Jørgen Frøkiær

Dehydration reverses vasopressin antagonist-induced diuresis and aquaporin-2 downregulation in rats

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Standard

Dehydration reverses vasopressin antagonist-induced diuresis and aquaporin-2 downregulation in rats. / Marples, D; Christensen, Birgitte Mønster; Frøkiær, Jørgen; Knepper, M A; Nielsen, Søren.

In: American Journal of Physiology (Consolidated), Vol. 275, No. 3 Pt 2, 09.1998, p. F400-9.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Harvard

Marples, D, Christensen, BM, Frøkiær, J, Knepper, MA & Nielsen, S 1998, 'Dehydration reverses vasopressin antagonist-induced diuresis and aquaporin-2 downregulation in rats', American Journal of Physiology (Consolidated), vol. 275, no. 3 Pt 2, pp. F400-9.

APA

Marples, D., Christensen, B. M., Frøkiær, J., Knepper, M. A., & Nielsen, S. (1998). Dehydration reverses vasopressin antagonist-induced diuresis and aquaporin-2 downregulation in rats. American Journal of Physiology (Consolidated), 275(3 Pt 2), F400-9.

CBE

Marples D, Christensen BM, Frøkiær J, Knepper MA, Nielsen S. 1998. Dehydration reverses vasopressin antagonist-induced diuresis and aquaporin-2 downregulation in rats. American Journal of Physiology (Consolidated). 275(3 Pt 2):F400-9.

MLA

Marples, D et al. "Dehydration reverses vasopressin antagonist-induced diuresis and aquaporin-2 downregulation in rats". American Journal of Physiology (Consolidated). 1998, 275(3 Pt 2). F400-9.

Vancouver

Marples D, Christensen BM, Frøkiær J, Knepper MA, Nielsen S. Dehydration reverses vasopressin antagonist-induced diuresis and aquaporin-2 downregulation in rats. American Journal of Physiology (Consolidated). 1998 Sep;275(3 Pt 2):F400-9.

Author

Marples, D ; Christensen, Birgitte Mønster ; Frøkiær, Jørgen ; Knepper, M A ; Nielsen, Søren. / Dehydration reverses vasopressin antagonist-induced diuresis and aquaporin-2 downregulation in rats. In: American Journal of Physiology (Consolidated). 1998 ; Vol. 275, No. 3 Pt 2. pp. F400-9.

Bibtex

@article{31afae0b040e4e5fb0f79b4a4820209f,
title = "Dehydration reverses vasopressin antagonist-induced diuresis and aquaporin-2 downregulation in rats",
abstract = "To examine the involvement of vasopressin and dehydration in the regulation of aquaporin-2 (AQP2) expression in rat kidney, we investigated the effects of treatment for 60 h with the specific V2-receptor antagonist OPC-31260 (OPC), alone and in conjunction with dehydration for the last 12 h. Changes in AQP2 protein and mRNA expression in kidney inner medulla were determined by Western and Northern blotting, and AQP2 distribution was analyzed by immunocytochemistry and immunoelectron microscopy. Treatment with OPC increased urine output fourfold, with a reciprocal decrease in urine osmolality. AQP2 expression decreased to 52 +/- 11% of control levels (n = 12, P <0.05), and AQP2 was found predominantly in intracellular vesicles in collecting duct principal cells. This is consistent with efficient blockade of the vasopressin-induced AQP2 delivery to the plasma membrane and with the observed increased diuresis. Consistent with this, AQP2 mRNA levels were also reduced in response to prolonged OPC treatment (30 +/- 10% of control levels, n = 9). Five days of treatment with furosemide, despite producing even greater polyuria than OPC, was not associated with downregulation of AQP2 levels, demonstrating that AQP2 downregulation is not secondary to increased urine flow rate or loss of medullary hypertonicity. During 12-h thirsting in the continued presence of OPC, urine output dropped dramatically, to levels not significantly different from that seen in (nonthirsted) control animals. In parallel with this, AQP2 levels rose to control levels. Control experiments confirmed continued effective receptor blockade. These results indicate that the V2-receptor antagonist causes a modest decrease in AQP2 expression that is not a consequence of increased urine flow rate or washout of medullary hypertonicity. However, this decrease is much less marked than that seen in some forms of acquired nephrogenic diabetes insipidus. In conjunction with the effects of thirsting, this suggests that modulation of AQP2 expression is mediated partly, but not exclusively, via V2 receptors.",
keywords = "Animals, Aquaporin 2, Aquaporin 6, Aquaporins, Benzazepines, Dehydration, Diuresis, Diuretics, Furosemide, Gene Expression, Immunohistochemistry, Ion Channels, Kidney Medulla, Male, Microscopy, Immunoelectron, Polyuria, RNA, Messenger, Rats, Rats, Wistar, Vasopressins, Water Deprivation",
author = "D Marples and Christensen, {Birgitte M{\o}nster} and J{\o}rgen Fr{\o}ki{\ae}r and Knepper, {M A} and S{\o}ren Nielsen",
year = "1998",
month = sep,
language = "English",
volume = "275",
pages = "F400--9",
journal = "American Journal of Physiology (Consolidated)",
issn = "0002-9513",
publisher = "American Physiological Society",
number = "3 Pt 2",

