scholarly journals STIM and Orai proteins: players in sexual differences in hypertension-associated vascular dysfunction?

2009 ◽  
Vol 118 (6) ◽  
pp. 391-396 ◽  
Author(s):  
Fernanda R.C. Giachini ◽  
R. Clinton Webb ◽  
Rita C. Tostes
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Dysfunction ◽  
Epidemiological Studies ◽  
Vascular Protection ◽  
Male And Female ◽  
Intracellular Store ◽  
Store Depletion ◽  
New Hypothesis ◽  
Ca2 Channels

Sex-associated differences in hypertension have been observed repeatedly in epidemiological studies; however, the mechanisms conferring vascular protection to females are not totally elucidated. Sex-related differences in intracellular Ca2+ handling or, more specifically, in mechanisms that regulate Ca2+ entry into vascular smooth muscle cells have been identified as players in sex-related differences in hypertension-associated vascular dysfunction. Recently, new signalling components that regulate Ca2+ influx, in conditions of intracellular store depletion, were identified: STIM1 (stromal interaction molecule 1), which works as an intracellular Ca2+ sensor; and Orai1, which is a component of the CRAC (Ca2+ release-activated Ca2+) channels. Together, these proteins reconstitute store-operated Ca2+ channel function. Disturbances in STIM1/Orai1 signalling have been implicated in pathophysiological conditions, including hypertension. In the present article, we analyse evidence for sex-related differences in Ca2+ handling and propose a new hypothesis where sex-related differences in STIM/Orai signalling may contribute to hypertension-associated vascular differences between male and female subjects.

5-Hydroxytryptamine induces transient Ca2+ influx through Ni2+-insensitive Ca2+ channels in rat vascular smooth muscle cells

1999 ◽  
Vol 380 (2-3) ◽  
pp. 163-170 ◽  
Author(s):  
Masahiko Hirafuji ◽  
Fumito Kawahara ◽  
Takashi Ebihara ◽  
Akihiro Nezu ◽  
Akihiko Tanimura ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Ca2 Channels

scholarly journals Farnesol Inhibits L-type Ca2+Channels in Vascular Smooth Muscle Cells

1997 ◽  
Vol 272 (51) ◽  
pp. 32240-32246 ◽  
Author(s):  
Jean-Baptiste Roullet ◽  
Ulrich C. Luft ◽  
Hong Xue ◽  
Justin Chapman ◽  
Rostislav Bychkov ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Ca2 Channels

scholarly journals Peripheral Coupling Sites Formed by STIM1 Govern the Contractility of Vascular Smooth Muscle Cells

2021 ◽  
Author(s):  
Vivek Krishnan ◽  
Sher Ali ◽  
Albert L. Gonzales ◽  
Pratish Thakore ◽  
Caoimhin S. Griffin ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Transmembrane Domain ◽  
Muscle Cells ◽  
Channel Activity ◽  
Resistance Arteries ◽  
Store Depletion ◽  
Domain Protein

Peripheral coupling between the sarcoplasmic reticulum (SR) and plasma membrane (PM) forms signaling complexes that regulate the membrane potential and contractility of vascular smooth muscle cells (VSMCs), although the mechanisms responsible for these membrane interactions are poorly understood. In many cells, STIM1 (stromal interaction molecule 1), a single transmembrane-domain protein that resides in the endoplasmic reticulum (ER), transiently moves to ER-PM junctions in response to depletion of ER Ca2+ stores and initiates store-operated Ca2+ entry (SOCE). Fully differentiated VSMCs express STIM1 but exhibit only marginal SOCE activity. We hypothesized that STIM1 is constitutively active in contractile VSMCs and maintains peripheral coupling. In support of this concept, we found that the number and size of SR-PM interacting sites were decreased and SR-dependent Ca2+ signaling processes were disrupted in freshly isolated cerebral artery SMCs from tamoxifen-inducible, SMC specific STIM1-knockout (Stim1-smKO) mice. VSMCs from Stim1-smKO mice also exhibited a reduction in nanoscale colocalization between Ca2+-release sites on the SR and Ca2+-activated ion channels on the PM, accompanied by diminished channel activity. Stim1-smKO mice were hypotensive and resistance arteries isolated from them displayed blunted contractility. These data suggest that STIM1 – independent of SR Ca2+ store depletion – is critically important for stable peripheral coupling in contractile VSMCs.

Direct Block of Ca2+ Channels by Calmidazolium in Cultured Vascular Smooth Muscle Cells

1999 ◽  
Vol 34 (4) ◽  
pp. 488-496 ◽  
Author(s):  
Masanori Sunagawa ◽  
Hisashi Yokoshiki ◽  
Takashi Seki ◽  
Mariko Nakamura ◽  
Patrick Laber ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Ca2 Channels

Abstract 34: Diminished Contractile Capability In Cerebral Vascular Smooth Muscle Cells In The TgF344-AD Rat Model Of Alzheimer's Disease

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Xing Fang ◽  
Huawei Zhang ◽  
Yedan Liu ◽  
Shaoxun Wang ◽  
Baoying Zheng ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Rat Model ◽  
Perfusion Pressure ◽  
Vascular Dysfunction ◽  
Muscle Cells ◽  
Model Of Alzheimer’S Disease ◽  
Cerebral Vascular

We recently reported that cerebral vascular dysfunction leads to impaired autoregulation of cerebral blood flow (CBF), neurovascular coupling (NVC), and blood-brain barrier (BBB) leakage. The present study examined if cerebral vascular dysfunction precedes cognitive impairment in the TgF344-AD (AD) rat model of Alzheimer's disease. In the present study, we confirmed that the AD rats develop learning and memory deficits beginning at 24-week of age using an eight-arm water maze. AD rats (n = 11) took a longer time to escape and displayed more errors than age-matched wildtype (WT) rats (n = 6). We also completed a longitudinal comparison of the myogenic response (MR) of the middle cerebral artery (MCA) and found that the MR was similar in AD and WT rats at 8- to 12-week of age when perfusion pressure was increased from 40 to 180 mmHg. However, the MR was significantly reduced in 16-week old AD rats (n = 6) as the inner diameter of the MCA only decreased by 8.2 ± 2.4% when perfusion pressure was increased from 40 to 180 mmHg compared with 14.5% ± 2.0% in age-matched WT rats (n = 6). The impaired MR of the MCA was exacerbated in AD rats with aging. Autoregulation of CBF AD rats (n = 4) in vivo was impaired in the surface and deep cortex at 24-week of age compared to age-matched WT rats (n = 4). Furthermore, we found the contractile capability of the cerebral vascular smooth muscle cells (VSMCs) isolated from AD rats (n = 4) was significantly reduced compared with WT rats (n = 4), detected by the reduction in size of 15.7 ± 0.9% vs. 25.4 ± 1.0% using a collagen gel-based assay kit. These results provide evidence that cerebral VSMC dysfunction, impaired MR, and autoregulation of CBF precede the development of memory and learning deficits in the TgF344-AD rat model. However, the underlying mechanisms for the loss of VSMCs contractility in this AD model overexpressing mutant human amyloid precursor protein ( APPsw ) and presenilin 1 ( PS1ΔE9 ) genes remain to be determined. Nevertheless, these results provide novel insight into the vascular contribution to AD.

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