Renovascular BK(Ca) channels are not activated in vivo under resting conditions and during agonist stimulation.

Linda Magnusson; Charlotte Mehlin Sørensen; Thomas Hartig Braunstein; Max Salomonsson; N.-H. Holstein-Rathlou

doi:10.1152/ajpregu.00337.2006

Renovascular BK(Ca) channels are not activated in vivo under resting conditions and during agonist stimulation.

Linda Magnusson, Charlotte Mehlin Sørensen, Thomas Hartig Braunstein, Max Salomonsson, N.-H. Holstein-Rathlou

17 Citations (Scopus)

Abstract

We investigated the role of large-conductance Ca(2+)-activated K(+) (BK(Ca)) channels for the basal renal vascular tone in vivo. Furthermore, the possible buffering by BK(Ca) of the vasoconstriction elicited by angiotensin II (ANG II) or norepinephrine (NE) was investigated. The possible activation of renal vascular BK(Ca) channels by cAMP was investigated by infusing forskolin. Renal blood flow (RBF) was measured in vivo using electromagnetic flowmetry or ultrasonic Doppler. Renal preinfusion of tetraethylammonium (TEA; 3.0 mumol/min) caused a small reduction of baseline RBF, but iberiotoxin (IBT; 0.3 nmol/min) did not have any effect. Renal injection of ANG II (1-4 ng) or NE (10-40 ng) produced a transient decrease in RBF. These responses were not affected by preinfusion of TEA or IBT. Renal infusion of the BK(Ca) opener NS-1619 (90.0 nmol/min) did not affect basal RBF or the response to NE, but it attenuated the response to ANG II. Coadministration of NS-1619 with TEA or IBT abolished this effect. Forskolin caused renal vasodilation that was not inhibited by IBT. The presence of BK(Ca) channels in the preglomerular vessels was confirmed by immunohistochemistry. Despite their presence, there is no indication for a major role for BK(Ca) channels in the control of basal renal tone in vivo. Furthermore, BK(Ca) channels do not have a buffering effect on the rat renal vascular responses to ANG II and NE. The fact that NS-1619 attenuates the ANG II response indicates that the renal vascular BK(Ca) channels can be activated under certain conditions.

Original language	English
Journal	American Journal of Physiology: Regulatory, Integrative and Comparative Physiology
Volume	292
Issue number	1
Pages (from-to)	R345-53
ISSN	0363-6119
DOIs	https://doi.org/10.1152/ajpregu.00337.2006
Publication status	Published - 2006

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Renovascular BK(Ca) channels are not activated in vivo under resting conditions and during agonist stimulation. / Magnusson, Linda; Sørensen, Charlotte Mehlin; Braunstein, Thomas Hartig et al.

In: American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, Vol. 292, No. 1, 2006, p. R345-53.

Research output: Contribution to journal › Journal article › Research › peer-review

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title = "Renovascular BK(Ca) channels are not activated in vivo under resting conditions and during agonist stimulation.",

abstract = "We investigated the role of large-conductance Ca(2+)-activated K(+) (BK(Ca)) channels for the basal renal vascular tone in vivo. Furthermore, the possible buffering by BK(Ca) of the vasoconstriction elicited by angiotensin II (ANG II) or norepinephrine (NE) was investigated. The possible activation of renal vascular BK(Ca) channels by cAMP was investigated by infusing forskolin. Renal blood flow (RBF) was measured in vivo using electromagnetic flowmetry or ultrasonic Doppler. Renal preinfusion of tetraethylammonium (TEA; 3.0 mumol/min) caused a small reduction of baseline RBF, but iberiotoxin (IBT; 0.3 nmol/min) did not have any effect. Renal injection of ANG II (1-4 ng) or NE (10-40 ng) produced a transient decrease in RBF. These responses were not affected by preinfusion of TEA or IBT. Renal infusion of the BK(Ca) opener NS-1619 (90.0 nmol/min) did not affect basal RBF or the response to NE, but it attenuated the response to ANG II. Coadministration of NS-1619 with TEA or IBT abolished this effect. Forskolin caused renal vasodilation that was not inhibited by IBT. The presence of BK(Ca) channels in the preglomerular vessels was confirmed by immunohistochemistry. Despite their presence, there is no indication for a major role for BK(Ca) channels in the control of basal renal tone in vivo. Furthermore, BK(Ca) channels do not have a buffering effect on the rat renal vascular responses to ANG II and NE. The fact that NS-1619 attenuates the ANG II response indicates that the renal vascular BK(Ca) channels can be activated under certain conditions.",

author = "Linda Magnusson and S{\o}rensen, {Charlotte Mehlin} and Braunstein, {Thomas Hartig} and Max Salomonsson and N.-H. Holstein-Rathlou",

note = "Keywords: Adenylate Cyclase; Angiotensin II; Animals; Benzimidazoles; Blood Pressure; Electromagnetic Fields; Forskolin; Immunohistochemistry; Large-Conductance Calcium-Activated Potassium Channels; Male; Muscle Tonus; Muscle, Smooth, Vascular; Norepinephrine; Peptides; Potassium Channel Blockers; Rats; Rats, Sprague-Dawley; Renal Circulation; Rheology; Stimulation, Chemical; Tetraethylammonium; Vasoconstrictor Agents",

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doi = "10.1152/ajpregu.00337.2006",

language = "English",

volume = "292",

pages = "R345--53",

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T1 - Renovascular BK(Ca) channels are not activated in vivo under resting conditions and during agonist stimulation.

