The Experts below are selected from a list of 285 Experts worldwide ranked by ideXlab platform

Oscar A Carretero - One of the best experts on this subject based on the ideXlab platform.

Hong Wang - One of the best experts on this subject based on the ideXlab platform.

  • Connecting Tubule glomerular feedback mediates tubuloglomerular feedback resetting after unilateral nephrectomy
    American Journal of Physiology-renal Physiology, 2018
    Co-Authors: Sumit R. Monu, Kristopher Kutskill, Edward L Peterson, Hong Wang, Nitin Kumar, J X Masjoanjuncos, Oscar A Carretero
    Abstract:

    Unilaterally nephrectomized rats (UNx) have higher glomerular capillary pressure (PGC) that can cause significant glomerular injury in the remnant kidney. PGC is controlled by the ratio of afferent...

  • effect of salt intake on afferent arteriolar dilatation role of Connecting Tubule glomerular feedback ctgf
    American Journal of Physiology-renal Physiology, 2017
    Co-Authors: Hong Wang, Edward L Peterson, Cesar A Romero, Sumit R. Monu, J. X. Masjoan Juncos, Oscar A Carretero
    Abstract:

    Afferent arteriole (Af-Art) resistance is modulated by two intrinsic nephron feedbacks: 1) the vasoconstrictor tubuloglomerular feedback (TGF) mediated by Na+-K+-2Cl− cotransporters (NKCC2) in the ...

  • Effect of salt intake on afferent arteriolar dilatation: role of Connecting Tubule glomerular feedback (CTGF).
    American Journal of Physiology-renal Physiology, 2017
    Co-Authors: Hong Wang, Edward L Peterson, Cesar A Romero, Sumit R. Monu, J. X. Masjoan Juncos, Oscar A Carretero
    Abstract:

    Afferent arteriole (Af-Art) resistance is modulated by two intrinsic nephron feedbacks: 1 ) the vasoconstrictor tubuloglomerular feedback (TGF) mediated by Na + -K + -2Cl − cotransporters (NKCC2) in the macula densa and blocked by furosemide and 2 ) the vasodilator Connecting Tubule glomerular feedback (CTGF), mediated by epithelial Na + channels (ENaC) in the Connecting Tubule and blocked by benzamil. High salt intake reduces Af-Art vasoconstrictor ability in Dahl salt-sensitive rats (Dahl SS). Previously, we measured CTGF indirectly, by differences between TGF responses with and without CTGF inhibition. We recently developed a new method to measure CTGF more directly by simultaneously inhibiting NKCC2 and the Na + /H + exchanger (NHE). We hypothesize that in vivo during simultaneous inhibition of NKCC2 and NHE, CTGF causes an Af-Art dilatation revealed by an increase in stop-flow pressure (P SF ) in Dahl SS and that is enhanced with a high salt intake. In the presence of furosemide alone, increasing nephron perfusion did not change the P SF in either Dahl salt-resistant rats (Dahl SR) or Dahl SS. When furosemide and an NHE inhibitor, dimethylamiloride, were perfused simultaneously, an increase in tubular flow caused Af-Art dilatation that was demonstrated by an increase in P SF. This increase was greater in Dahl SS [4.5 ± 0.4 (SE) mmHg] than in Dahl SR (2.5 ± 0.3 mmHg; P

  • Connecting Tubule glomerular feedback mediates tubuloglomerular feedback resetting after unilateral nephrectomy
    American Journal of Physiology-renal Physiology, 2017
    Co-Authors: Sumit R. Monu, Kristopher Kutskill, Edward L Peterson, Hong Wang, J. X. Masjoan-juncos, Nitin Kumar, Oscar A Carretero
    Abstract:

    Unilaterally nephrectomized rats (UNx) have higher glomerular capillary pressure (PGC) that can cause significant glomerular injury in the remnant kidney. PGC is controlled by the ratio of afferent (Af-Art) and efferent arteriole resistance. Af-Art resistance in turn is regulated by two intrinsic feedback mechanisms: 1) Tubuloglomerular feedback (TGF) that causes Af-Art constriction in response to increased NaCl in the macula densa and 2) Connecting Tubule glomerular feedback (CTGF) that causes Af-Art dilatation in response to an increase in NaCl transport in the Connecting Tubule via the epithelial sodium channel (ENaC). Resetting of TGF post-UNx can allow systemic pressure to be transmitted to the glomerulus and cause renal damage, but the mechanism behind this resetting is unclear. Since CTGF is an Af-Art dilatory mechanism, we hypothesized that CTGF is increased after UNx, and contributes to TGF resetting. To test this hypothesis, we performed UNx in Sprague Dawley (SD) rats. Twenty-four hours after surgery, we performed micropuncture of individual nephrons and measured stop-flow pressure (PSF). PSF is an indirect measurement of PGC. Maximal TGF response at 40nl/min was 8.9 ± 1.24 mmHg in sham-UNx rats and 1.39 ± 1.02 mmHg in UNx rats indicating TGF resetting after UNx. When CTGF was inhibited with the ENaC blocker Benzamil (1μM/L), the TGF response was 12.29 ± 2.01 mmHg in UNx rats and 13.03 ± 1.25 mmHg in sham-UNx rats, indicating restoration of the TGF responses in UNx. We conclude that enhanced CTGF contributes to TGF resetting after UNx.

  • abstract p325 enhanced afferent arteriole dilatation in dahl salt sensitive rats dahlss role of Connecting Tubule glomerular feedback ctgf
    Hypertension, 2016
    Co-Authors: Hong Wang, Branislava Janic, Cesar A Romero, Edwards Peterson, Oscar A Carretero
    Abstract:

    Afferent arteriole (Af-Art) resistance is modulated by 2 intrinsic nephron feedbacks: the vasoconstrictor tubuloglomerular feedback (TGF) and the vasodilator CTGF. TGF is mediated by NKCC2 channel in the macula densa and blocked by furosemide; and CTGF is mediated by ENaC in the Connecting Tubule and blocked by benzamil. Previously we measured CTGF indirectly, by differences between TGF response with and without CTGF blocker benzamil. Thus, using this indirect measurement we reported that Dahl SS have greater CTGF than Dahl salt-resistant rats (Dahl SR). We have recently developed a new method to measure CTGF more directly and we found that when we simultaneously blocked TGF with furosemide and CTGF with benzamil, the increasing tubular perfusion caused Af-Art constriction (TGF-like) that is mediated by the NHE. W e hypothesize that in vivo during simultaneous inhibition of NKCC2 and the NHE, CTGF causes an Af-Art dilatation revealed by an increase in stop-flow pressure (P SF ) and that is greater in Dahl SS than in Dahl SR in a high salt diet. In the presence of furosemide alone, increasing nephron perfusion did not change the P SF in neither Dahl SS nor Dahl SR. When we blocked both, NKCC2 with furosemide and NHE with DMA, increase in tubular flow caused Af-Art dilation that was demonstrated by an increase in P SF . This increase was greater in Dahl SS (5.1±0.4 mmHg) than in Dahl SR (2.9±0.3 mmHg; P

Jeffrey L Garvin - One of the best experts on this subject based on the ideXlab platform.

  • abstract 118 role of Connecting Tubule glomerular feedback in tubuloglomerular feedback resetting after unilateral nephrectomy
    Hypertension, 2015
    Co-Authors: Sumit R. Monu, Branislava Janic, Kristopher Kutskill, Jeffrey L Garvin, Hong Wang, Cesar A Romero, Juan Xavier Juncos, Ed Peterson, Oscar A Carretero
    Abstract:

