Publication

Impaired renal vascular response to a D-1-like receptor agonist but not to an ACE inhibitor in conscious spontaneously hypertensive rats

de Vries, P. A. M., Navis, G. J., De Jong, P. E. & de Zeeuw, D., Aug-1999, In : Journal of Cardiovascular Pharmacology. 34, 2, p. 191 - 198 8 p.

Research output: Contribution to journalArticleAcademicpeer-review

APA

de Vries, P. A. M., Navis, G. J., De Jong, P. E., & de Zeeuw, D. (1999). Impaired renal vascular response to a D-1-like receptor agonist but not to an ACE inhibitor in conscious spontaneously hypertensive rats. Journal of Cardiovascular Pharmacology, 34(2), 191 - 198.

Author

de Vries, P.A.M. ; Navis, Ger Jan ; De Jong, P.E. ; de Zeeuw, Dick. / Impaired renal vascular response to a D-1-like receptor agonist but not to an ACE inhibitor in conscious spontaneously hypertensive rats. In: Journal of Cardiovascular Pharmacology. 1999 ; Vol. 34, No. 2. pp. 191 - 198.

Harvard

de Vries, PAM, Navis, GJ, De Jong, PE & de Zeeuw, D 1999, 'Impaired renal vascular response to a D-1-like receptor agonist but not to an ACE inhibitor in conscious spontaneously hypertensive rats', Journal of Cardiovascular Pharmacology, vol. 34, no. 2, pp. 191 - 198.

Standard

Impaired renal vascular response to a D-1-like receptor agonist but not to an ACE inhibitor in conscious spontaneously hypertensive rats. / de Vries, P.A.M.; Navis, Ger Jan; De Jong, P.E.; de Zeeuw, Dick.

In: Journal of Cardiovascular Pharmacology, Vol. 34, No. 2, 08.1999, p. 191 - 198.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

de Vries PAM, Navis GJ, De Jong PE, de Zeeuw D. Impaired renal vascular response to a D-1-like receptor agonist but not to an ACE inhibitor in conscious spontaneously hypertensive rats. Journal of Cardiovascular Pharmacology. 1999 Aug;34(2):191 - 198.


BibTeX

@article{d604c70338054e61b33f2e5942d935a4,
title = "Impaired renal vascular response to a D-1-like receptor agonist but not to an ACE inhibitor in conscious spontaneously hypertensive rats",
abstract = "The natriuretic response to a dopamine 1-like receptor agonist is blunted in spontaneously hypertensive rats (SHRs). Whether the renal vasodilator response to D-1-like receptor stimulation in SHRs is defective also is unclear. To determine whether the renal hemodynamic response to a D-1-like receptor is impaired in SHR, we examined the effect of a continuous infusion of the D-1-like receptor agonist fenoldopam (2 mu g/kg/min) on systemic and renal hemodynamics in conscious SHRs and Wistar-Kyoto (WKY) rats. As an active control, we used an equivalent antihypertensive dosage of captopril (10 mg/kg). Fenoldopam significantly increased effective renal plasma flow (ERPF) in WKY rats (+22 +/- 5{\%}; p <0.01), whereas this response was absent in SHRs (+7 +/- 3{\%}; NS). Mean arterial pressure (MAP) was significantly reduced in SHRs (-11 +/- 2{\%}; p <0.001), demonstrating a systemic vasodilator response to fenoldopam in SHRs. The reduction in renal vascular resistance (RVR) was more pronounced in WKY rats (-24 +/- 2{\%}) than in SHRs (-13 +/- 4{\%}; p <0.05). Captopril significantly increased ERPF in SHRs (+16 +/- 3{\%}; p <0.001), demonstrating a preserved renal vasodilatory capacity in SHRs. The blunting of the renal vasodilatory response to fenoldopam in SHRs is present during a high as well as a low sodium intake. In conscious SHRs, the renal vasodilatory response to a D-1-like receptor agonist is impaired, whereas the blood pressure response is more pronounced. The preserved renal vasodilatory response to captopril indicates that the defective vasodilatory response in SHRs is functional rather than due to altered structural properties of the renal vascular bed.",
keywords = "renal function, blood pressure, SHRs, dopamine-, D-1-like receptor agonist, ACE inhibitor, CONVERTING ENZYME-INHIBITORS, GLOMERULAR-FILTRATION RATE, RENIN-ANGIOTENSIN SYSTEM, PLASMA-FLOW, DOPAMINE, FENOLDOPAM, SODIUM, ANESTHESIA, MODULATION, EXCRETION",
author = "{de Vries}, P.A.M. and Navis, {Ger Jan} and {De Jong}, P.E. and {de Zeeuw}, Dick",
note = "Article 7",
year = "1999",
month = "8",
language = "English",
volume = "34",
pages = "191 -- 198",
journal = "Journal of Cardiovascular Pharmacology",
issn = "0160-2446",
number = "2",

}

RIS

TY - JOUR

T1 - Impaired renal vascular response to a D-1-like receptor agonist but not to an ACE inhibitor in conscious spontaneously hypertensive rats

AU - de Vries, P.A.M.

