The Experts below are selected from a list of 1944 Experts worldwide ranked by ideXlab platform

Geert-jan Tangelder - One of the best experts on this subject based on the ideXlab platform.

  • direct vasoconstrictor effect of prostaglandin e2 on renal Interlobular Arteries role of the ep3 receptor
    American Journal of Physiology-renal Physiology, 2007
    Co-Authors: William F Van Rodijnen, Iolente J Korstjens, Natalee Legerstee, Piet M Ter Wee, Geert-jan Tangelder
    Abstract:

    Evidence indicates that prostaglandin E2 (PGE2) preferentially affects preglomerular renal vessels. However, whether this is limited to small-caliber arterioles or whether larger vessels farther up...

  • Direct vasoconstrictor effect of prostaglandin E2 on renal Interlobular Arteries: role of the EP3 receptor.
    American journal of physiology. Renal physiology, 2006
    Co-Authors: William F Van Rodijnen, Iolente J Korstjens, Natalee Legerstee, Piet M Ter Wee, Geert-jan Tangelder
    Abstract:

    Evidence indicates that prostaglandin E(2) (PGE(2)) preferentially affects preglomerular renal vessels. However, whether this is limited to small-caliber arterioles or whether larger vessels farther upstream also respond to PGE(2) is currently unclear. In the present study, we first investigated the effects of PGE(2) along the preglomerular vascular tree and subsequently focused on proximal Interlobular Arteries (ILAs). Proximal ILAs in hydronephrotic rat kidneys as well as isolated vessels from normal kidneys constricted in response to PGE(2), both under basal conditions and after the induction of vascular tone. By contrast, smaller vessels, i.e., distal ILAs and afferent arterioles, exhibited PGE(2)-induced vasodilation. Endothelium removal and pretreatment of single, isolated proximal ILAs with an EP1 receptor blocker (SC51322, 1 micromol/l) or a thromboxane A(2) receptor blocker (SQ29548, 1 micromol/l) did not prevent vasoconstriction to PGE(2). Furthermore, in the presence of SC51322, responses of these vessels to PGE(2) and the EP1/EP3 agonist sulprostone were superimposable, indicating that PGE(2)-induced vasoconstriction is mediated by EP3 receptors on smooth muscle cells. Immunohistochemical staining of proximal ILAs confirmed the presence of EP3 receptor protein on these cells and the endothelium. Adding PGE(2) to normal isolated kidneys induced a biphasic flow response, i.e., an initial flow increase at PGE(2) concentrations

  • Renal microvascular actions of angiotensin II fragments.
    American Journal of Physiology-renal Physiology, 2002
    Co-Authors: William F Van Rodijnen, Geert-jan Tangelder, Ton A. Van Lambalgen, Michiel H. Van Wijhe, Piet M. Ter Wee
    Abstract:

    In the present study, we investigated renal microvascular responses to ANG-(1-7) and ANG IV. Diameter changes of small Interlobular Arteries, afferent arterioles, and efferent arterioles were assessed by using isolated perfused hydronephrotic rat kidneys. ANG-(1-7) and ANG IV concentration dependently decreased the diameters of all investigated renal microvessel, however, with a much lower potency than ANG II. The ANG II type 1 receptor blocker irbesartan completely reversed the responses to ANG-(1-7) and ANG IV, whereas the ANG II type 2 receptor blocker PD-123319 had no effect. Both ANG-(1-7) and ANG IV failed to alter renal microvascular constriction induced by ANG II. In addition, subnanomolar concentrations of ANG-(1-7) had no effect on the myogenic-induced tone of Interlobular Arteries and afferent arterioles. Thus our data indicate that at high concentrations, ANG-(1-7) and ANG IV are able to activate the ANG II type 1 receptor, thereby inducing renal microvascular constriction. The failure of ANG-(1-7) and ANG IV to reduce ANG II- and pressure-induced constrictions suggests that these fragments do not exert a vasodilator and/or ANG II antagonistic action in the kidney.

