co-Authors: En Yin Lai, Anton Wellstein, William J Welch, Glenn Solis, Zaiming Luo, Kathy K Griendling, Margarida Mendonca, Christopher S Wilcox
    Abstract:

    High salt, Ang II (angiotensin II), and reactive oxygen species enhance progression of chronic kidney disease. We tested the hypothesis that a high salt intake generates specific reactive oxygen species to enhance Ang II contractions of Afferent Arterioles from mice with reduced renal mass (RRM). C57BL/6 mice were subjected to surgical RRM or sham operations and received 6% or 0.4% NaCl salt diet for 3 months. Ang II contractions were measured in perfused Afferent Arterioles and superoxide (O2-) and hydrogen peroxide (H2O2) by fluorescence microscopy. RRM enhanced the Afferent arteriolar gene expression for p47phox and neutrophil oxidase (NOX) 2 and high salt intake in RRM mice enhanced gene expression for angiotensin type 1 receptors, POLDIP2 and NOX4 and reduced catalase. High salt in mice with RRM enhanced arteriolar O2- and H2O2 generation and maximal contractions to Ang II (10-6 mol/L) that were dependent on O2- because they were prevented by gene deletion of p47phox and on H2O2 because they were prevented by transgenic smooth muscle cell expression of catalase (tgCAT-SMC) and POLDIP2 gene deletion. Three months of tempol normalized arteriolar reactive oxygen species and Ang II contractions. However, arteriolar contractions to lower concentrations of Ang II (10-8 to 10-11 mol/L) were paradoxically inhibited by H2O2 and POLDIP2. In conclusion, both O2- from p47phox/NOX2 and H2O2 from NOX4/POLDIP2 enhance maximal arteriolar Ang II contractions from RRM mice during high salt, but H2O2 and NOX4/POLDIP2 reduce the sensitivity to lower concentrations of Ang II by >100-fold. Tempol prevents all of these changes in function.

  • superoxide and hydrogen peroxide counterregulate myogenic contractions in renal Afferent Arterioles from a mouse model of chronic kidney disease
    Kidney International, 2017
    Co-Authors: En Yin Lai, William J Welch, Glenn Solis, Zaiming Luo, Kathy K Griendling, Robert W Taylor, Pedro A Jose, Anton Wellsten, Christopher S Wilcox
    Abstract:

    Myogenic contractions protect kidneys from barotrauma but are impaired in chronic kidney disease (CKD). Since myogenic contractions are enhanced by superoxide but impaired by hydrogen peroxide, we tested the hypothesis that they are counterregulated by superoxide and H 2 O 2 from NOX2/p47phox and/or NOX4/POLDIP2 in CKD. Myogenic contraction in isolated perfused Afferent Arterioles from mice with surgical 5/6 nephrectomy or sham operations fed a 6% sodium chloride diet was measured directly while superoxide and H 2 O 2 were measured by fluorescence microscopy. Compared to sham-operated animals, an increase in perfusion pressure of Arterioles from CKD mice doubled superoxide (21 versus 11%), increased H 2 O 2 seven-fold (29 versus 4%), and reduced myogenic contractions profoundly (-1 versus -14%). Myogenic contractions were impaired further by PEG-superoxide dismutase or in Arterioles from p47phox-/- (versus wild type) mice but became supra-normal by PEG-catalase or in mice with transgenic expression of catalase in vascular smooth muscle cells (-11 versus -1%). Single Arterioles from mice with CKD expressed over 40% more mRNA and protein for NOX4 and POLDIP2. Myogenic responses in Arterioles from POLDIP2 +/- (versus wild type) mice with CKD had over an 85% reduction in H 2 O 2 , but preserved superoxide and a normal myogenic response. Tempol administration to CKD mice for 3 months decreased Afferent arteriolar superoxide and H 2 O 2 and maintained myogenic contractions. Thus, Afferent arteriolar superoxide generated by NOX2/p47phox opposes H 2 O 2 generated by NOX4/POLDIP2 whose upregulation in Afferent Arterioles from mice with CKD accounts for impaired myogenic contractions.

