The role of eNOS on the compensatory regulation of vascular tonus by H 2 S in mouse carotid arteries

Nitric Oxide ◽  
2017 ◽  
Vol 69 ◽  
pp. 45-50 ◽  
Author(s):  
Elif Ertuna ◽  
Annemarieke E. Loot ◽  
Ingrid Fleming ◽  
Gunay Yetik-Anacak
1989 ◽  
Vol 9 (5) ◽  
pp. 640-645 ◽  
Author(s):  
V. MacMillan

In this study, the cerebral hemisphere content of calcium as well as selected parameters of oxidative metabolism and electrophysiological function were assessed in normoglycemic and hyperglycemic rats that were exposed to ischemia produced by electrocautery of the vertebral arteries and reversible occlusion of the carotid arteries. In hyperglycemic animals, 0.5 h of ischemia was associated with large accumulations of lactate (27 mmol/kg), whereas normoglycemic animals showed lesser lactate accumulation (17 mmol/kg). At this sampling time (0.5 h of ischemia), both groups of ischemic animals showed tissue calcium contents that were unchanged from preischemic control levels. In normoglycemic animals, release of the carotid clamps and recirculation for 1.5–24 h was associated with normalization of lactate, ATP and phosphocreatine, clinical behavior, and EEC During this 24 h of recirculation, cerebral calcium levels showed no changes. Hyperglycemic ischemic animals recirculated for 1.5–24 h showed a persistent lactic acidosis, depressed ATP and phosphocreatine, gross EEG abnormalities, seizures, and a high mortality rate. Again, during this 24 h period, cerebral calcium content showed no changes from preischemic control or from the matched saline-treated group. These data suggest that significant accumulation of calcium in brain tissue is not an early event in ischemic-hyperglycemic brain damage, and thus does not provide support for a role of calcium in the production of this form of ischemic damage.


2008 ◽  
Vol 294 (3) ◽  
pp. H1183-H1187 ◽  
Author(s):  
Kristen M. Park ◽  
Mario Trucillo ◽  
Nicolas Serban ◽  
Richard A. Cohen ◽  
Victoria M. Bolotina

Store-operated channels (SOC) and store-operated Ca2+ entry are known to play a major role in agonist-induced constriction of smooth muscle cells (SMC) in conduit vessels. In microvessels the role of SOC remains uncertain, in as much as voltage-gated L-type Ca2+ (CaL2+) channels are thought to be fully responsible for agonist-induced Ca2+ influx and vasoconstriction. We present evidence that SOC and their activation via a Ca2+-independent phospholipase A2 (iPLA2)-mediated pathway play a crucial role in agonist-induced constriction of cerebral, mesenteric, and carotid arteries. Intracellular Ca2+ in SMC and intraluminal diameter were measured simultaneously in intact pressurized vessels in vitro. We demonstrated that 1) Ca2+ and contractile responses to phenylephrine (PE) in cerebral and carotid arteries were equally abolished by nimodipine (a CaL2+ inhibitor) and 2-aminoethyl diphenylborinate (an inhibitor of SOC), suggesting that SOC and CaL2+ channels may be involved in agonist-induced constriction of cerebral arteries, and 2) functional inhibition of iPLA2β totally inhibited PE-induced Ca2+ influx and constriction in cerebral, mesenteric, and carotid arteries, whereas K+-induced Ca2+ influx and vasoconstriction mediated by CaL2+ channels were not affected. Thus iPLA2-dependent activation of SOC is crucial for agonist-induced Ca2+ influx and vasoconstriction in cerebral, mesenteric, and carotid arteries. We propose that, on PE-induced depletion of Ca2+ stores, nonselective SOC are activated via an iPLA2-dependent pathway and may produce a depolarization of SMC, which could trigger a secondary activation of CaL2+ channels and lead to Ca2+ entry and vasoconstriction.


1995 ◽  
Vol 25 (2) ◽  
pp. 380A
Author(s):  
Alfredo E. Rodríguez ◽  
Mario Fernández ◽  
Eduardo Mele ◽  
Ernesto Peyregne ◽  
Néstor A. Pérez Baliño

2002 ◽  
Vol 282 (1) ◽  
pp. R131-R138 ◽  
Author(s):  
Arlin B. Blood ◽  
Yu Zhao ◽  
Wen Long ◽  
Lubo Zhang ◽  
Lawrence D. Longo

Recently, we reported that, whereas in cerebral arteries of the adult a majority of norepinephrine (NE)-induced increase in intracellular Ca2+ concentration ([Ca2+]i) comes from release of the sarcoplasmic reticulum (SR) Ca2+ stores, in the fetus the SR Ca2+ stores are relatively small, and NE-induced increase in [Ca2+]i results mainly from activation of plasma membrane L-type Ca2+ channels (20). In an effort to establish further the role of L-type Ca2+ channels in the developing cerebral arteries, we tested the hypothesis that, in the fetus, increased reliance on plasmalemmal L-type Ca2+ channels is mediated, in part, by increased L-type Ca2+ channel density. We used3H-labeled (+)isopropyl-4-(2,1,3-benzoxadiazol-4-y1)-1,4-dihydro-(2,6-dimethyl-5-methoxycarbonyl)pyridine-3-carboxylate (PN200–110, isradipine) to measure L-type Ca2+ channel density (Bmax) in the cerebral arteries, common carotid artery (CCA), and descending aortae of fetal (∼140 gestation days), newborn (7–10 days), and adult sheep. In the cerebral and common carotid arteries, Bmax values (fmol/mg protein) of fetuses and newborns were significantly greater than those of adults. Western immunoblotting assay also revealed that the density of L-type Ca2+ channel protein in the cerebral arteries and CCA was about twofold greater in the fetus than the adult. Finally, compared with the adult, fetal cerebral arteries demonstrated a significantly greater maximum tension and [Ca2+]i in response to stimulation with the L-type Ca2+ channel agonist Bay K 8644. In addition, Bay K 8644-stimulated fetal vessels demonstrated a maximal tension and [Ca2+]isimilar to that observed in response to stimulation with 10−4 NE. These results support the idea that fetal cerebrovascular smooth muscle relies more on extracellular Ca2+ and L-type Ca2+ channels for contraction than does the adult and that this increased reliance is mediated, in part, by greater L-type Ca2+ channel density. This may have important implications in the regulation of cerebral blood flow in the developing organism.