AU - Navis, Ger Jan

AU - De Jong, P.E.

AU - de Zeeuw, Dick

N1 - Article 7

PY - 1999/8

Y1 - 1999/8

N2 - The natriuretic response to a dopamine 1-like receptor agonist is blunted in spontaneously hypertensive rats (SHRs). Whether the renal vasodilator response to D-1-like receptor stimulation in SHRs is defective also is unclear. To determine whether the renal hemodynamic response to a D-1-like receptor is impaired in SHR, we examined the effect of a continuous infusion of the D-1-like receptor agonist fenoldopam (2 mu g/kg/min) on systemic and renal hemodynamics in conscious SHRs and Wistar-Kyoto (WKY) rats. As an active control, we used an equivalent antihypertensive dosage of captopril (10 mg/kg). Fenoldopam significantly increased effective renal plasma flow (ERPF) in WKY rats (+22 +/- 5%; p <0.01), whereas this response was absent in SHRs (+7 +/- 3%; NS). Mean arterial pressure (MAP) was significantly reduced in SHRs (-11 +/- 2%; p <0.001), demonstrating a systemic vasodilator response to fenoldopam in SHRs. The reduction in renal vascular resistance (RVR) was more pronounced in WKY rats (-24 +/- 2%) than in SHRs (-13 +/- 4%; p <0.05). Captopril significantly increased ERPF in SHRs (+16 +/- 3%; p <0.001), demonstrating a preserved renal vasodilatory capacity in SHRs. The blunting of the renal vasodilatory response to fenoldopam in SHRs is present during a high as well as a low sodium intake. In conscious SHRs, the renal vasodilatory response to a D-1-like receptor agonist is impaired, whereas the blood pressure response is more pronounced. The preserved renal vasodilatory response to captopril indicates that the defective vasodilatory response in SHRs is functional rather than due to altered structural properties of the renal vascular bed.

AB - The natriuretic response to a dopamine 1-like receptor agonist is blunted in spontaneously hypertensive rats (SHRs). Whether the renal vasodilator response to D-1-like receptor stimulation in SHRs is defective also is unclear. To determine whether the renal hemodynamic response to a D-1-like receptor is impaired in SHR, we examined the effect of a continuous infusion of the D-1-like receptor agonist fenoldopam (2 mu g/kg/min) on systemic and renal hemodynamics in conscious SHRs and Wistar-Kyoto (WKY) rats. As an active control, we used an equivalent antihypertensive dosage of captopril (10 mg/kg). Fenoldopam significantly increased effective renal plasma flow (ERPF) in WKY rats (+22 +/- 5%; p <0.01), whereas this response was absent in SHRs (+7 +/- 3%; NS). Mean arterial pressure (MAP) was significantly reduced in SHRs (-11 +/- 2%; p <0.001), demonstrating a systemic vasodilator response to fenoldopam in SHRs. The reduction in renal vascular resistance (RVR) was more pronounced in WKY rats (-24 +/- 2%) than in SHRs (-13 +/- 4%; p <0.05). Captopril significantly increased ERPF in SHRs (+16 +/- 3%; p <0.001), demonstrating a preserved renal vasodilatory capacity in SHRs. The blunting of the renal vasodilatory response to fenoldopam in SHRs is present during a high as well as a low sodium intake. In conscious SHRs, the renal vasodilatory response to a D-1-like receptor agonist is impaired, whereas the blood pressure response is more pronounced. The preserved renal vasodilatory response to captopril indicates that the defective vasodilatory response in SHRs is functional rather than due to altered structural properties of the renal vascular bed.

KW - renal function

KW - blood pressure

KW - SHRs

KW - dopamine-

KW - D-1-like receptor agonist

KW - ACE inhibitor

KW - CONVERTING ENZYME-INHIBITORS

KW - GLOMERULAR-FILTRATION RATE

KW - RENIN-ANGIOTENSIN SYSTEM

KW - PLASMA-FLOW

KW - DOPAMINE

KW - FENOLDOPAM

KW - SODIUM

KW - ANESTHESIA

KW - MODULATION

KW - EXCRETION

M3 - Article

VL - 34

SP - 191

EP - 198

JO - Journal of Cardiovascular Pharmacology

JF - Journal of Cardiovascular Pharmacology

SN - 0160-2446

IS - 2

ER -

ID: 2004388