  • Increased hydrogen peroxide impairs angiotensin II contractions of Afferent Arterioles in mice after renal ischaemia-reperfusion injury.
    Acta physiologica (Oxford England), 2016
    Co-Authors: Qian Huang, Andreas Patzak, Qiaoling Wang, Suping Zhang, Shan Jiang, Liang Zhao, Michael Hultström, Christopher S Wilcox
    Abstract:

    AIM Renal ischaemia-reperfusion injury (IRI) increases angiotensin II (Ang II) and reactive oxygen species (ROS) that are potent modulators of vascular function. However, the roles of individual ROS and their interaction with Ang II are not clear. Here we tested the hypothesis that IRI modulates renal Afferent arteriolar responses to Ang II via increasing superoxide (O2-) or hydrogen peroxide (H2 O2 ). METHODS Renal Afferent Arterioles were isolated and perfused from C57BL/6 mice 24 h after IRI or sham surgery. Responses to Ang II or noradrenaline were assessed by measuring arteriolar diameter. Production of H2 O2 and O2- was assessed in Afferent Arterioles and renal cortex. Activity of SOD and catalase, and mRNA expressions of Ang II receptors were assessed in pre-glomerular Arterioles and renal cortex. RESULTS Afferent Arterioles from mice after IRI had a reduced maximal contraction to Ang II (-27±2 vs. -42±1%, P 

En Yin Lai – One of the best experts on this subject based on the ideXlab platform.

  • high salt enhances reactive oxygen species and angiotensin ii contractions of glomerular Afferent Arterioles from mice with reduced renal mass
    Hypertension, 2018
    Co-Authors: En Yin Lai, Anton Wellstein, William J Welch, Glenn Solis, Zaiming Luo, Kathy K Griendling, Margarida Mendonca, Christopher S Wilcox
    Abstract:

    High salt, Ang II (angiotensin II), and reactive oxygen species enhance progression of chronic kidney disease. We tested the hypothesis that a high salt intake generates specific reactive oxygen species to enhance Ang II contractions of Afferent Arterioles from mice with reduced renal mass (RRM). C57BL/6 mice were subjected to surgical RRM or sham operations and received 6% or 0.4% NaCl salt diet for 3 months. Ang II contractions were measured in perfused Afferent Arterioles and superoxide (O2-) and hydrogen peroxide (H2O2) by fluorescence microscopy. RRM enhanced the Afferent arteriolar gene expression for p47phox and neutrophil oxidase (NOX) 2 and high salt intake in RRM mice enhanced gene expression for angiotensin type 1 receptors, POLDIP2 and NOX4 and reduced catalase. High salt in mice with RRM enhanced arteriolar O2- and H2O2 generation and maximal contractions to Ang II (10-6 mol/L) that were dependent on O2- because they were prevented by gene deletion of p47phox and on H2O2 because they were prevented by transgenic smooth muscle cell expression of catalase (tgCAT-SMC) and POLDIP2 gene deletion. Three months of tempol normalized arteriolar reactive oxygen species and Ang II contractions. However, arteriolar contractions to lower concentrations of Ang II (10-8 to 10-11 mol/L) were paradoxically inhibited by H2O2 and POLDIP2. In conclusion, both O2- from p47phox/NOX2 and H2O2 from NOX4/POLDIP2 enhance maximal arteriolar Ang II contractions from RRM mice during high salt, but H2O2 and NOX4/POLDIP2 reduce the sensitivity to lower concentrations of Ang II by >100-fold. Tempol prevents all of these changes in function.