    Tubuloglomerular feedback (TGF) and Connecting Tubule glomerular feedback (CTGF) autoregulate nephronal afferent arteriolar resistance. In TGF, the macula densa signals the afferent arteriole to constrict when NaCl transport is enhanced by increased luminal NaCl, via sodium[[Unable to Display Character: –]]potassium-2-chloride cotransporter-2 (NKCC2). CTGF is mediated by Connecting Tubule sodium transport via epithelial sodium channel (ENaC) and dilates the afferent arteriole. Attenuation or resetting of TGF occurs after unilateral nephrectomy (UNX), but the mechanism behind this resetting remains unclear. This TGF resetting after UNX has been implicated in progressive glomerular damage due to sustained increase in glomerular capillary pressure. Since TGF is attenuated after UNX, we sought to test the hypothesis that CTGF is enhanced and that it contributes to TGF resetting after UNX. To test this hypothesis, we performed right side UNX in Sprague Dawley (SD) rats. 24 hours after surgery, we performed micropuncture of individual rat nephrons while measuring stop-flow pressure (PSF), which is an index of glomerular capillary pressure and afferent arteriolar tone. PSF decreases with an increase in afferent arteriolar tone. TGF response was measured as a decrease in PSF induced by switching late proximal perfusion from 0,10,20,30 and 40nl/min. Maximal TGF response was 1.3 ± 1.7 mmHg in UNX rats while 8.2 ± 0.9 mmHg in sham-UNX rats indicating a TGF resetting in UNX rats. When CTGF was inhibited with the ENaC blocker Benzamil (1μM), TGF response was 10±1.2 mmHg in UNX rats and 14.8± 1.3 mmHg in sham-UNX rats, indicating the restoration of TGF responses in UNX. We conclude that enhanced CTGF contributes to the TGF resetting after 24 hours of UNX. Enhanced CTGF may be responsible for glomerular damage post UNX.

  • aldosterone sensitizes Connecting Tubule glomerular feedback via the aldosterone receptor gpr30
    American Journal of Physiology-renal Physiology, 2014
    Co-Authors: Martin A Dambrosio, Kristopher Kutskill, Edward L Peterson, Jeffrey L Garvin, Pablo Leung, Hong Wang, Oscar A Carretero
    Abstract:

    Increasing Na delivery to epithelial Na channels (ENaC) in the Connecting Tubule (CNT) dilates the afferent arteriole (Af-Art), a process we call Connecting Tubule glomerular feedback (CTGF). We hy...

  • response to prostaglandin e2 mediates Connecting Tubule glomerular feedback
    Hypertension, 2014
    Co-Authors: Martin A Dambrosio, Jeffrey L Garvin, Hong Wang, Oscar A Carretero
    Abstract:

    We thank Elijovich and Laffer1 for their interest in our article. First, we clarify that prostaglandin E2 is not the only mediator of Connecting Tubule glomerular feedback (CTGF). We had previously reported that about half of the CTGF response is mediated by epoxyeicosatrienoic acids, with the other half attributable to a prostaglandin,2 which …

  • prostaglandin e2 mediates Connecting Tubule glomerular feedback
    Hypertension, 2013
    Co-Authors: Martin A Dambrosio, Jeffrey L Garvin, Hong Wang, Oscar A Carretero
    Abstract:

    We read with interest the publication of Ren et al1 about prostaglandin E2 being the major mediator of the Connecting Tubule glomerular feedback (CTGF) response (afferent arteriolar vasodilation in response to an increase in distal Na tubular delivery). The same group of authors has previously shown that an impairment of macula densa …

  • Connecting Tubule glomerular feedback in hypertension
    Hypertension, 2013
    Co-Authors: Hong Wang, Jeffrey L Garvin, Martin A Dambrosio, Oscar A Carretero
    Abstract:

