Effects of Ca(2+) channel activity on renal hemodynamics during acute attenuation of NO synthesis in the rat

R Kramp, P Fourmanoir, L Ladrière, E Joly, C Gerbaux, A El Hajjam, N Caron

Research output: Contribution to journalArticle

Abstract

In cultured vascular muscle cells, nitric oxide (NO) has been shown to inhibit voltage-dependent Ca(2+) channels, which are involved in renal blood flow (RBF) autoregulation. Therefore, our purpose was to specify in vivo the effects of this interaction on RBF autoregulation. To do so, hemodynamics were investigated in anesthetized rats during Ca(2+) channel blockade before or after acute NO synthesis inhibition. Rats were treated intravenously with vehicle (n = 10), 0.3 mg/kg body wt N(G)-nitro-L-arginine-methyl ester (L-NAME; n = 7), 4.5 microg. kg body wt(-1). min(-1) nifedipine (n = 8) alone, or with nifedipine infused before (n = 8), after (n = 8), or coadministered with L-NAME (n = 10). Baseline renal vascular resistance (RVR) averaged 14.0 +/- 1.2 resistance units and did not change after vehicle. RVR increased or decreased significantly by 27 and 29% after L-NAME or nifedipine, respectively. Nifedipine reversed, but did not prevent, RVR increase after or coadministered with L-NAME. RBF autoregulation was maintained after L-NAME, but the autoregulatory pressure limit (P(A)) was significantly lowered by 15 mmHg. Nifedipine pretreatment or coadministration with L-NAME limited P(A) resetting or suppressed autoregulation at higher doses. Results were similar with verapamil. Intrarenal blockade of Ca(2+)-activated K(+) channels also prevented autoregulatory resetting by L-NAME (n = 8). These findings suggest NO inhibits voltage-dependent Ca(2+) channels and thereby modulates RBF autoregulatory efficiency.
Original languageEnglish
Pages (from-to)F561-9
JournalAm. J. Physiol. Renal Physiol.
Volume278
Issue number4
Publication statusPublished - Apr 2000

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NG-Nitroarginine Methyl Ester
Nitric Oxide
Hemodynamics
Kidney
Nifedipine
Renal Circulation
Homeostasis
Vascular Resistance
Verapamil
Muscle Cells
Blood Vessels
Pressure

Keywords

  • Renal Circulation
  • Animals
  • Vascular Resistance
  • Blood Pressure
  • Calcium Channel Blockers
  • Hemodynamics
  • Enzyme Inhibitors
  • Homeostasis
  • Nitric Acid
  • Nifedipine
  • Calcium Channels
  • Rats
  • NG-Nitroarginine Methyl Ester
  • Rats, Wistar
  • Time Factors
  • Male

Cite this

Kramp, R., Fourmanoir, P., Ladrière, L., Joly, E., Gerbaux, C., El Hajjam, A., & Caron, N. (2000). Effects of Ca(2+) channel activity on renal hemodynamics during acute attenuation of NO synthesis in the rat. Am. J. Physiol. Renal Physiol., 278(4), F561-9.
Kramp, R ; Fourmanoir, P ; Ladrière, L ; Joly, E ; Gerbaux, C ; El Hajjam, A ; Caron, N. / Effects of Ca(2+) channel activity on renal hemodynamics during acute attenuation of NO synthesis in the rat. In: Am. J. Physiol. Renal Physiol. 2000 ; Vol. 278, No. 4. pp. F561-9.
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Kramp, R, Fourmanoir, P, Ladrière, L, Joly, E, Gerbaux, C, El Hajjam, A & Caron, N 2000, 'Effects of Ca(2+) channel activity on renal hemodynamics during acute attenuation of NO synthesis in the rat', Am. J. Physiol. Renal Physiol., vol. 278, no. 4, pp. F561-9.

Effects of Ca(2+) channel activity on renal hemodynamics during acute attenuation of NO synthesis in the rat. / Kramp, R; Fourmanoir, P; Ladrière, L; Joly, E; Gerbaux, C; El Hajjam, A; Caron, N.