  • glucose dilates renal Afferent Arterioles via glucose transporter 1
    American Journal of Physiology-renal Physiology, 2018
    Co-Authors: Jie Zhang, En Yin Lai, Shan Jiang, Jin Wei, Kaypong Yip, Lei Wang, Ruisheng Liu
    Abstract:

    Glomerular hyperfiltration often occurs during the early stage of diabetes. An acute glucose infuinfusion increases glomerular filtfiltratione (GFR). The involvement of tubuloglomerular feedback response and direct effect of glucose on the Afferent Arterioles (Af-Arts) have been suggested. However, the signaling pathways to trigger Af-Art dilatation have not been fully identified. Therefore, in the present study we tested our hypothesis that an increase of glucose concentration enhances endothelial nitric oxide synthesis (NOS3) activity and dilates the Af-Arts via glucose transporter 1 (GLUT1) using isolated mouse Af-Arts with perfusion. We isolated and microperfused the Af-Arts from non-diabetic C57BL/6 mice. The Af-Arts were preconstricted with norepinephrine (NE, 1 µM). When we switched the D-glucose concentration from low (5 mM) to high (30 mM) in the perfusate, the preconstricted Af-Arts significantly dilated by 37.8{plus minus}7.1%, but L-glucose did not trigger the dilation. GLUT1 mRNA was identified i…

  • superoxide and hydrogen peroxide counterregulate myogenic contractions in renal Afferent Arterioles from a mouse model of chronic kidney disease
    Kidney International, 2017
    Co-Authors: En Yin Lai, William J Welch, Glenn Solis, Zaiming Luo, Kathy K Griendling, Robert W Taylor, Pedro A Jose, Anton Wellsten, Christopher S Wilcox
    Abstract:

    Myogenic contractions protect kidneys from barotrauma but are impaired in chronic kidney disease (CKD). Since myogenic contractions are enhanced by superoxide but impaired by hydrogen peroxide, we tested the hypothesis that they are counterregulated by superoxide and H 2 O 2 from NOX2/p47phox and/or NOX4/POLDIP2 in CKD. Myogenic contraction in isolated perfused Afferent Arterioles from mice with surgical 5/6 nephrectomy or sham operations fed a 6% sodium chloride diet was measured directly while superoxide and H 2 O 2 were measured by fluorescence microscopy. Compared to sham-operated animals, an increase in perfusion pressure of Arterioles from CKD mice doubled superoxide (21 versus 11%), increased H 2 O 2 seven-fold (29 versus 4%), and reduced myogenic contractions profoundly (-1 versus -14%). Myogenic contractions were impaired further by PEG-superoxide dismutase or in Arterioles from p47phox-/- (versus wild type) mice but became supra-normal by PEG-catalase or in mice with transgenic expression of catalase in vascular smooth muscle cells (-11 versus -1%). Single Arterioles from mice with CKD expressed over 40% more mRNA and protein for NOX4 and POLDIP2. Myogenic responses in Arterioles from POLDIP2 +/- (versus wild type) mice with CKD had over an 85% reduction in H 2 O 2 , but preserved superoxide and a normal myogenic response. Tempol administration to CKD mice for 3 months decreased Afferent arteriolar superoxide and H 2 O 2 and maintained myogenic contractions. Thus, Afferent arteriolar superoxide generated by NOX2/p47phox opposes H 2 O 2 generated by NOX4/POLDIP2 whose upregulation in Afferent Arterioles from mice with CKD accounts for impaired myogenic contractions.

Andreas Patzak – One of the best experts on this subject based on the ideXlab platform.

  • Extravasal albumin concentration modulates contractile responses of renal Afferent Arterioles
    Acta physiologica (Oxford England), 2017
    Co-Authors: Xiang Gao, En Yin Lai, Zhi Zhao Liu, H. Mohammed, Diana Braun, Zhengbing Zhuge, Ming Liu, Leif Jansson, Mattias Carlström, Andreas Patzak
    Abstract:

    AIM Afferent Arterioles (AA) hold a key position in the regulation of renal blood flow and glomerular filtfiltratione. Being the effector site of tubuloglomerular feedback, the Afferent arteriole contributes to the renal handling of sodium and fluid. Dehydration goes along with increased renal interstitial protein concentration. Here, the hypothesis was tested that extravasal protein concentration directly modulates Afferent arteriolar tone, a mechanism which may contribute to body fluid volume control. METHOD The effect of increased extravasal albumin concentration on the vascular reactivity was investigated in renal AA and interlobar arteries of mice, in rat renal AA and in pancreatic islet Arterioles. RESULTS Albumin (2 and 4% in the bath solution) significantly potentiated the contractile response of renal Afferent Arterioles induced by angiotensin II and adenosine, as well as their combination, compared to the control situation (0.1% albumin). Albumin did not influence the contractility of larger renal vessels or pancreatic islet Arterioles. Mimicking the increase in the osmolality induced by 4% albumin by applying mannitol to the bath solution also increased the response of renal Arterioles to Ang II. However, the effect was smaller compared to that of albumin. The nitric oxide bioavailability, measured by DAF-FM fluorescence, was reduced in Afferent Arterioles exposed to 4% albumin. CONCLUSION The protein-induced modulation of AA tone is mediated by the increased osmolality as well as by NO scavenging. The results suggest a possible contribution of these mechanisms to the control of extracellular fluid volume via adjustment of renal blood flow and glomerular filtfiltratione.

  • Increased hydrogen peroxide impairs angiotensin II contractions of Afferent Arterioles in mice after renal ischaemia-reperfusion injury.
    Acta physiologica (Oxford England), 2016
    Co-Authors: Qian Huang, Andreas Patzak, Qiaoling Wang, Suping Zhang, Shan Jiang, Liang Zhao, Michael Hultström, Christopher S Wilcox
    Abstract:

    AIM Renal ischaemia-reperfusion injury (IRI) increases angiotensin II (Ang II) and reactive oxygen species (ROS) that are potent modulators of vascular function. However, the roles of individual ROS and their interaction with Ang II are not clear. Here we tested the hypothesis that IRI modulates renal Afferent arteriolar responses to Ang II via increasing superoxide (O2-) or hydrogen peroxide (H2 O2 ). METHODS Renal Afferent Arterioles were isolated and perfused from C57BL/6 mice 24 h after IRI or sham surgery. Responses to Ang II or noradrenaline were assessed by measuring arteriolar diameter. Production of H2 O2 and O2- was assessed in Afferent Arterioles and renal cortex. Activity of SOD and catalase, and mRNA expressions of Ang II receptors were assessed in pre-glomerular Arterioles and renal cortex. RESULTS Afferent Arterioles from mice after IRI had a reduced maximal contraction to Ang II (-27±2 vs. -42±1%, P 

  • increased hydrogen peroxide impairs angiotensin ii contractions of Afferent Arterioles in mice after renal ischaemia reperfusion injury
    Acta Physiologica, 2016
    Co-Authors: Qian Huang, Christopher S Wilcox, Andreas Patzak, Qiaoling Wang, Suping Zhang, Shan Jiang, Liang Zhao, Michael Hultström, En Yin Lai
    Abstract:

    AIM Renal ischaemia-reperfusion injury (IRI) increases angiotensin II (Ang II) and reactive oxygen species (ROS) that are potent modulators of vascular function. However, the roles of individual ROS and their interaction with Ang II are not clear. Here we tested the hypothesis that IRI modulates renal Afferent arteriolar responses to Ang II via increasing superoxide (O2-) or hydrogen peroxide (H2 O2 ). METHODS Renal Afferent Arterioles were isolated and perfused from C57BL/6 mice 24 h after IRI or sham surgery. Responses to Ang II or noradrenaline were assessed by measuring arteriolar diameter. Production of H2 O2 and O2- was assessed in Afferent Arterioles and renal cortex. Activity of SOD and catalase, and mRNA expressions of Ang II receptors were assessed in pre-glomerular Arterioles and renal cortex. RESULTS Afferent Arterioles from mice after IRI had a reduced maximal contraction to Ang II (-27±2 vs. -42±1%, P < 0.001), but retained a normal contraction to noradrenaline. Arterioles after IRI had a 38% increase in H2 O2 (P < 0.001) and a 45% decrease in catalase activity (P < 0.01). Contractions were reduced in normal Arterioles after incubation with H2 O2 (-22±2 vs. -42±1%, P < 0.05) similar to the effects of IRI. However, the impaired contractions were normalized by incubation with PEG catalase despite a reduced AT1 R expression. CONCLUSIONS Renal IRI in mice selectively impairs Afferent arteriolar responses to Ang II because of H2 O2 accumulation that is caused by a reduced catalase activity. This could serve to buffer the effect of Ang II after IRI and may be a protective mechanism.