    In Dahl salt-sensitive rats (Dahl SS), glomerular capillary pressure increases in response to high salt intake and this is accompanied by significant glomerular injury compared with spontaneously hypertensive rats with similar blood pressure. Glomerular capillary pressure is controlled mainly by afferent arteriolar resistance, which is regulated by the vasoconstrictor Tubule glomerular feedback (TGF) and the vasodilator Connecting TGF (CTGF). We hypothesized that Dahl SS have a decreased TGF response and enhanced TGF resetting compared with spontaneously hypertensive rats, and that these differences are attributable in part to an increase in CTGF. In vivo, using micropuncture we measured stop-flow pressure (a surrogate of glomerular capillary pressure). TGF was calculated as the maximal decrease in stop-flow pressure caused by increasing nephron perfusion, TGF resetting as the attenuation in TGF induced by high salt diet, and CTGF as the difference in TGF response before and during CTGF inhibition with benzamil. Compared with spontaneously hypertensive rats, Dahl SS had (1) lower TGF responses in normal (6.6±0.1 versus 11.0±0.2 mm Hg; P P P P

Martin A Dambrosio - One of the best experts on this subject based on the ideXlab platform.

  • aldosterone sensitizes Connecting Tubule glomerular feedback via the aldosterone receptor gpr30
    American Journal of Physiology-renal Physiology, 2014
    Co-Authors: Martin A Dambrosio, Kristopher Kutskill, Edward L Peterson, Jeffrey L Garvin, Pablo Leung, Hong Wang, Oscar A Carretero
    Abstract:

    Increasing Na delivery to epithelial Na channels (ENaC) in the Connecting Tubule (CNT) dilates the afferent arteriole (Af-Art), a process we call Connecting Tubule glomerular feedback (CTGF). We hy...

  • response to prostaglandin e2 mediates Connecting Tubule glomerular feedback
    Hypertension, 2014
    Co-Authors: Martin A Dambrosio, Jeffrey L Garvin, Hong Wang, Oscar A Carretero
    Abstract:

    We thank Elijovich and Laffer1 for their interest in our article. First, we clarify that prostaglandin E2 is not the only mediator of Connecting Tubule glomerular feedback (CTGF). We had previously reported that about half of the CTGF response is mediated by epoxyeicosatrienoic acids, with the other half attributable to a prostaglandin,2 which …

  • prostaglandin e2 mediates Connecting Tubule glomerular feedback
    Hypertension, 2013
    Co-Authors: Martin A Dambrosio, Jeffrey L Garvin, Hong Wang, Oscar A Carretero
    Abstract:

    We read with interest the publication of Ren et al1 about prostaglandin E2 being the major mediator of the Connecting Tubule glomerular feedback (CTGF) response (afferent arteriolar vasodilation in response to an increase in distal Na tubular delivery). The same group of authors has previously shown that an impairment of macula densa …

  • Connecting Tubule glomerular feedback in hypertension
    Hypertension, 2013
    Co-Authors: Hong Wang, Jeffrey L Garvin, Martin A Dambrosio, Oscar A Carretero
    Abstract:

    In Dahl salt-sensitive rats (Dahl SS), glomerular capillary pressure increases in response to high salt intake and this is accompanied by significant glomerular injury compared with spontaneously hypertensive rats with similar blood pressure. Glomerular capillary pressure is controlled mainly by afferent arteriolar resistance, which is regulated by the vasoconstrictor Tubule glomerular feedback (TGF) and the vasodilator Connecting TGF (CTGF). We hypothesized that Dahl SS have a decreased TGF response and enhanced TGF resetting compared with spontaneously hypertensive rats, and that these differences are attributable in part to an increase in CTGF. In vivo, using micropuncture we measured stop-flow pressure (a surrogate of glomerular capillary pressure). TGF was calculated as the maximal decrease in stop-flow pressure caused by increasing nephron perfusion, TGF resetting as the attenuation in TGF induced by high salt diet, and CTGF as the difference in TGF response before and during CTGF inhibition with benzamil. Compared with spontaneously hypertensive rats, Dahl SS had (1) lower TGF responses in normal (6.6±0.1 versus 11.0±0.2 mm Hg; P P P P