  • Reduced Reactivity of Renal Microvessels to Pressure and Angiotensin II in Fawn-Hooded Rats
    Hypertension, 2002
    Co-Authors: William F Van Rodijnen, Geert-jan Tangelder, Ton A. Van Lambalgen, Richard P. E. Van Dokkum, Abraham P. Provoost, Piet M. Ter Wee
    Abstract:

    Fawn-Hooded rats possess an increased risk to develop glomerular damage. Both an impaired control of preglomerular resistance and an elevated postglomerular resistance have been implicated. In the present study, we directly assessed the myogenic reactivity of distal Interlobular Arteries and afferent arterioles from hypertensive and normotensive Fawn-Hooded rats compared with Sprague-Dawley and Wistar rats, which are known to be resistant for developing renal disease. Pressure-response curves were made in isolated perfused hydronephrotic kidneys from these rats. In addition, increasing concentrations of angiotensin II were added to the perfusate to determine the reactivity of Interlobular Arteries, afferent arterioles, and efferent arterioles to this peptide. Preglomerular vessels from hypertensive and normotensive Fawn-Hooded rats exhibited an impaired reactivity to both pressure and angiotensin II compared with that of Sprague-Dawley and Wistar rats. Basal efferent arteriolar diameters were similar among the 4 strains of rat. In addition, efferent arterioles from hypertensive and normotensive Fawn-Hooded rats displayed a reduced sensitivity to angiotensin II. Our observations demonstrate that in Fawn-Hooded rats, 2 components of preglomerular resistance control are impaired: the myogenic and the angiotensin II response. In addition, efferent arteriolar reactivity to angiotensin II is not elevated but lowered in these rats. Therefore, a deficit in preglomerular resistance control is the most important intrinsic factor involved in the increased susceptibility of Fawn-hooded rats to develop renal disease.

Hamid Nasri - One of the best experts on this subject based on the ideXlab platform.

  • catastrophic antiphospholipid syndrome presented with sudden renal failure and history of long lasting psychosis and hypertension in a 42 years old women
    Journal of nephropathology, 2013
    Co-Authors: Saeed Mardani, Hamid Nasri
    Abstract:

    The catastrophic variant of the antiphospholipid syndrome (CAPS), which is also named as Asherson’s syndrome (1-4), is defined as a potential life-threatening variant of this syndrome, which is characterized by multiple small-vessel thrombosis that can lead to multiorgan failure, particularly renal deterioration (2-4). A renal small-vessel nephropathy, defined as antiphospholipid syndrome nephropathy (APS nephropathy; APSN), has been described (3,4). This vaso-occlusive disease mainly affects arterioles, Interlobular Arteries and glomerular tufts. However, interstitial area and tubules may subsequently be involved (2-7).

  • Hypertension and renal failure with right arm pulse weakness in a 65 years old man
    Journal of nephropathology, 2012
    Co-Authors: Hamid Nasri
    Abstract:

    Implication for health policy/practice/research/medical education: Antiphospholipid syndrome (APS) is being increasingly recognized as an important cause of kidney injury due to thrombosis at any location within the renal vasculature. The term antiphospholipid syndrome nephropathy (APSN) refers to the kidney damage caused by vascular lesions in the glomeruli, arterioles and/ or Interlobular Arteries in patients with antiphospholipid antibodies. APSN manifests with hypertension, acute and/or chronic kidney failure, and often a lowgrade proteinuria.

William F Van Rodijnen - One of the best experts on this subject based on the ideXlab platform.

  • direct vasoconstrictor effect of prostaglandin e2 on renal Interlobular Arteries role of the ep3 receptor
    American Journal of Physiology-renal Physiology, 2007
    Co-Authors: William F Van Rodijnen, Iolente J Korstjens, Natalee Legerstee, Piet M Ter Wee, Geert-jan Tangelder
    Abstract:

    Evidence indicates that prostaglandin E2 (PGE2) preferentially affects preglomerular renal vessels. However, whether this is limited to small-caliber arterioles or whether larger vessels farther up...