William J Welch – One of the best experts on this subject based on the ideXlab platform.

  • high salt enhances reactive oxygen species and angiotensin ii contractions of glomerular Afferent Arterioles from mice with reduced renal mass
    Hypertension, 2018
    Co-Authors: En Yin Lai, Anton Wellstein, William J Welch, Glenn Solis, Zaiming Luo, Kathy K Griendling, Margarida Mendonca, Christopher S Wilcox
    Abstract:

    High salt, Ang II (angiotensin II), and reactive oxygen species enhance progression of chronic kidney disease. We tested the hypothesis that a high salt intake generates specific reactive oxygen species to enhance Ang II contractions of Afferent Arterioles from mice with reduced renal mass (RRM). C57BL/6 mice were subjected to surgical RRM or sham operations and received 6% or 0.4% NaCl salt diet for 3 months. Ang II contractions were measured in perfused Afferent Arterioles and superoxide (O2-) and hydrogen peroxide (H2O2) by fluorescence microscopy. RRM enhanced the Afferent arteriolar gene expression for p47phox and neutrophil oxidase (NOX) 2 and high salt intake in RRM mice enhanced gene expression for angiotensin type 1 receptors, POLDIP2 and NOX4 and reduced catalase. High salt in mice with RRM enhanced arteriolar O2- and H2O2 generation and maximal contractions to Ang II (10-6 mol/L) that were dependent on O2- because they were prevented by gene deletion of p47phox and on H2O2 because they were prevented by transgenic smooth muscle cell expression of catalase (tgCAT-SMC) and POLDIP2 gene deletion. Three months of tempol normalized arteriolar reactive oxygen species and Ang II contractions. However, arteriolar contractions to lower concentrations of Ang II (10-8 to 10-11 mol/L) were paradoxically inhibited by H2O2 and POLDIP2. In conclusion, both O2- from p47phox/NOX2 and H2O2 from NOX4/POLDIP2 enhance maximal arteriolar Ang II contractions from RRM mice during high salt, but H2O2 and NOX4/POLDIP2 reduce the sensitivity to lower concentrations of Ang II by >100-fold. Tempol prevents all of these changes in function.

  • superoxide and hydrogen peroxide counterregulate myogenic contractions in renal Afferent Arterioles from a mouse model of chronic kidney disease
    Kidney International, 2017
    Co-Authors: En Yin Lai, William J Welch, Glenn Solis, Zaiming Luo, Kathy K Griendling, Robert W Taylor, Pedro A Jose, Anton Wellsten, Christopher S Wilcox
    Abstract:

    Myogenic contractions protect kidneys from barotrauma but are impaired in chronic kidney disease (CKD). Since myogenic contractions are enhanced by superoxide but impaired by hydrogen peroxide, we tested the hypothesis that they are counterregulated by superoxide and H 2 O 2 from NOX2/p47phox and/or NOX4/POLDIP2 in CKD. Myogenic contraction in isolated perfused Afferent Arterioles from mice with surgical 5/6 nephrectomy or sham operations fed a 6% sodium chloride diet was measured directly while superoxide and H 2 O 2 were measured by fluorescence microscopy. Compared to sham-operated animals, an increase in perfusion pressure of Arterioles from CKD mice doubled superoxide (21 versus 11%), increased H 2 O 2 seven-fold (29 versus 4%), and reduced myogenic contractions profoundly (-1 versus -14%). Myogenic contractions were impaired further by PEG-superoxide dismutase or in Arterioles from p47phox-/- (versus wild type) mice but became supra-normal by PEG-catalase or in mice with transgenic expression of catalase in vascular smooth muscle cells (-11 versus -1%). Single Arterioles from mice with CKD expressed over 40% more mRNA and protein for NOX4 and POLDIP2. Myogenic responses in Arterioles from POLDIP2 +/- (versus wild type) mice with CKD had over an 85% reduction in H 2 O 2 , but preserved superoxide and a normal myogenic response. Tempol administration to CKD mice for 3 months decreased Afferent arteriolar superoxide and H 2 O 2 and maintained myogenic contractions. Thus, Afferent arteriolar superoxide generated by NOX2/p47phox opposes H 2 O 2 generated by NOX4/POLDIP2 whose upregulation in Afferent Arterioles from mice with CKD accounts for impaired myogenic contractions.