  • abstract 552 aldosterone enhances Connecting Tubule glomerular feedback ctgf
    Hypertension, 2013
    Co-Authors: Martin A Dambrosio, Jeffrey L Garvin, Pablo Leung, Hong Wang, Oscar A Carretero
    Abstract:

    Increasing Na delivery to the Connecting Tubule (CNT) stimulates epithelial Na channels (ENaC) and dilates the afferent arteriole (Af-Art), a process we call Connecting Tubule glomerular feedback (CTGF). We hypothesize that aldosterone (aldo) enhances CTGF via a nongenomic mechanism that stimulates CNT ENaC via GPR30 and/or mineralocorticoid receptors (MR). Rabbit Af-Arts and their adherent CNTs were microdissected and simultaneously perfused. Two consecutive CTGF curves were elicited by increasing luminal NaCl in the CNT. Addition of aldo 10 -8 M to the CNT potentiated CTGF, seen as a left-shift in the concentration of NaCl that elicited a half-maximal response (EC 50 ), see Figure. The MR blocker eplerenone (10 -5 M) prevented the enhancement of CTGF by aldo (control EC 50 = 32.4 ± 2.3 mM; aldo + eplerenone EC 50 = 35.4 ± 1.7 mM; n = 7). Neither the transcription inhibitor actinomycin D (5x10 -6 M) nor the translation inhibitor cycloheximide (10 -5 M) prevented the effect of aldo (control EC 50 = 33.0 ± 2.0 mM; aldo + actinomycin D EC 50 = 15.4 ± 1.5 mM; n = 6; P 50 = 33.2 ± 2.4 mM; aldo + cycloheximide EC 50 = 11.2 ± 1.3 mM; n = 6; P via a nongenomic effect possibly involving MR and/or GPR30 receptors. Enhanced CTGF induced by aldosterone may contribute to renal damage by causing increases in Af-Art dilation and glomerular capillary pressure (glomerular barotrauma). Figure. Control CTGF (○) seen as dilation of norepinephrine-preconstricted Af-Arts induced by increasing NaCl in the CNT. Aldo 10 -8 M (•) enhanced CTGF (n = 6; * P P P vs . control). Vertical dashed lines indicate EC 50 .

Edward L Peterson - One of the best experts on this subject based on the ideXlab platform.

  • role of Connecting Tubule glomerular feedback in obesity related renal damage
    American Journal of Physiology-renal Physiology, 2018
    Co-Authors: Sumit R. Monu, Edward L Peterson, Mani Maheshwari, Oscar A Carretero
    Abstract:

    Zucker obese rats (ZOR) have higher glomerular capillary pressure (PGC) that can cause renal damage. PGC is controlled by afferent (Af-Art) and efferent arteriole (Ef-Art) resistance. Af-Art resist...

  • Connecting Tubule glomerular feedback mediates tubuloglomerular feedback resetting after unilateral nephrectomy
    American Journal of Physiology-renal Physiology, 2018
    Co-Authors: Sumit R. Monu, Kristopher Kutskill, Edward L Peterson, Hong Wang, Nitin Kumar, J X Masjoanjuncos, Oscar A Carretero
    Abstract:

    Unilaterally nephrectomized rats (UNx) have higher glomerular capillary pressure (PGC) that can cause significant glomerular injury in the remnant kidney. PGC is controlled by the ratio of afferent...

  • effect of salt intake on afferent arteriolar dilatation role of Connecting Tubule glomerular feedback ctgf
    American Journal of Physiology-renal Physiology, 2017
    Co-Authors: Hong Wang, Edward L Peterson, Cesar A Romero, Sumit R. Monu, J. X. Masjoan Juncos, Oscar A Carretero
    Abstract:

    Afferent arteriole (Af-Art) resistance is modulated by two intrinsic nephron feedbacks: 1) the vasoconstrictor tubuloglomerular feedback (TGF) mediated by Na+-K+-2Cl− cotransporters (NKCC2) in the ...

