Sheep mesenteric arteries are more sensitive to S-nitrosothiol-mediated vasodilation than femoral arteries due to an L-type calcium channel-dependent mechanism

Nitric Oxide ◽  
2014 ◽  
Vol 42 ◽  
pp. 132
Author(s):  
Taiming Liu ◽  
Hobe Schroeder ◽  
Meijuan Zhang ◽  
Sean Wilson ◽  
Gordon Power ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Mesenteric Arteries ◽  
Femoral Arteries ◽  
Channel Dependent ◽  
Dependent Mechanism

scholarly journals S-nitrosothiols dilate the mesenteric artery more potently than the femoral artery by a cGMP and L-type calcium channel-dependent mechanism

Nitric Oxide ◽  
2016 ◽  
Vol 58 ◽  
pp. 20-27 ◽  
Author(s):  
Taiming Liu ◽  
Hobe J. Schroeder ◽  
Meijuan Zhang ◽  
Sean M. Wilson ◽  
Michael H. Terry ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Femoral Artery ◽  
Mesenteric Artery ◽  
Channel Dependent ◽  
Dependent Mechanism

scholarly journals Rap1 Signaling Prevents L-Type Calcium Channel-Dependent Neurotransmitter Release

2013 ◽  
Vol 33 (17) ◽  
pp. 7245-7252 ◽  
Author(s):  
J. Subramanian ◽  
L. Dye ◽  
A. Morozov
Keyword(s):  
Calcium Channel ◽  
Neurotransmitter Release ◽  
Channel Dependent

Effect of nifedipine on calcium-induced contractions to potassium in the aorta and mesenteric arteries of spontaneously hypertensive and normotensive rats

1986 ◽  
Vol 64 (3) ◽  
pp. 310-314 ◽  
Author(s):  
M. S. Kannan ◽  
A. E. Seip ◽  
D. J. Crankshaw
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Effective Concentration ◽  
Mesenteric Arteries ◽  
Induced Responses ◽  
Shr Rats ◽  
Free Medium ◽  
Spontaneously Hypertensive ◽  
Calcium Dependence

Graded contractions to cumulative additions of calcium in the presence of KCl were obtained in strips of aorta and mesenteric arteries of normotensive (WKY) and spontaneously hypertensive (SHR) rats. In calcium-free medium, a maximally effective concentration of KCl produced a response that was larger in the mesenteric arteries (43–51% of control) than in the aorta (12–14% of control). The calcium channel blocker nifedipine (NFD, up to 10−7 M) did not significantly alter these calcium-insensitive responses. The Ca2+-induced responses were inhibited by NFD, in a concentration-dependent fashion, in both vessel types of WKY and SHR rats. The aortic responses were more sensitive to inhibition by NFD than the responses of mesenteric arteries. Moreover, the aortic responses of WKY were inhibited to a greater extent than those of the SHR. The results suggest: (a) a differential calcium dependence of contractions to KCl in the vessels studied; (b) that aortic responses are dependent on NFD-sensitive voltage-sensitive Ca2+ channels to a greater extent than the responses of mesenteric arteries; and (c) that hypertension results in a decreased sensitivity of the aorta Ca2+ channels to NFD.

scholarly journals Mechanisms of NMDA Receptor- and Voltage-Gated L-Type Calcium Channel-Dependent Hippocampal LTP Critically Rely on Proteolysis That Is Mediated by Distinct Metalloproteinases

2017 ◽  
Vol 37 (5) ◽  
pp. 1240-1256 ◽  
Author(s):  
Grzegorz Wiera ◽  
Daria Nowak ◽  
Inge van Hove ◽  
Piotr Dziegiel ◽  
Lieve Moons ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Calcium Channel ◽  
Voltage Gated ◽  
Channel Dependent

Cytochrome P-450 epoxygenase products contribute to attenuated vasoconstriction after chronic hypoxia

2003 ◽  
Vol 285 (1) ◽  
pp. H127-H136 ◽  
Author(s):  
Scott Earley ◽  
Andrzej Pastuszyn ◽  
Benjimen R. Walker
Keyword(s):  
Chronic Hypoxia ◽  
Barometric Pressure ◽  
Mesenteric Arteries ◽  
Resting Membrane Potential ◽  
Epoxyeicosatrienoic Acids ◽  
Resistance Arteries ◽  
Protein Levels ◽  
Acid Metabolites ◽  
Channel Dependent ◽  
Cytochrome P 450

The systemic vasculature exhibits attenuated vasoconstriction following chronic hypoxia (CH) that is associated with endothelium-dependent vascular smooth muscle (VSM) cell hyperpolarization. We hypothesized that increased production of arachidonic acid metabolites such as the cyclooxygenase product prostacyclin or cytochrome P-450 (CYP) epoxygenase-derived epoxyeicosatrienoic acids (EETs) contributes to VSM cell hyperpolarization following CH. VSM cell resting membrane potential ( Em) was measured in superior mesenteric artery strips isolated from rats with control barometric pressure (Pb, ≅630 Torr) and CH (Pb, 380 Torr for 48 h). VSM cell Em was normalized between groups following administration of the CYP inhibitors 17-octadecynoic acid and SKF-525A. VSM cell hyperpolarization after CH was not altered by cyclooxygenase inhibition, whereas the selective CYP2C9 inhibitor sulfaphenazole normalized VSM cell Em between groups. Iberiotoxin also normalized VSM cell Em, which suggests that large-conductance, Ca2+-activated K+ (BKCa) channel activity is increased after CH. Sulfaphenazole administration restored phenylephrine-induced and myogenic vasoconstriction and Ca2+ responses of mesenteric resistance arteries isolated from CH rats to control levels. Western blot experiments demonstrated that CYP2C9 protein levels were greater in mesenteric arteries from CH rats. In addition, 11,12-EET levels were elevated in endothelial cells from CH rats compared with controls. We conclude that enhanced CYP2C9 expression and 11,12-EET production following CH contributes to BKCa channel-dependent VSM cell hyperpolarization and attenuated vasoreactivity.