  • differential effects of superoxide and hydrogen peroxide on myogenic signaling membrane potential and contractions of mouse renal Afferent Arterioles
    American Journal of Physiology-renal Physiology, 2016
    Co-Authors: En Yin Lai, Anton Wellstein, William J Welch, Christopher S Wilcox
    Abstract:

    Myogenic contraction is the principal component of renal autoregulation that protects the kidney from hypertensive barotrauma. Contractions are initiated by a rise in perfusion pressure that signals a reduction in membrane potential (Em) of vascular smooth muscle cells to activate voltage-operated Ca(2+) channels. Since ROS have variable effects on myogenic tone, we investigated the hypothesis that superoxide (O2 (·-)) and H2O2 differentially impact myogenic contractions. The myogenic contractions of mouse isolated and perfused single Afferent Arterioles were assessed from changes in luminal diameter with increasing perfusion pressure (40-80 mmHg). O2 (·-), H2O2, and Em were assessed by fluorescence microscopy during incubation with paraquat to increase O2 (·-) or with H2O2 Paraquat enhanced O2 (·-) generation and myogenic contractions (-42 ± 4% vs. -19 ± 4%, P < 0.005) that were blocked by SOD but not by catalase and signaled via PKC. In contrast, H2O2 inhibited the effects of paraquat and reduced myogenic contractions (-10 ± 1% vs. -19 ± 2%, P < 0.005) and signaled via PKG. O2 (·-) activated Ca(2+)-activated Cl(-) channels that reduced Em, whereas H2O2 activated Ca(2+)-activated and voltage-gated K(+) channels that increased Em Blockade of voltage-operated Ca(2+) channels prevented the enhanced myogenic contractions with paraquat without preventing the reduction in Em Myogenic contractions were independent of the endothelium and largely independent of nitric oxide. We conclude that O2 (·-) and H2O2 activate different signaling pathways in vascular smooth muscle cells linked to discreet membrane channels with opposite effects on Em and voltage-operated Ca(2+) channels and therefore have opposite effects on myogenic contractions.

Shoji Kimura – One of the best experts on this subject based on the ideXlab platform.

  • Effects of angiotensin II on isolated rabbit Afferent Arterioles.
    Japanese Journal of Pharmacology, 2019
    Co-Authors: Hiroyuki Yoshida, Toshiaki Tamaki, Shoji Kimura, Ikumasa Takenaka
    Abstract:

    We examined the effects of angiotensin II (Ang II) on isolated rabbit Afferent Arterioles to assess the direct effect of Ang II at the resistance vessel level in the kidney. We microdissected the superficial Afferent arteriole from the kidney of New Zealand White rabbits. The Afferent arteriole was cannulated with a micropipette system, and the intraluminal pressure was set at 80 mmHg. Ang II did not change the lumen diameter of the Afferent Arterioles. After the Afferent Arterioles were pretreated with aspirin DL-lysine or indomethacin, Ang II (10-7 M) caused transient vasoconstriction in the Afferent Arterioles. Ang II (10-7 M) caused persistent constriction in the Afferent Arterioles pretreated with NG-nitro-L-arginine (10-4 M). Physiological doses of Ang II decresed the lumen diameter of the isolated Afferent Arterioles pretreated with NG-nitro-L-arginine and aspirin DL-lysine. Dup753 (10-6 M), an AT1-receptor antagonist, abolished the vasoconstrictor effects of Ang II. These findings suggest that the isolated rabbit Afferent arteriole has AT1 receptors, and the vasoconstrictor response of Ang II is counteracted by vasodilatory prostaglandins and nitric oxide.

