Measurement of Membrane Potential and Intracellular Ca2+ of Arteriolar Endothelium and Smooth Muscle in Vivo

Chen, Yifan; Rivers, Richard J.

doi:10.1006/mvre.2001.2315

Cited by 12 publications

(23 citation statements)

References 12 publications

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“…This is consistent with the abundant literature showing a link between hyperpolarization and remote vasodilation (6,9,15,25); depolarization has similarly been demonstrated to occur with many remote vasoconstrictor agents (46). Lin and Duling (32) additionally tested remote vasoconstrictor responses with ischemia but did not test recovery of responses after the single ischemic event.…”

Section: Discussionsupporting

confidence: 78%

Initiation of remote microvascular preconditioning requires K_ATP channel activity

Mabanta

Valane

Borne

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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The purpose of this study was to investigate vascular preconditioning of individual microvascular networks. Prior work shows that exposure of downstream arterioles to specific agonists preconditions upstream arterioles so that they exhibit an altered local vasoactive response [remote microvascular preconditioning (RMP)]. We hypothesized that mitochondrial ATP-sensitive K+ (K(ATP)) channels were involved in stimulation of RMP. Arteriolar diameter (approximately 15 microm) was observed approximately 1,000 microm upstream of the remote exposure site in the cheek pouch of pentobarbital sodium-anesthetized (70 mg/kg) male hamsters (n = 104); all agonists were applied via micropipette. RMP was initiated by application of pinacidil (Pin), diazoxide (DZ), sodium nitroprusside (SNP), or bradykinin (BK) to the downstream vessel. After 15 min, RMP was apparent at the upstream observation site from testing of local vasoactive responses to L-arginine. Pin, DZ, SNP, and BK each stimulated RMP. To evaluate a specific role for mitochondrial K(ATP) channels in this response, 5-hydroxydecanoate was applied (via a 2nd pipette) during downstream stimulation with agonist. 5-Hydroxydecanoate blocked RMP initiated by Pin, DZ, or SNP, suggesting that mitochondrial K(ATP) channels are involved before SNP signal transduction. To verify this, we applied N(omega)-nitro-L-arginine during DZ or SNP stimulation. RMP was blocked during SNP, but not during DZ, stimulation. Thus stimulation of the RMP response requires mitochondrial K(ATP) channel activity after stimulation by nitric oxide donors.

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Section: Discussionsupporting

confidence: 78%

Initiation of remote microvascular preconditioning requires K_ATP channel activity

Mabanta

Valane

Borne

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…We therefore sought to apply a recently developed technique that utilizes a ratiometric voltage-sensitive fluorescent dye, di-8-ANEPPS, to measure changes in membrane potential. Di-8-ANEPPS has been used successfully for that purpose in a variety of tissues, including the endothelium from intact pressurized peripheral blood vessels (1,2,10,11,41). In the present study, we demonstrated that luminally applied di-8-ANEPPS could be confined to the endothelium and used to indicate changes in endothelial V m in a pressurized cerebral artery preparation.…”

Section: Discussionsupporting

confidence: 51%

“…This dye has previously been utilized to indicate changes in endothelial membrane potential in intact peripheral microvessels (1,2,10,41). Selective endothelial loading of di-8-ANEPPS was achieved by delivering di-8-ANEPPS (10 M/0.1% pluronic) luminally for 10 min followed by a 10-min washout period.…”

Section: Methodsmentioning

confidence: 99%

Role of endothelial intermediate conductance K_Cachannels in cerebral EDHF-mediated dilations

Marrelli

Eckmann

Hunte

2003

American Journal of Physiology-Heart and Circulatory Physiology

112

138

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“…Nonratiometric dyes were used to monitor uncalibrated [Ca 2ϩ ] i changes in endothelial cells in vivo (8,32); the latter study employed the genetically encoded, but nonratiometric, fluorochrome, GCaMP-2. On the other hand, the ratiometric dye, fura PE-3 was used to estimate [Ca 2ϩ ] i in myocytes and endothelial cells (4). Especially in intact arteries, however, calibration of Ca 2ϩ -sensitive fluorochromes, such as fura 2 (18) and fura PE-3 (4), is severely limited by problems such as dye sequestration in organelles and dye leakage (28).…”

Section: Discussionmentioning

confidence: 99%

In vivo assessment of artery smooth muscle [Ca²⁺]_i and MLCK activation in FRET-based biosensor mice

Zhang

Chen

Raina³

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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The cellular mechanisms that control arterial diameter in vivo, particularly in hypertension, are uncertain. Here, we report a method that permits arterial intracellular Ca(2+) concentration ([Ca(2+)](i)), myosin light-chain kinase (MLCK) activation, and artery external diameter to be recorded simultaneously with arterial blood pressure (BP) in living mice under 1.5% isofluorane anesthesia. The method also enables an assessment of local receptor activity on [Ca(2+)](i), MLCK activity, and diameter in arteries, uncomplicated by systemic effects. Transgenic mice that express, in smooth muscle, a Ca(2+)/calmodulin-activated, Förster resonance energy transfer (FRET)-based "ratiometric", exogenous MLCK biosensor were used. Vasoactive substances were administered either intravenously or locally to segments of exposed femoral or cremaster arteries. In the basal state, mean BP was approximately 90 mmHg, femoral arteries were constricted to 65% of their passive diameter, MLCK fractional activation was 0.14, and [Ca(2+)](i) was 131 nM. Phenylephrine (300 ng/g wt iv) elevated mean BP transiently to approximately 110 mmHg, decreased heart rate, increased femoral artery [Ca(2+)](i) to 244 nM and fractional MLCK activation to 0.24, and decreased artery diameter by 23%. In comparison, local application of 1.0 muM phenylephrine raised [Ca(2+)](i) to 279 nM and fractional MLCK activation to 0.26, and reduced diameter by 25%, but did not affect BP or heart rate. Intravital FRET imaging of exogenous MLCK biosensor mice permits quantification of changes in [Ca(2+)](i) and MLCK activation that accompany small changes in BP. Based on the observed variance of the FRET data, this method should enable the detection of a difference in basal [Ca(2+)](i) of 29 nM between two groups of 12 mice with a significance of P < 0.05.

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Measurement of Membrane Potential and Intracellular Ca2+ of Arteriolar Endothelium and Smooth Muscle in Vivo

Cited by 12 publications

References 12 publications

Initiation of remote microvascular preconditioning requires K_ATP channel activity

Initiation of remote microvascular preconditioning requires K_ATP channel activity

Role of endothelial intermediate conductance K_Cachannels in cerebral EDHF-mediated dilations

In vivo assessment of artery smooth muscle [Ca²⁺]_i and MLCK activation in FRET-based biosensor mice

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Measurement of Membrane Potential and Intracellular Ca2+ of Arteriolar Endothelium and Smooth Muscle in Vivo

Cited by 12 publications

References 12 publications

Initiation of remote microvascular preconditioning requires KATP channel activity

Initiation of remote microvascular preconditioning requires KATP channel activity

Role of endothelial intermediate conductance KCachannels in cerebral EDHF-mediated dilations

In vivo assessment of artery smooth muscle [Ca2+]i and MLCK activation in FRET-based biosensor mice

Contact Info

Product

Resources

About

Initiation of remote microvascular preconditioning requires K_ATP channel activity

Initiation of remote microvascular preconditioning requires K_ATP channel activity

Role of endothelial intermediate conductance K_Cachannels in cerebral EDHF-mediated dilations

In vivo assessment of artery smooth muscle [Ca²⁺]_i and MLCK activation in FRET-based biosensor mice