scholarly journals Aberrant Exon 8/8a Splicing by Downregulated PTBP (Polypyrimidine Tract-Binding Protein) 1 Increases Ca V 1.2 Dihydropyridine Resistance to Attenuate Vasodilation

2020 ◽  
Vol 40 (10) ◽  
pp. 2440-2453
Author(s):  
Jianzhen Lei ◽  
Xiaoxin Liu ◽  
Miaomiao Song ◽  
Yingying Zhou ◽  
Jia Fan ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Binding Protein ◽  
Expression Patterns ◽  
Mesenteric Arteries ◽  
Channel Blockers ◽  
Polypyrimidine Tract ◽  
Polypyrimidine Tract Binding ◽  
Polypyrimidine Tract Binding Protein

Objective: Calcium channel blockers, such as dihydropyridines, are commonly used to inhibit enhanced activity of vascular Ca V 1.2 channels in hypertension. However, patients who are insensitive to such treatments develop calcium channel blocker-resistant hypertension. The function of Ca V 1.2 channel is diversified by alternative splicing, and the splicing factor PTBP (polypyrimidine tract-binding protein) 1 influences the utilization of mutually exclusive exon 8/8a of the Ca V 1.2 channel during neuronal development. Nevertheless, whether and how PTBP1 makes a role in the calcium channel blocker sensitivity of vascular Ca V 1.2 channels, and calcium channel blocker-induced vasodilation remains unknown. Approach and Results: We detected high expression of PTBP1 and, inversely, low expression of exon 8a in Ca V 1.2 channels (Ca V 1.2 E8a ) in rat arteries. In contrast, the opposite expression patterns were observed in brain and heart tissues. In comparison to normotensive rats, the expressions of PTBP1 and Ca V 1.2 E8a channels were dysregulated in mesenteric arteries of hypertensive rats. Notably, PTBP1 expression was significantly downregulated, and Ca V 1.2 E8a channels were aberrantly increased in dihydropyridine-resistant arteries compared with dihydropyridine-sensitive arteries of rats and human. In rat vascular smooth muscle cells, PTBP1 knockdown resulted in shifting of Ca V 1.2 exon 8 to 8a. Using patch-clamp recordings, we demonstrated a concomitant reduction of sensitivity of Ca V 1.2 channels to nifedipine, due to the higher expression of Ca V 1.2 E8a isoform. In vascular myography experiments, small interfering RNA-mediated knockdown of PTBP1 attenuated nifedipine-induced vasodilation of rat mesenteric arteries. Conclusions: PTBP1 finely modulates the sensitivities of Ca V 1.2 channels to dihydropyridine by shifting the utilization of exon 8/8a and resulting in changes of responses in dihydropyridine-induced vasodilation.

scholarly journals Vulnerability of the retinal microvasculature to oxidative stress: ion channel-dependent mechanisms

2012 ◽  
Vol 302 (9) ◽  
pp. C1413-C1420 ◽  
Author(s):  
Masanori Fukumoto ◽  
Atsuko Nakaizumi ◽  
Ting Zhang ◽  
Stephen I. Lentz ◽  
Maho Shibata ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ionic Currents ◽  
Blue Dye ◽  
Adult Rat ◽  
Retinal Microvasculature ◽  
Independent Mechanism ◽  
Pathophysiological Condition ◽  
Channel Dependent ◽  
Microvascular Cells ◽  
Dependent Mechanism

Although oxidative stress is a hallmark of important vascular disorders such as diabetic retinopathy, it remains unclear why the retinal microvasculature is particularly vulnerable to this pathophysiological condition. We postulated that redox-sensitive ion channels may play a role. Using H2O2 to cause oxidative stress in microvascular complexes freshly isolated from the adult rat retina, we assessed ionic currents, cell viability, intracellular oxidants, and cell calcium by using perforated-patch recordings, trypan blue dye exclusion, and fura-2 fluorescence, respectively. Supporting a role for the oxidant-sensitive ATP-sensitive K (KATP) channels, we found that these channels are activated during exposure of retinal microvessels to H2O2. Furthermore, their inhibition by glibenclamide significantly lessened H2O2-induced microvascular cell death. Additional experiments established that by increasing the influx of calcium into microvascular cells, the KATP channel-mediated hyperpolarization boosted the vulnerability of these cells to oxidative stress. In addition to the KATP channel-dependent mechanism for increasing the lethality of oxidative stress, we also found that the vulnerability of cells in the capillaries, but not in the arterioles, was further boosted by a KATP channel-independent mechanism, which our experiments indicated involves the oxidant-induced activation of calcium-permeable nonspecific cation channels. Taken together, our findings support a working model in which both KATP channel-independent and KATP channel-dependent mechanisms render the capillaries of the retina particularly vulnerable to oxidative stress. Identification of these previously unappreciated mechanisms for boosting the lethality of oxidants may provide new targets for pharmacologically limiting damage to the retinal microvasculature during periods of oxidative stress.

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