In: Am. J. Physiol. Renal Physiol., Vol. 278, No. 4, 04.2000, p. F561-9.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Effects of Ca(2+) channel activity on renal hemodynamics during acute attenuation of NO synthesis in the rat

AU - Kramp, R

AU - Fourmanoir, P

AU - Ladrière, L

AU - Joly, E

AU - Gerbaux, C

AU - El Hajjam, A

AU - Caron, N

PY - 2000/4

Y1 - 2000/4

N2 - In cultured vascular muscle cells, nitric oxide (NO) has been shown to inhibit voltage-dependent Ca(2+) channels, which are involved in renal blood flow (RBF) autoregulation. Therefore, our purpose was to specify in vivo the effects of this interaction on RBF autoregulation. To do so, hemodynamics were investigated in anesthetized rats during Ca(2+) channel blockade before or after acute NO synthesis inhibition. Rats were treated intravenously with vehicle (n = 10), 0.3 mg/kg body wt N(G)-nitro-L-arginine-methyl ester (L-NAME; n = 7), 4.5 microg. kg body wt(-1). min(-1) nifedipine (n = 8) alone, or with nifedipine infused before (n = 8), after (n = 8), or coadministered with L-NAME (n = 10). Baseline renal vascular resistance (RVR) averaged 14.0 +/- 1.2 resistance units and did not change after vehicle. RVR increased or decreased significantly by 27 and 29% after L-NAME or nifedipine, respectively. Nifedipine reversed, but did not prevent, RVR increase after or coadministered with L-NAME. RBF autoregulation was maintained after L-NAME, but the autoregulatory pressure limit (P(A)) was significantly lowered by 15 mmHg. Nifedipine pretreatment or coadministration with L-NAME limited P(A) resetting or suppressed autoregulation at higher doses. Results were similar with verapamil. Intrarenal blockade of Ca(2+)-activated K(+) channels also prevented autoregulatory resetting by L-NAME (n = 8). These findings suggest NO inhibits voltage-dependent Ca(2+) channels and thereby modulates RBF autoregulatory efficiency.

AB - In cultured vascular muscle cells, nitric oxide (NO) has been shown to inhibit voltage-dependent Ca(2+) channels, which are involved in renal blood flow (RBF) autoregulation. Therefore, our purpose was to specify in vivo the effects of this interaction on RBF autoregulation. To do so, hemodynamics were investigated in anesthetized rats during Ca(2+) channel blockade before or after acute NO synthesis inhibition. Rats were treated intravenously with vehicle (n = 10), 0.3 mg/kg body wt N(G)-nitro-L-arginine-methyl ester (L-NAME; n = 7), 4.5 microg. kg body wt(-1). min(-1) nifedipine (n = 8) alone, or with nifedipine infused before (n = 8), after (n = 8), or coadministered with L-NAME (n = 10). Baseline renal vascular resistance (RVR) averaged 14.0 +/- 1.2 resistance units and did not change after vehicle. RVR increased or decreased significantly by 27 and 29% after L-NAME or nifedipine, respectively. Nifedipine reversed, but did not prevent, RVR increase after or coadministered with L-NAME. RBF autoregulation was maintained after L-NAME, but the autoregulatory pressure limit (P(A)) was significantly lowered by 15 mmHg. Nifedipine pretreatment or coadministration with L-NAME limited P(A) resetting or suppressed autoregulation at higher doses. Results were similar with verapamil. Intrarenal blockade of Ca(2+)-activated K(+) channels also prevented autoregulatory resetting by L-NAME (n = 8). These findings suggest NO inhibits voltage-dependent Ca(2+) channels and thereby modulates RBF autoregulatory efficiency.

KW - Renal Circulation

KW - Animals

KW - Vascular Resistance

KW - Blood Pressure

KW - Calcium Channel Blockers

KW - Hemodynamics

KW - Enzyme Inhibitors

KW - Homeostasis

KW - Nitric Acid

KW - Nifedipine

KW - Calcium Channels

KW - Rats

KW - NG-Nitroarginine Methyl Ester

KW - Rats, Wistar

KW - Time Factors

KW - Male

M3 - Article

C2 - 10751216

VL - 278

SP - F561-9

JO - Am. J. Physiol. Renal Physiol.

JF - Am. J. Physiol. Renal Physiol.

IS - 4

ER -

Kramp R, Fourmanoir P, Ladrière L, Joly E, Gerbaux C, El Hajjam A et al. Effects of Ca(2+) channel activity on renal hemodynamics during acute attenuation of NO synthesis in the rat. Am. J. Physiol. Renal Physiol. 2000 Apr;278(4):F561-9.