  • Effect of salt intake on afferent arteriolar dilatation: role of Connecting Tubule glomerular feedback (CTGF).
    American Journal of Physiology-renal Physiology, 2017
    Co-Authors: Hong Wang, Edward L Peterson, Cesar A Romero, Sumit R. Monu, J. X. Masjoan Juncos, Oscar A Carretero
    Abstract:

    Afferent arteriole (Af-Art) resistance is modulated by two intrinsic nephron feedbacks: 1 ) the vasoconstrictor tubuloglomerular feedback (TGF) mediated by Na + -K + -2Cl − cotransporters (NKCC2) in the macula densa and blocked by furosemide and 2 ) the vasodilator Connecting Tubule glomerular feedback (CTGF), mediated by epithelial Na + channels (ENaC) in the Connecting Tubule and blocked by benzamil. High salt intake reduces Af-Art vasoconstrictor ability in Dahl salt-sensitive rats (Dahl SS). Previously, we measured CTGF indirectly, by differences between TGF responses with and without CTGF inhibition. We recently developed a new method to measure CTGF more directly by simultaneously inhibiting NKCC2 and the Na + /H + exchanger (NHE). We hypothesize that in vivo during simultaneous inhibition of NKCC2 and NHE, CTGF causes an Af-Art dilatation revealed by an increase in stop-flow pressure (P SF ) in Dahl SS and that is enhanced with a high salt intake. In the presence of furosemide alone, increasing nephron perfusion did not change the P SF in either Dahl salt-resistant rats (Dahl SR) or Dahl SS. When furosemide and an NHE inhibitor, dimethylamiloride, were perfused simultaneously, an increase in tubular flow caused Af-Art dilatation that was demonstrated by an increase in P SF. This increase was greater in Dahl SS [4.5 ± 0.4 (SE) mmHg] than in Dahl SR (2.5 ± 0.3 mmHg; P

  • Connecting Tubule glomerular feedback mediates tubuloglomerular feedback resetting after unilateral nephrectomy
    American Journal of Physiology-renal Physiology, 2017
    Co-Authors: Sumit R. Monu, Kristopher Kutskill, Edward L Peterson, Hong Wang, J. X. Masjoan-juncos, Nitin Kumar, Oscar A Carretero
    Abstract:

    Unilaterally nephrectomized rats (UNx) have higher glomerular capillary pressure (PGC) that can cause significant glomerular injury in the remnant kidney. PGC is controlled by the ratio of afferent (Af-Art) and efferent arteriole resistance. Af-Art resistance in turn is regulated by two intrinsic feedback mechanisms: 1) Tubuloglomerular feedback (TGF) that causes Af-Art constriction in response to increased NaCl in the macula densa and 2) Connecting Tubule glomerular feedback (CTGF) that causes Af-Art dilatation in response to an increase in NaCl transport in the Connecting Tubule via the epithelial sodium channel (ENaC). Resetting of TGF post-UNx can allow systemic pressure to be transmitted to the glomerulus and cause renal damage, but the mechanism behind this resetting is unclear. Since CTGF is an Af-Art dilatory mechanism, we hypothesized that CTGF is increased after UNx, and contributes to TGF resetting. To test this hypothesis, we performed UNx in Sprague Dawley (SD) rats. Twenty-four hours after surgery, we performed micropuncture of individual nephrons and measured stop-flow pressure (PSF). PSF is an indirect measurement of PGC. Maximal TGF response at 40nl/min was 8.9 ± 1.24 mmHg in sham-UNx rats and 1.39 ± 1.02 mmHg in UNx rats indicating TGF resetting after UNx. When CTGF was inhibited with the ENaC blocker Benzamil (1μM/L), the TGF response was 12.29 ± 2.01 mmHg in UNx rats and 13.03 ± 1.25 mmHg in sham-UNx rats, indicating restoration of the TGF responses in UNx. We conclude that enhanced CTGF contributes to TGF resetting after UNx.