  • Direct vasoconstrictor effect of prostaglandin E2 on renal Interlobular Arteries: role of the EP3 receptor.
    American journal of physiology. Renal physiology, 2006
    Co-Authors: William F Van Rodijnen, Iolente J Korstjens, Natalee Legerstee, Piet M Ter Wee, Geert-jan Tangelder
    Abstract:

    Evidence indicates that prostaglandin E(2) (PGE(2)) preferentially affects preglomerular renal vessels. However, whether this is limited to small-caliber arterioles or whether larger vessels farther upstream also respond to PGE(2) is currently unclear. In the present study, we first investigated the effects of PGE(2) along the preglomerular vascular tree and subsequently focused on proximal Interlobular Arteries (ILAs). Proximal ILAs in hydronephrotic rat kidneys as well as isolated vessels from normal kidneys constricted in response to PGE(2), both under basal conditions and after the induction of vascular tone. By contrast, smaller vessels, i.e., distal ILAs and afferent arterioles, exhibited PGE(2)-induced vasodilation. Endothelium removal and pretreatment of single, isolated proximal ILAs with an EP1 receptor blocker (SC51322, 1 micromol/l) or a thromboxane A(2) receptor blocker (SQ29548, 1 micromol/l) did not prevent vasoconstriction to PGE(2). Furthermore, in the presence of SC51322, responses of these vessels to PGE(2) and the EP1/EP3 agonist sulprostone were superimposable, indicating that PGE(2)-induced vasoconstriction is mediated by EP3 receptors on smooth muscle cells. Immunohistochemical staining of proximal ILAs confirmed the presence of EP3 receptor protein on these cells and the endothelium. Adding PGE(2) to normal isolated kidneys induced a biphasic flow response, i.e., an initial flow increase at PGE(2) concentrations

  • Renal microvascular actions of angiotensin II fragments.
    American Journal of Physiology-renal Physiology, 2002
    Co-Authors: William F Van Rodijnen, Geert-jan Tangelder, Ton A. Van Lambalgen, Michiel H. Van Wijhe, Piet M. Ter Wee
    Abstract:

    In the present study, we investigated renal microvascular responses to ANG-(1-7) and ANG IV. Diameter changes of small Interlobular Arteries, afferent arterioles, and efferent arterioles were assessed by using isolated perfused hydronephrotic rat kidneys. ANG-(1-7) and ANG IV concentration dependently decreased the diameters of all investigated renal microvessel, however, with a much lower potency than ANG II. The ANG II type 1 receptor blocker irbesartan completely reversed the responses to ANG-(1-7) and ANG IV, whereas the ANG II type 2 receptor blocker PD-123319 had no effect. Both ANG-(1-7) and ANG IV failed to alter renal microvascular constriction induced by ANG II. In addition, subnanomolar concentrations of ANG-(1-7) had no effect on the myogenic-induced tone of Interlobular Arteries and afferent arterioles. Thus our data indicate that at high concentrations, ANG-(1-7) and ANG IV are able to activate the ANG II type 1 receptor, thereby inducing renal microvascular constriction. The failure of ANG-(1-7) and ANG IV to reduce ANG II- and pressure-induced constrictions suggests that these fragments do not exert a vasodilator and/or ANG II antagonistic action in the kidney.

  • Reduced Reactivity of Renal Microvessels to Pressure and Angiotensin II in Fawn-Hooded Rats
    Hypertension, 2002
    Co-Authors: William F Van Rodijnen, Geert-jan Tangelder, Ton A. Van Lambalgen, Richard P. E. Van Dokkum, Abraham P. Provoost, Piet M. Ter Wee
    Abstract:

    Fawn-Hooded rats possess an increased risk to develop glomerular damage. Both an impaired control of preglomerular resistance and an elevated postglomerular resistance have been implicated. In the present study, we directly assessed the myogenic reactivity of distal Interlobular Arteries and afferent arterioles from hypertensive and normotensive Fawn-Hooded rats compared with Sprague-Dawley and Wistar rats, which are known to be resistant for developing renal disease. Pressure-response curves were made in isolated perfused hydronephrotic kidneys from these rats. In addition, increasing concentrations of angiotensin II were added to the perfusate to determine the reactivity of Interlobular Arteries, afferent arterioles, and efferent arterioles to this peptide. Preglomerular vessels from hypertensive and normotensive Fawn-Hooded rats exhibited an impaired reactivity to both pressure and angiotensin II compared with that of Sprague-Dawley and Wistar rats. Basal efferent arteriolar diameters were similar among the 4 strains of rat. In addition, efferent arterioles from hypertensive and normotensive Fawn-Hooded rats displayed a reduced sensitivity to angiotensin II. Our observations demonstrate that in Fawn-Hooded rats, 2 components of preglomerular resistance control are impaired: the myogenic and the angiotensin II response. In addition, efferent arteriolar reactivity to angiotensin II is not elevated but lowered in these rats. Therefore, a deficit in preglomerular resistance control is the most important intrinsic factor involved in the increased susceptibility of Fawn-hooded rats to develop renal disease.

Götz M. Richter - One of the best experts on this subject based on the ideXlab platform.

  • Standard microspheres–histopathological findings.
    2018
    Co-Authors: Dominik F. Vollherbst, Theresa Gockner, Kerstin Holzer, Carolin Mogler, Paul Flechsig, Alexander Harms, Christopher L. Schlett, Philippe L. Pereira, Götz M. Richter
    Abstract:

    SMS.a. HE staining. Microspheres in the Interlobular Arteries (black asterisk). Note the blood retention within the sinusoids (white arrowheads), which is a potential sign of embolization-related reactive hyperemia. There were no qualitative differences regarding the histopathological findings between the standard and the radiopaque microspheres for the acute setting.

  • Iodized oil–histopathological findings.
    2018
    Co-Authors: Dominik F. Vollherbst, Theresa Gockner, Kerstin Holzer, Carolin Mogler, Paul Flechsig, Alexander Harms, Christopher L. Schlett, Philippe L. Pereira, Götz M. Richter
    Abstract:

    A IO.a. MG staining. Preparation artefacts due to degreasing of iodized oil during routine histopathological work-up appear as oval cavities within the sinusoids (black asterisk). Note the integrity of the liver lobule and periportal field (white arrowhead). B IO.sa. Sudan III staining. Iodized oil in Interlobular Arteries (white arrowheads). C IO.sa. HE staining. Infiltration of the periportal fields by lymphocytes, plasma cells and eosinophilic granulocytes (white arrowhead). Note the absence of parenchymal necrosis.

  • Iodized oil–standard CT findings.
    2018
    Co-Authors: Dominik F. Vollherbst, Theresa Gockner, Kerstin Holzer, Carolin Mogler, Paul Flechsig, Alexander Harms, Christopher L. Schlett, Philippe L. Pereira, Götz M. Richter
    Abstract:

    A IO.a. Non-enhanced CT 2 hours after embolization with 0.5 mL iodized oil. Linear hyperdensities (blue asterisk) corresponding to an occluded subsegmental artery (arterial enhancement) and patchy hyperdensities (red asterisk) corresponding to occluded Interlobular Arteries and sinusoids (parenchymal enhancement). B IO.sa. Non-enhanced CT 2 hours after embolization. Note the lower arterial (blue asterisk) and parenchymal (red asterisk) enhancement compared to A. C IO.sa. Non-enhanced CT 7 days after embolization. Note the less intense arterial (blue asterisk) and parenchymal (red asterisk) enhancement compared to B.

  • Radiopaque microspheres–histopathological findings.
    2018
    Co-Authors: Dominik F. Vollherbst, Theresa Gockner, Kerstin Holzer, Carolin Mogler, Paul Flechsig, Alexander Harms, Christopher L. Schlett, Philippe L. Pereira, Götz M. Richter
    Abstract:

    A RMS.a. HE staining. Incipient sinusoidal penetration of microspheres (white arrowhead). B RMS.sa. HE staining. Multiple microspheres within a subsegmental artery (white arrowheads). There were only mild inflammatory changes compared to iodized oil, but signs of cell death were present. C RMS.sa. HE staining. Focal areas of parenchymal necrosis, represented by anucleate hepatocytes (white arrowhead). The black asterisk indicates the central vein. D RMS-HEP.sa. HE staining. Seven days after embolization, there were large areas of severe confluent parenchymal necrosis (black arrowhead), accompanied by a hemorrhagic rim (white arrowheads) with necrosis of the periportal fields. Note the microspheres within the subsegmental (black asterisk) and Interlobular Arteries (white asterisk).