AU - Magnusson, Linda

AU - Sørensen, Charlotte Mehlin

AU - Braunstein, Thomas Hartig

AU - Salomonsson, Max

AU - Holstein-Rathlou, N.-H.

N1 - Keywords: Adenylate Cyclase; Angiotensin II; Animals; Benzimidazoles; Blood Pressure; Electromagnetic Fields; Forskolin; Immunohistochemistry; Large-Conductance Calcium-Activated Potassium Channels; Male; Muscle Tonus; Muscle, Smooth, Vascular; Norepinephrine; Peptides; Potassium Channel Blockers; Rats; Rats, Sprague-Dawley; Renal Circulation; Rheology; Stimulation, Chemical; Tetraethylammonium; Vasoconstrictor Agents

PY - 2006

Y1 - 2006

N2 - We investigated the role of large-conductance Ca(2+)-activated K(+) (BK(Ca)) channels for the basal renal vascular tone in vivo. Furthermore, the possible buffering by BK(Ca) of the vasoconstriction elicited by angiotensin II (ANG II) or norepinephrine (NE) was investigated. The possible activation of renal vascular BK(Ca) channels by cAMP was investigated by infusing forskolin. Renal blood flow (RBF) was measured in vivo using electromagnetic flowmetry or ultrasonic Doppler. Renal preinfusion of tetraethylammonium (TEA; 3.0 mumol/min) caused a small reduction of baseline RBF, but iberiotoxin (IBT; 0.3 nmol/min) did not have any effect. Renal injection of ANG II (1-4 ng) or NE (10-40 ng) produced a transient decrease in RBF. These responses were not affected by preinfusion of TEA or IBT. Renal infusion of the BK(Ca) opener NS-1619 (90.0 nmol/min) did not affect basal RBF or the response to NE, but it attenuated the response to ANG II. Coadministration of NS-1619 with TEA or IBT abolished this effect. Forskolin caused renal vasodilation that was not inhibited by IBT. The presence of BK(Ca) channels in the preglomerular vessels was confirmed by immunohistochemistry. Despite their presence, there is no indication for a major role for BK(Ca) channels in the control of basal renal tone in vivo. Furthermore, BK(Ca) channels do not have a buffering effect on the rat renal vascular responses to ANG II and NE. The fact that NS-1619 attenuates the ANG II response indicates that the renal vascular BK(Ca) channels can be activated under certain conditions.

AB - We investigated the role of large-conductance Ca(2+)-activated K(+) (BK(Ca)) channels for the basal renal vascular tone in vivo. Furthermore, the possible buffering by BK(Ca) of the vasoconstriction elicited by angiotensin II (ANG II) or norepinephrine (NE) was investigated. The possible activation of renal vascular BK(Ca) channels by cAMP was investigated by infusing forskolin. Renal blood flow (RBF) was measured in vivo using electromagnetic flowmetry or ultrasonic Doppler. Renal preinfusion of tetraethylammonium (TEA; 3.0 mumol/min) caused a small reduction of baseline RBF, but iberiotoxin (IBT; 0.3 nmol/min) did not have any effect. Renal injection of ANG II (1-4 ng) or NE (10-40 ng) produced a transient decrease in RBF. These responses were not affected by preinfusion of TEA or IBT. Renal infusion of the BK(Ca) opener NS-1619 (90.0 nmol/min) did not affect basal RBF or the response to NE, but it attenuated the response to ANG II. Coadministration of NS-1619 with TEA or IBT abolished this effect. Forskolin caused renal vasodilation that was not inhibited by IBT. The presence of BK(Ca) channels in the preglomerular vessels was confirmed by immunohistochemistry. Despite their presence, there is no indication for a major role for BK(Ca) channels in the control of basal renal tone in vivo. Furthermore, BK(Ca) channels do not have a buffering effect on the rat renal vascular responses to ANG II and NE. The fact that NS-1619 attenuates the ANG II response indicates that the renal vascular BK(Ca) channels can be activated under certain conditions.

U2 - 10.1152/ajpregu.00337.2006

DO - 10.1152/ajpregu.00337.2006

M3 - Journal article

C2 - 16973937

SN - 0363-6119

VL - 292

SP - R345-53

JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology

JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology

IS - 1

ER -

Renovascular BK(Ca) channels are not activated in vivo under resting conditions and during agonist stimulation.

Abstract

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