Abstract
Our goal in this review is to provide a comprehensive, integrated view of the numerous signaling pathways that are activated by α1-adrenoceptors and control actin-myosin interactions (i.e., crossbridge cycling and force generation) in mammalian arterial smooth muscle. These signaling pathways may be categorized broadly as leading either to thick (myosin) filament regulation or to thin (actin) filament regulation. Thick filament regulation encompasses both “Ca2+ activation” and “Ca2+-sensitization” as it involves both activation of myosin light chain kinase (MLCK) by Ca2+-calmodulin and regulation of myosin light chain phosphatase (MLCP) activity. With respect to Ca2+ activation, adrenergically induced Ca2+ transients in individual smooth muscle cells of intact arteries are now being shown by high resolution imaging to be sarcoplasmic reticulum-dependent asynchronous propagating Ca2+ waves. These waves differ from the spatially uniform increases in [Ca2+] previously assumed. Similarly, imaging during adrenergic activation has revealed the dynamic translocation, to membranes and other subcellular sites, of protein kinases (e.g., Ca2+-activated protein kinases, PKCs) that are involved in regulation of MLCP and thus in “Ca2+ sensitization” of contraction. Thin filament regulation includes the possible disinhibition of actin-myosin interactions by phosphorylation of CaD, possibly by mitogen-activated protein (MAP) kinases that are also translocated during adrenergic activation. An hypothesis for the mechanisms of adrenergic activation of small arteries is advanced. This involves asynchronous Ca2+ waves in individual SMC, synchronous Ca2+ oscillations (at high levels of adrenergic activation), Ca2+ sparks, “Ca2+-sensitization” by PKC and Rho-associated kinase (ROK), and thin filament mechanisms.
The French version of this article is available in the form of electronic supplementary material and can be obtained by using the Springer Link server located at http://dx.doi.org/10.1007/s10254-003-0019-8
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Abbreviations
- 2-APB:
-
2-Aminoethoxydiphenylborate
- ABS-1:
-
Actin binding sequence no. 1
- BK:
-
Large conductance potassium channel
- CaD:
-
Caldesmon
- CaM:
-
Calmodulin
- CaMKinase II:
-
Calmodulin kinase II
- CaP:
-
Calponin
- CICR:
-
Ca2+-induced Ca2+ release
- CPA:
-
Cyclopiazonic acid
- CPI-17:
-
Protein kinase C-potentiated 17 kDa inhibitor protein
- 2,4-DCB:
-
2,4-Dichlorobenzamil
- DAG:
-
Diacylglycerol
- DHP:
-
Dihydropyridine
- DOG:
-
1,2-Dioctanoyl-sn-glycerol
- ERK:
-
Extracellular-regulated kinase
- FDS:
-
Frequent discharge sites
- FRAP:
-
Fluorescence recovery after photobleaching
- FRET:
-
Fluorescence resonance energy transfer
- GEF:
-
Guanine nucleotide exchange factor
- GS17C:
-
Fluorophore peptide antagonist of caldesmon
- HA-1077:
-
1-(5-Isoquinolinesulfonyl)homopiperazine, Di-HCl Salt
- IICR:
-
InsP3−induced Ca2+ release
- ILK:
-
Integrin-linked kinase
- InsP3R:
-
1,4,5-Trisphosphate receptor
- IVC:
-
Inferior vena cava
- jCaTs:
-
Junctional calcium transients
- LC20:
-
20,000 Da light chain of smooth muscle myosin
- M20:
-
Small noncatalytic subunit of myosin phosphatase
- M130:
-
Large noncatalytic subunit of myosin phosphatase
- MAP kinase:
-
Mitogen-activated protein kinase
- MEK:
-
MAPK kinase
- ML-9:
-
1-(5-Chloronaphthalene-1-sulfonyl)-1H-hexahydro-1,4-diazepine hydrochloride
- MLCK:
-
Myosin light chain kinase
- MLCP:
-
Myosin light chain phosphatase
- MLC20 :
-
Myosin light chain 20
- MP:
-
Myosin phosphatase
- MYPT1:
-
Targeting subunit of myosin phosphatase
- NCX:
-
Na/Ca exchanger
- NE:
-
Norepinephrine
- p160ROCK:
-
A rho kinase
- PAK:
-
P21-activated kinase
- PE:
-
Phenylephrine
- PGF2α:
-
Prostaglandin factor 2α
- PKC:
-
Protein kinase C
- PKC-α:
-
Protein kinase C-α
- PKN:
-
Rho effector, protein kinase C-related kinase
- PL:
-
Plasmalemma
- PLC:
-
Phospholipase C
- PL-jSR:
-
Plasmalemma-junctional sarcoplasmic reticulum
- PMA:
-
Phorbol 12-myristate 13-acetate
- PP1c:
-
Catalytic subunit of myosin phosphatase
- PSF:
-
Point spread function
- PMCA:
-
Plasmalemma Ca2+ pumping ATPase
- PM-SR:
-
Plasma membrane-sarcoplasmic reticulum
- ROK:
-
Rho-associated kinase
- RYR:
-
Ryanodine receptor
- SBB:
-
Superficial buffer barrier
- SERCA:
-
Sarcoplasmic reticulum Ca2+ ATPase
- Ser/Thr:
-
Serine/threonine
- SMC:
-
Smooth muscle cell
- SMPP-1M:
-
Smooth muscle phosphatase-1M
- SOC:
-
Store-operated channels
- SR:
-
Sarcoplasmic reticulum
- STOCs:
-
Spontaneous transient outward currents
- TnI:
-
Inhibitory subunit troponin I
- TPEN:
-
N,N,N′N′-tetrakis (2-pyridylmethyl) ethylenediamine
- Tyr:
-
Tyrosine
- UTP:
-
Uridine 5′-triphosphate
- VSMC:
-
Vascular smooth muscle cells
- ZIP kinase:
-
Zipper interacting protein kinase
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Ca2+ waves in the muscle cells of rat resistance arteries during α1-adrenoceptor activation.
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Wier, W.G., Morgan, K.G. (2003). α1-Adrenergic signaling mechanisms in contraction of resistance arteries. In: Reviews of Physiology, Biochemistry and Pharmacology. Reviews of Physiology, Biochemistry and Pharmacology, vol 150. Springer, Berlin, Heidelberg. https://doi.org/10.1007/s10254-003-0019-8
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