  • Radiopaque microspheres–standard CT findings.
    2018
    Co-Authors: Dominik F. Vollherbst, Theresa Gockner, Kerstin Holzer, Carolin Mogler, Paul Flechsig, Alexander Harms, Christopher L. Schlett, Philippe L. Pereira, Götz M. Richter
    Abstract:

    A RMS.a. Non-enhanced CT 2 hours after embolization. Marked linear hyperdensity (blue asterisk) corresponding to an occluded subsegmental artery (arterial enhancement). The type of arterial enhancement was comparable to iodized oil. B RMS.sa. Non-enhanced CT 2 hours after embolization. Linear (blue asterisk) and patchy hyperdensities (red asterisk) corresponding to occluded subsegmental and Interlobular Arteries and sinusoids (arterial and parenchymal enhancement). Note the more intense arterial and parenchymal enhancement compared to A. The type of arterial and parenchymal enhancement was comparable with iodized oil. C RMS-HEP.sa. Non-enhanced CT 2 hours after embolization. Note the more intense arterial (blue asterisk) and parenchymal enhancement (red asterisk) than A and B. D RMS-HEP.sa. Non-enhanced CT 7 days after embolization. Note the weaker arterial (blue asterisk) and parenchymal (red asterisk) enhancement compared to C. Note the hypodense areas in the embolized liver parenchyma (blue arrowhead) representing tissue necrosis.

Iolente J Korstjens - One of the best experts on this subject based on the ideXlab platform.

  • direct vasoconstrictor effect of prostaglandin e2 on renal Interlobular Arteries role of the ep3 receptor
    American Journal of Physiology-renal Physiology, 2007
    Co-Authors: William F Van Rodijnen, Iolente J Korstjens, Natalee Legerstee, Piet M Ter Wee, Geert-jan Tangelder
    Abstract:

    Evidence indicates that prostaglandin E2 (PGE2) preferentially affects preglomerular renal vessels. However, whether this is limited to small-caliber arterioles or whether larger vessels farther up...

  • Direct vasoconstrictor effect of prostaglandin E2 on renal Interlobular Arteries: role of the EP3 receptor.
    American journal of physiology. Renal physiology, 2006
    Co-Authors: William F Van Rodijnen, Iolente J Korstjens, Natalee Legerstee, Piet M Ter Wee, Geert-jan Tangelder
    Abstract:

    Evidence indicates that prostaglandin E(2) (PGE(2)) preferentially affects preglomerular renal vessels. However, whether this is limited to small-caliber arterioles or whether larger vessels farther upstream also respond to PGE(2) is currently unclear. In the present study, we first investigated the effects of PGE(2) along the preglomerular vascular tree and subsequently focused on proximal Interlobular Arteries (ILAs). Proximal ILAs in hydronephrotic rat kidneys as well as isolated vessels from normal kidneys constricted in response to PGE(2), both under basal conditions and after the induction of vascular tone. By contrast, smaller vessels, i.e., distal ILAs and afferent arterioles, exhibited PGE(2)-induced vasodilation. Endothelium removal and pretreatment of single, isolated proximal ILAs with an EP1 receptor blocker (SC51322, 1 micromol/l) or a thromboxane A(2) receptor blocker (SQ29548, 1 micromol/l) did not prevent vasoconstriction to PGE(2). Furthermore, in the presence of SC51322, responses of these vessels to PGE(2) and the EP1/EP3 agonist sulprostone were superimposable, indicating that PGE(2)-induced vasoconstriction is mediated by EP3 receptors on smooth muscle cells. Immunohistochemical staining of proximal ILAs confirmed the presence of EP3 receptor protein on these cells and the endothelium. Adding PGE(2) to normal isolated kidneys induced a biphasic flow response, i.e., an initial flow increase at PGE(2) concentrations