  • Role of Nitric Oxide in Desmopressin-Induced Vasodilation of Microperfused Rabbit Afferent Arterioles.
    Hypertension research : official journal of the Japanese Society of Hypertension, 1997
    Co-Authors: Kayo Kiyomoto, Toshiaki Tamaki, Shoji Kimura, Atsufumi Tomohiro, Akira Nishiyama, Yasuharu Aki, Youichi Abe
    Abstract:

    We have previously reported that desmopressin (dDAVP) increased the lumen diameter of norepinephrine (NE)-constricted isolated microperfused rabbit Afferent Arterioles. In this study, we examined the role of nitric oxide in dDAVP-induced vasodilation of Afferent Arterioles. We microdissected a superficial Afferent arteriole from the kidney of a New Zealand white rabbit. Each Afferent arteriole was cannulated with a pipette system and microperfused in vitro at 60 mmHg. dDAVP increased the lumen diameter of NE-preconstricted rabbit Afferent Arterioles dose-dependently. dDAVP-induced vasodilation was abolished by pretreatment with NG-nitro-L-arginine (L-NNA, 10(-4)M) (L-NNA + NE, 6.7 +/- 1.1 microns; L-NNA + NE + dDAVP, 7.3 +/- 1.4 microns, n = 8). dDAVP increased the lumen diameter of NE-preconstricted Afferent Arterioles pretreated with L-NNA and L-arginine (10(-2)M) (L-NNA + L-arginine + NE, 6.1 +/- 1.1 microns; L-NNA + L-arginine + NE + dDAVP, 8.7 +/- 0.9 microns*; *p < 0.05, n = 6). Aspirin-DL-lysine (10(-4)M) did not influence dDAVP-induced Afferent arteriolar vasodilation (aspirin + NE, 6.4 +/- 0.8 microns; aspirin + NE + dDAVP, 9.6 +/- 1.3 microns *; *p < 0.05, n = 5). These results suggest that nitric oxide may be responsible for dDAVP-induced Afferent arteriolar vasodilation.

  • Vasodilation induced by vasopressin V2 receptor stimulation in Afferent Arterioles
    Kidney International, 1996
    Co-Authors: Toshiaki Tamaki, Kayo Kiyomoto, Hong He, Atsufumi Tomohiro, Akira Nishiyama, Shoji Kimura
    Abstract:

    Vasodilation induced by vasopressin V2 receptor stimulation in Afferent Arterioles. We have previously reported that vasopressin (AVP) V2 receptor stimulation increased renal blood flow in dogs anesthetized with pentobarbital. In this study, we examined the direct effects of AVP on Afferent Arterioles to clarify the role played by V2 receptors in regulating Afferent arteriolar tone. We microdissected a superficial Afferent arteriole with glomerulus from the kidney of a New Zealand White rabbit. Each Afferent arteriole was cannulated with a pipette system and microperfused in vitro at 60mm Hg. The effects of vasoactive substances were evaluated by changes in the lumen diameter of Afferent Arterioles. We found that AVP decreased the lumen diameter of microperfused Afferent Arterioles dose-dependently and that a VI antagonist, OPC21268, inhibited the vasoconstrictor action of AVP. However, AVP 10 −8 M increased the lumen diameter of norepinephrine (NE)-constricted Afferent Arterioles pretreated with OPC21268 (OPC+NE, 8.2 ± 0.7 µ m; OPC+NE+AVP, 9.9 ± 0.9 µ m*; * P N = 13). This vasodilatory effect of AVP was abolished by pretreatment with a V2 antagonist, OPC31260. Desmopressin (dDAVP), a V2 agonist, increased the lumen diameter of the NE-constricted Afferent Arterioles (NE, 7.4 ± 0.9 µ m; NE+dDAVP, 10.1 ± 0.7 µ m*; *P