scholarly journals Vasomotor Reaction to Cyclooxygenase-1-Mediated Prostacyclin Synthesis in Carotid Arteries from Two-Kidney-One-Clip Hypertensive Mice

PLoS ONE ◽  
2015 ◽  
Vol 10 (8) ◽  
pp. e0136738 ◽  
Author(s):  
Bin Liu ◽  
Zhenhua Li ◽  
Yingzhan Zhang ◽  
Wenhong Luo ◽  
Jiling Zhang ◽  
...  
1981 ◽  
Author(s):  
R B Philp ◽  
I Francey

Recently we reported that acetylsalicylic acid (ASA) 100 mg/kg i.v. had no antithrombotic effect in a rat model of arterial thrombosis whereas 200 mg/kg i.v. had significant antithrombotic activity. The present study investigates salicylate kinetics at the non-protective level. Carotid arteries of urethane-anesthetized rats were injured electrically (1 mA, DC, for 1 min) and thrombogenesis measured by recording downstream temperature. Right and left side injuries were compared before and after ASA, 100 mg/kg i.v. Blood samples were collected at various times post injection and serum assayed for salicylate content by Trinder’s method. All salicylate levels are reported as mg/dL ± SEM. Control injuries produced a temperature fall of 1.4°C ± 0.08 (SEM) and post ASA injuries a fall of 1.8°C ± 0.17 (SEM) (P < .1 > .05). Serum salicylate was 20 mg ± 4.58 1 min post injection and the calculated lh was 40 min with decay following first order kinetics. The intraperitoneal injection of ASA 200 mg/kg produced a serum salicylate level of 8.1 ± 1.55 5 min post injection with a peak of 19 ± 2.03 30 min post injection. Both absorption and elimination followed first order kinetics with Th values of 10 and 44 min respectively. Urine collected 40 min post injection contained 9.4 ± 3.38 free salicylate which increased to about 40 following chemical digestion, indicating the presence of metabolites. The results indicate that serum salicylate levels < 20 do not offer antithrombotic protection in this model and that this level is achieved only briefly following ASA 100 mg/kg i.v. or 200 mg/kg i.p. The brief half-life of ASA in the rat has implications for the interpretation of data concerning the inhibition of prostacyclin synthesis by vessel wall. The wide variation in effective ASA doses reported for various animal models of thrombosis is probably a function of the nature of the model rather than of efficient prostacyclin synthesis.


1994 ◽  
Vol 75 (1) ◽  
pp. 33-40 ◽  
Author(s):  
A J North ◽  
T S Brannon ◽  
L B Wells ◽  
W B Campbell ◽  
P W Shaul

2013 ◽  
Vol 698 (1-3) ◽  
pp. 354-361 ◽  
Author(s):  
Bin Liu ◽  
Wenhong Luo ◽  
Yingzhan Zhang ◽  
Hui Li ◽  
Ningxia Zhu ◽  
...  

2012 ◽  
Vol 302 (9) ◽  
pp. F1133-F1140 ◽  
Author(s):  
Bin Liu ◽  
Wenhong Luo ◽  
Yingzhan Zhang ◽  
Hui Li ◽  
Ningxia Zhu ◽  
...  

This study aimed to determine whether PGI2 would be evoked by the endogenous endothelial B2 receptor agonist bradykinin (BK) in the porcine interlobular renal artery and, if so, to determine how it would influence the vasomotor reaction, and the specific cyclooxygenase (COX) isoform(s) involved in its synthesis. The production of the PGI2 metabolite 6-keto-PGF1α was analyzed with HPLC-mass spectroscopy, while vasomotor reaction to PGI2 or BK was determined with isometric force measurement. Results showed that BK evoked an increase in the production of 6-keto-PGF1α, which was abolished by endothelial denudation that removed COX-1 expression, or was reduced by COX-1 inhibition. Interestingly, PGI2 evoked a potent contraction, which was prevented by antagonizing thromboxane-prostanoid (TP) receptors and was not enhanced by antagonizing the vasodilator PGI2 (IP) receptors. The IP receptor agonists MRE-269 and iloprost did not induce any relaxation. Moreover, iloprost, which is also a PGI2 analog, caused a contraction, which was sensitive to TP receptor antagonism, but was to a significantly lesser extent than that of PGI2. Indeed, IP receptors were not detected by RT-PCR or Western blotting in the vessel. Following nitric oxide synthase (NOS) inhibition, BK also evoked an endothelium-dependent contraction, which was blocked by TP receptor antagonism. In addition, inhibition of COX-1 (but not COX-2) impeded the vasoconstrictor activity of BK and expedited the relaxation induced by the agonist in NOS-intact vessels. These results demonstrate that in the porcine interlobular renal artery BK evokes endothelial COX-1-mediated PGI2 synthesis, which mainly leads to the activation of TP receptors and a vasoconstrictor response, possibly due to a scarcity of vasodilator activity mediated by IP receptors. Also, our data suggested that the effect of a PGI2 analog on TP receptors could be reduced compared with that of PGI2 due to modified structure as with iloprost.


1963 ◽  
Vol 205 (4) ◽  
pp. 749-753 ◽  
Author(s):  
C. Y. Chai ◽  
Norman N. Share ◽  
S. C. Wang

Fifty-three vagotomized cats under chloralose were studied for cardiac augmentation, cardioacceleration, and vasomotor reaction on direct stimulation of the medulla oblongata and via reflex activations. Cardiac augmentation as well as other cardiovascular responses could be induced on stimulation of the dorsal medulla or the central cut end of the sciatic nerves, or on occlusion of the carotid arteries. The augmentation and other responses remained essentially unchanged regardless of the presence or absence of the rostral neural structures, including the hypothalamus. The results confirm and support the concept that a central control mechanism for vasomotor reaction and cardioacceleration as well as augmentation resides in the dorsal region of the lower brain stem.


Author(s):  
A. Trillo

There are conflicting reports regarding some fine structural details of arteries from several animal species. Buck denied the existence of a sub-endothelial space, while Karrer and Keech described a space of variable width which separates the endothelium from the underlying internal elastic lamina in aortas of aging rats and mice respectively.The present communication deals with the ultrastrueture of the interface between the endothelial cell layer and the internal elastic lamina as observed in carotid arteries from rabbits of varying ages.


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