2020 ◽  
pp. 25-29
Author(s):  
A. G. Shapovalova ◽  
V. G. Rapovka ◽  
A. O. Sobolevskaya ◽  
T. N. Negoda

The literature data is presented covering epidemiological significance of acute cerebrovascular accidents (CVA) in‑ cidence in patients with brachiocephalic arteries lesion. The role of atherosclerotic lesion of carotid arteries in the develop‑ ment of ischemic cerebral stroke is shown. The basic methods for diagnosis of carotid arteries lesion has been analyzed as well as their availability and informative value. A comparative analysis of modern methods for surgical treatment of athero‑ sclerotic lesion of carotid arteries such as carotid endarterectomy (classic and eversion), endovascular procedure has been done. The main advantages and disadvantages of these treatment methods, indications and contraindications for their use are described. The timing of cerebral revascularization in the acute and delayed periods of ischemic stroke was estimated. The role of bilateral lesion of the carotid territory is shown as well as approaches to the treatment strategy of such patients.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
V Genkel ◽  
I Baturina ◽  
I Emelyanov ◽  
I Shaposhnik ◽  
I Dolgushin

Abstract Background The role of NK-cells and NKT-cells and their subtypes at various stages of the development of atherosclerosis is poorly understood. It was previously shown that CD3+CD56+CD8+ cells can secrete pro-inflammatory cytokines and an increase in their number has been established in patients with active Behçet's Disease and Multiple Sclerosis. Purpose To study the relationship between the number of activated CD3+CD56+CD8+ cells and the echogenicity of plaques in patients with carotid atherosclerosis. Methods The study included 40 patients, 21 (52.5%) men and 19 (47.5%) women who underwent carotid ultrasound and immunological studies. The median age was 53.5 (46.7; 57.0) years. All patients underwent duplex ultrasound scanning of the carotid arteries. If an atherosclerotic plaque was detected, its image was saved and exported to Adobe Photoshop CS6® followed by analysis of the gray-scale median (GSM) of the plaque. Hypoechoic was considered a carotid plaque whose GSM values were less than 50. The number of CD3+CD56+CD8+CD11b+ cells was evaluated by flow cytometry using a flow cytometer. Results Among the examined patients, carotid plaques were detected in 31 (77.5%) participants. The average values of GSM visualized plaques were 58.0 (46.0; 71.5). Atherosclerotic plaques with GSM <50 were detected in 11 (35.5%) patients. In patients with hypoechoic carotid plaques, the number of CD3+CD56+CD8+CD11b+ cells was statistically significantly higher – 352 (55.0; 505) cells/uL versus 66.0 (15.5; 138) cells/uL in patients with plaques whose GSM values were more than 50 (p=0.020). Based on the results of correlation analysis it was established inverse relationship between number of CD3+CD56+CD8+CD11b+ cells and GSM of plaques (r=−0.427; p=0.016). According to the results of the ROC-analysis, an increase in the number of activated NKT-CD8+ cells over 46.5 cells/uL was a predictor of the presence of hypoechogenic carotid plaques with a sensitivity of 81.8% and a specificity of 45.0% (see Figure 1). Conclusion In patients with hypoechoic carotid plaques, the number of CD3+CD56+CD8+CD11b+ cells was significantly higher in comparison with other patients. An increase in the number of activated NKT-CD8+ cells over 46.5 cells/uL was a predictor of the presence of hypoechoic carotid plaques with sensitivity of 81.8% and specificity of 45.0% Figure 1 Funding Acknowledgement Type of funding source: None


1981 ◽  
Vol 241 (3) ◽  
pp. R163-R166
Author(s):  
R. F. Munzner ◽  
D. G. Ward ◽  
D. S. Gann

To examine the role of right atrial receptors in mediating reflex vascular responses we measured, in cats anesthetized with chloralose/urethan, changes in mean arterial pressure (MAP) in response to volume pulsation of the right atrium (+/- 1 ml, 1 Hz). Changes in MAP were measured 1) with pressure in the carotid arteries normal and vagus nerves intact: right atrial pulsation led to a very small and transient fall in MAP; 2) with pressure in the carotid arteries at 75 mmHg and the vagus nerves intact: right atrial pulsation led to a larger and sustained fall in MAP; 3) with pressure in the carotid arteries at 75 mmHg and the vagus nerves cooled or sectioned bilaterally: right atrial pulsation of the right atrium led only to a very small and transient fall in MAP. These data suggest strongly that signals from right atrial receptors traveling in the vagus nerves mediate a reflex change in MAP that is normally masked by signals from carotid receptors.


Dermatology ◽  
1966 ◽  
Vol 133 (4) ◽  
pp. 262-272 ◽  
Author(s):  
B. Gözsy ◽  
L. Kátó
Keyword(s):  

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