}

RIS

TY - JOUR

T1 - Dehydration reverses vasopressin antagonist-induced diuresis and aquaporin-2 downregulation in rats

AU - Marples, D

AU - Christensen, Birgitte Mønster

AU - Frøkiær, Jørgen

AU - Knepper, M A

AU - Nielsen, Søren

PY - 1998/9

Y1 - 1998/9

N2 - To examine the involvement of vasopressin and dehydration in the regulation of aquaporin-2 (AQP2) expression in rat kidney, we investigated the effects of treatment for 60 h with the specific V2-receptor antagonist OPC-31260 (OPC), alone and in conjunction with dehydration for the last 12 h. Changes in AQP2 protein and mRNA expression in kidney inner medulla were determined by Western and Northern blotting, and AQP2 distribution was analyzed by immunocytochemistry and immunoelectron microscopy. Treatment with OPC increased urine output fourfold, with a reciprocal decrease in urine osmolality. AQP2 expression decreased to 52 +/- 11% of control levels (n = 12, P <0.05), and AQP2 was found predominantly in intracellular vesicles in collecting duct principal cells. This is consistent with efficient blockade of the vasopressin-induced AQP2 delivery to the plasma membrane and with the observed increased diuresis. Consistent with this, AQP2 mRNA levels were also reduced in response to prolonged OPC treatment (30 +/- 10% of control levels, n = 9). Five days of treatment with furosemide, despite producing even greater polyuria than OPC, was not associated with downregulation of AQP2 levels, demonstrating that AQP2 downregulation is not secondary to increased urine flow rate or loss of medullary hypertonicity. During 12-h thirsting in the continued presence of OPC, urine output dropped dramatically, to levels not significantly different from that seen in (nonthirsted) control animals. In parallel with this, AQP2 levels rose to control levels. Control experiments confirmed continued effective receptor blockade. These results indicate that the V2-receptor antagonist causes a modest decrease in AQP2 expression that is not a consequence of increased urine flow rate or washout of medullary hypertonicity. However, this decrease is much less marked than that seen in some forms of acquired nephrogenic diabetes insipidus. In conjunction with the effects of thirsting, this suggests that modulation of AQP2 expression is mediated partly, but not exclusively, via V2 receptors.

AB - To examine the involvement of vasopressin and dehydration in the regulation of aquaporin-2 (AQP2) expression in rat kidney, we investigated the effects of treatment for 60 h with the specific V2-receptor antagonist OPC-31260 (OPC), alone and in conjunction with dehydration for the last 12 h. Changes in AQP2 protein and mRNA expression in kidney inner medulla were determined by Western and Northern blotting, and AQP2 distribution was analyzed by immunocytochemistry and immunoelectron microscopy. Treatment with OPC increased urine output fourfold, with a reciprocal decrease in urine osmolality. AQP2 expression decreased to 52 +/- 11% of control levels (n = 12, P <0.05), and AQP2 was found predominantly in intracellular vesicles in collecting duct principal cells. This is consistent with efficient blockade of the vasopressin-induced AQP2 delivery to the plasma membrane and with the observed increased diuresis. Consistent with this, AQP2 mRNA levels were also reduced in response to prolonged OPC treatment (30 +/- 10% of control levels, n = 9). Five days of treatment with furosemide, despite producing even greater polyuria than OPC, was not associated with downregulation of AQP2 levels, demonstrating that AQP2 downregulation is not secondary to increased urine flow rate or loss of medullary hypertonicity. During 12-h thirsting in the continued presence of OPC, urine output dropped dramatically, to levels not significantly different from that seen in (nonthirsted) control animals. In parallel with this, AQP2 levels rose to control levels. Control experiments confirmed continued effective receptor blockade. These results indicate that the V2-receptor antagonist causes a modest decrease in AQP2 expression that is not a consequence of increased urine flow rate or washout of medullary hypertonicity. However, this decrease is much less marked than that seen in some forms of acquired nephrogenic diabetes insipidus. In conjunction with the effects of thirsting, this suggests that modulation of AQP2 expression is mediated partly, but not exclusively, via V2 receptors.

KW - Animals

KW - Aquaporin 2

KW - Aquaporin 6

KW - Aquaporins

KW - Benzazepines

KW - Dehydration

KW - Diuresis

KW - Diuretics

KW - Furosemide

KW - Gene Expression

KW - Immunohistochemistry

KW - Ion Channels

KW - Kidney Medulla

KW - Male

KW - Microscopy, Immunoelectron

KW - Polyuria

KW - RNA, Messenger

KW - Rats

KW - Rats, Wistar

KW - Vasopressins

KW - Water Deprivation

M3 - Journal article

C2 - 9729513

VL - 275

SP - F400-9

JO - American Journal of Physiology (Consolidated)

JF - American Journal of Physiology (Consolidated)

SN - 0002-9513

IS - 3 Pt 2

ER -