Intercellular calcium signaling and nitric oxide feedback during constriction of rabbit renal afferent arterioles

Torben Rene Uhrenholt, J Schjerning, Paul M. G. Vanhoutte, Boye L. Jensen, O Skøtt

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Resumé

 
Udgivelsesdato: 2007-Apr
OriginalsprogEngelsk
TidsskriftAmerican Journal of Physiology - Renal Physiology
Vol/bind292
Udgave nummer4
Sider (fra-til)F1124-31
Antal sider8
ISSN0363-6127
DOI
StatusUdgivet - 1. apr. 2007

Fingeraftryk

Constriction
Nitric Oxide
Rabbits
Kidney
Vasoconstriction
Smooth Muscle
Coloring Agents
Fura-2
Optical Imaging
Vascular Smooth Muscle
Fluorescence Microscopy
Acetylcholine
Endothelium
lime

Citer dette

@article{3c6c4560d97211dc860c000ea68e967b,
title = "Intercellular calcium signaling and nitric oxide feedback during constriction of rabbit renal afferent arterioles",
abstract = "Vasoconstriction and increase in the intracellular calcium concentration ([Ca(2+)](i)) of vascular smooth muscle cells may cause an increase of endothelial cell [Ca(2+)](i), which, in turn, augments nitric oxide (NO) production and inhibits smooth muscle cell contraction. This hypothesis was tested in microperfused rabbit renal afferent arterioles, using fluorescence imaging microscopy with the calcium-sensitive dye fura-2 and the NO-sensitive dye 4-amino-5-methylamino-2',7'-difluorescein. Both dyes were loaded into smooth muscle and endothelium. Depolarization with 100 mmol/l KCl led to a transient vasoconstriction which was converted into a sustained response by N-nitro-l-arginine methyl ester (l-NAME). Depolarization increased smooth muscle cell [Ca(2+)](i) from 162 +/- 15 nmol/l to a peak of 555 +/- 70 nmol/l (n = 7), and this response was inhibited by 80{\%} by the l-type calcium channel blocker calciseptine. After a delay of 10 s, [Ca(2+)](i) increased in endothelial cells immediately adjacent to reactive smooth muscle cells, and this calcium wave spread in a nonregenerative fashion laterally into the endothelial cell layer with a velocity of 1.2 microm/s. Depolarization with 100 mmol/l KCl led to a significant increase in NO production ([NO](i)) which was inhibited by l-NAME (n = 5). Acetylcholine caused a rapid increase in endothelial [Ca(2+)](i), which did not transfer to the smooth muscle cells. l-NAME treatment did not affect changes in smooth muscle [Ca(2+)](i) after depolarization, but it did increase the calcium sensitivity of the contractile apparatus. We conclude that depolarization increases smooth muscle [Ca(2+)](i) which is transferred to the endothelial cells and stimulates NO production which curtails vasoconstriction by reducing the calcium sensitivity of the contractile apparatus.",
keywords = "Acetylcholine, Animals, Arterioles, Calcium, Calcium Signaling, Endothelial Cells, Feedback, Male, Microscopy, Fluorescence, NG-Nitroarginine Methyl Ester, Nitric Oxide, Perfusion, Potassium Chloride, Rabbits, Vasoconstriction",
author = "Uhrenholt, {Torben Rene} and J Schjerning and Vanhoutte, {Paul M. G.} and Jensen, {Boye L.} and O Sk{\o}tt",
year = "2007",
month = "4",
day = "1",
doi = "10.1152/ajprenal.00420.2006",
language = "English",
volume = "292",
pages = "F1124--31",
journal = "American Journal of Physiology: Renal Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
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}

Intercellular calcium signaling and nitric oxide feedback during constriction of rabbit renal afferent arterioles. / Uhrenholt, Torben Rene; Schjerning, J; Vanhoutte, Paul M. G.; Jensen, Boye L.; Skøtt, O.

I: American Journal of Physiology - Renal Physiology, Bind 292, Nr. 4, 01.04.2007, s. F1124-31.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

TY - JOUR

T1 - Intercellular calcium signaling and nitric oxide feedback during constriction of rabbit renal afferent arterioles

AU - Uhrenholt, Torben Rene

AU - Schjerning, J

AU - Vanhoutte, Paul M. G.

AU - Jensen, Boye L.

