ROLE OF ENDOTHELIUM AND VASOCONSTRICTOR PROSTANOIDS IN NOREPINEPHRINE-INDUCED VASOCONSTRICTION IN ISOLATED RAT COMMON CAROTID ARTERIES

2000 ◽  
Vol 22 (5) ◽  
pp. 543-554 ◽  
Author(s):  
Naoki Furuhashi ◽  
Seiji Miyazaki ◽  
Masanori Kamura ◽  
Shoichi Emura ◽  
Keigo Yasuda
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.


1989 ◽  
Vol 9 (4) ◽  
pp. 500-505 ◽  
Author(s):  
Bjarne Grøgaard ◽  
Ludwig Schürer ◽  
Bengt Gerdin ◽  
Karl E. Arfors

The role of polymorphonuclear leukocytes (PMNLs) in postischemic delayed hypoperfusion in the rat brain was investigated. Cerebral ischemia was accomplished by reversible bilateral occlusion of the common carotid arteries for 15 min combined with bleeding to an MABP of 50 mm Hg. The animals of one group were depleted of their circulating PMNLs by intraperitoneal injections of an antineutrophil serum (ANS) prior to the experiment. All animals included in this group had fewer than 0.2 × 109 circulating PMNLs/L at the start of the experiments. In another group ANS was injected intravenously for 5 min starting 2 min after the ischemic insult. After 4 min of recirculation, the number of circulating PMNLs in this group was below 10% of the normal. Control animals were injected with the same amount of normal sheep serum or were not treated at all. Sixty minutes after termination of ischemia, the local blood flow in previously ischemic cerebral structures was 40–50% of the normal as measured with the [14C]iodoantipyrine technique. In animals treated with ANS prior to the ischemic insult, the postischemic blood flow in the frontal, sensorimotor, and parietal cortex as well as caudoputamen and thalamus was significantly higher than that in non-ANS-treated animals. Treatment with ANS immediately after the ischemic period caused no improvement of the local CBF. It is concluded that PMNLs are involved in the cerebral postischemic flow derangements seen in this model. Their effects seem to be exerted during ischemia or immediately upon reinstitution of blood flow.


2016 ◽  
Vol 4 (01) ◽  
pp. 19-30
Author(s):  
Neema Kanyal

Objective: To investigate the Role of Rauwolfia serpentina in stroke induced experimental dementia. Methods: Methanolic root extract of Rauwolfia serpentina(RS) at a dose of 10mg/kg,20mg/kg and 40mg/kg;p.o. was studied against global cerebral ischemia induced dementia by occluding both common carotid arteries. RS at a dose of 10mg/kg, 20mg/kg and 40mg/kg;p.o. were administered for 14 days before and 7 days after both common carotid arteries occlusion(BCCAO) and were continued during behavioral testing i.e. Morris water maze test and elevated plus maze test. At the end of all experiment mice brain were removed and TBARS level, SOD level and infract size were determined.Results : Occlusion of both common carotid arteries significantly increased escape latency time(ELT) during acquisition trial and decrease, time spent in target quadrant on morris water maze, an increase in escape latency time was also observed on elevated plus maze when measured after 7 days of occlusion.Furthermore, TBARS levels, SOD levels and infract size were also increased when measured after 12 days of occlusion. Administration of RS specially at a dose of 20mg/kg and 40mg/kg;p.o. significantly attenuated these alteration and show neuroprotective effect against oxidative stress, infract size and learning and memory impairment. Conclusions: These finding suggest that Rauwolfia serpentina may have a promising role as a prophylactic drug in stroke induced experimental dementia due to its neuroprotective effect. The phenolic compound like phenolic acid, flavanoids and tannins present in the plant.


2020 ◽  
Vol 80 (1) ◽  
pp. 79-88
Author(s):  
Kampei Shimizu ◽  
Hiroharu Kataoka ◽  
Hirohiko Imai ◽  
Yuto Yamamoto ◽  
Tomohiro Yamada ◽  
...  

Abstract Past studies have elucidated the crucial role of macrophage-mediated inflammation in the growth of intracranial aneurysms (IAs), but the contributions of hemodynamics are unclear. Considering the size of the arteries, we induced de novo aneurysms at the bifurcations created by end-to-side anastomoses with the bilateral common carotid arteries in rats. Sequential morphological data of induced aneurysms were acquired by magnetic resonance angiography. Computational fluid dynamics analyses and macrophage imaging by ferumoxytol were performed. Using this model, we found that de novo saccular aneurysms with a median size of 3.2 mm were induced in 20/45 (44%) of animals. These aneurysms mimicked human IAs both in morphology and pathology. We detected the focal growth of induced aneurysms between the 10th and 17th day after the anastomosis. The regional maps of hemodynamic parameters demonstrated the area exposed to low wall shear stress (WSS) and high oscillatory shear index (OSI) colocalized with the regions of growth. WSS values were significantly lower in the growing regions than in ones without growth. Macrophage imaging showed colocalization of macrophage infiltration with the growing regions. This experimental model demonstrates the potential contribution of low WSS and high OSI to the macrophage-mediated growth of saccular aneurysms.


1965 ◽  
Vol 208 (2) ◽  
pp. 219-223 ◽  
Author(s):  
Leonard Share

This investigation was directed toward the clarification of the role of left atrial stretch receptors in the regulation of the blood level of vasopressin. Occlusion of both common carotid arteries in the anesthetized dog resulted in a marked elevation of the plasma titer of ADH. This response was blocked by the simultaneous inflation of a balloon in the left atrium. Balloon inflation was ineffective in the vagotomized dog. It is concluded that activation of stretch receptors in the wall of the left atrium results in an inhibition of the release of ADH from the neurohypophysis and that the afferent nerve fibers for these receptors are carried by the vagi.


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