AU - Skøtt, O

PY - 2007/4/1

Y1 - 2007/4/1

N2 - Vasoconstriction and increase in the intracellular calcium concentration ([Ca(2+)](i)) of vascular smooth muscle cells may cause an increase of endothelial cell [Ca(2+)](i), which, in turn, augments nitric oxide (NO) production and inhibits smooth muscle cell contraction. This hypothesis was tested in microperfused rabbit renal afferent arterioles, using fluorescence imaging microscopy with the calcium-sensitive dye fura-2 and the NO-sensitive dye 4-amino-5-methylamino-2',7'-difluorescein. Both dyes were loaded into smooth muscle and endothelium. Depolarization with 100 mmol/l KCl led to a transient vasoconstriction which was converted into a sustained response by N-nitro-l-arginine methyl ester (l-NAME). Depolarization increased smooth muscle cell [Ca(2+)](i) from 162 +/- 15 nmol/l to a peak of 555 +/- 70 nmol/l (n = 7), and this response was inhibited by 80% by the l-type calcium channel blocker calciseptine. After a delay of 10 s, [Ca(2+)](i) increased in endothelial cells immediately adjacent to reactive smooth muscle cells, and this calcium wave spread in a nonregenerative fashion laterally into the endothelial cell layer with a velocity of 1.2 microm/s. Depolarization with 100 mmol/l KCl led to a significant increase in NO production ([NO](i)) which was inhibited by l-NAME (n = 5). Acetylcholine caused a rapid increase in endothelial [Ca(2+)](i), which did not transfer to the smooth muscle cells. l-NAME treatment did not affect changes in smooth muscle [Ca(2+)](i) after depolarization, but it did increase the calcium sensitivity of the contractile apparatus. We conclude that depolarization increases smooth muscle [Ca(2+)](i) which is transferred to the endothelial cells and stimulates NO production which curtails vasoconstriction by reducing the calcium sensitivity of the contractile apparatus.

AB - Vasoconstriction and increase in the intracellular calcium concentration ([Ca(2+)](i)) of vascular smooth muscle cells may cause an increase of endothelial cell [Ca(2+)](i), which, in turn, augments nitric oxide (NO) production and inhibits smooth muscle cell contraction. This hypothesis was tested in microperfused rabbit renal afferent arterioles, using fluorescence imaging microscopy with the calcium-sensitive dye fura-2 and the NO-sensitive dye 4-amino-5-methylamino-2',7'-difluorescein. Both dyes were loaded into smooth muscle and endothelium. Depolarization with 100 mmol/l KCl led to a transient vasoconstriction which was converted into a sustained response by N-nitro-l-arginine methyl ester (l-NAME). Depolarization increased smooth muscle cell [Ca(2+)](i) from 162 +/- 15 nmol/l to a peak of 555 +/- 70 nmol/l (n = 7), and this response was inhibited by 80% by the l-type calcium channel blocker calciseptine. After a delay of 10 s, [Ca(2+)](i) increased in endothelial cells immediately adjacent to reactive smooth muscle cells, and this calcium wave spread in a nonregenerative fashion laterally into the endothelial cell layer with a velocity of 1.2 microm/s. Depolarization with 100 mmol/l KCl led to a significant increase in NO production ([NO](i)) which was inhibited by l-NAME (n = 5). Acetylcholine caused a rapid increase in endothelial [Ca(2+)](i), which did not transfer to the smooth muscle cells. l-NAME treatment did not affect changes in smooth muscle [Ca(2+)](i) after depolarization, but it did increase the calcium sensitivity of the contractile apparatus. We conclude that depolarization increases smooth muscle [Ca(2+)](i) which is transferred to the endothelial cells and stimulates NO production which curtails vasoconstriction by reducing the calcium sensitivity of the contractile apparatus.

KW - Acetylcholine

KW - Animals

KW - Arterioles

KW - Calcium

KW - Calcium Signaling

KW - Endothelial Cells

KW - Feedback

KW - Male

KW - Microscopy, Fluorescence

KW - NG-Nitroarginine Methyl Ester

KW - Nitric Oxide

KW - Perfusion

KW - Potassium Chloride

KW - Rabbits

KW - Vasoconstriction

U2 - 10.1152/ajprenal.00420.2006

DO - 10.1152/ajprenal.00420.2006

M3 - Journal article

VL - 292

SP - F1124-31

JO - American Journal of Physiology: Renal Physiology

JF - American Journal of Physiology: Renal Physiology

SN - 1931-857X

IS - 4

ER -