scholarly journals The role of bradykinin, AT2 and angiotensin 1-7 receptors in the EDRF-dependent vasodilator effect of angiotensin II on the isolated mesenteric vascular bed of the rat

2004 ◽  
Vol 141 (5) ◽  
pp. 860-866 ◽  
Author(s):  
R Soares De Moura ◽  
A C Resende ◽  
A F Emiliano ◽  
T Tano ◽  
A C Mendes-Ribeiro ◽  
...  
2007 ◽  
Vol 85 (10) ◽  
pp. 1038-1046 ◽  
Author(s):  
Banafsheh Afsharimani ◽  
Leila Moezi ◽  
Hamed Sadeghipour ◽  
Bahareh Rahimzadeh-Rofouyi ◽  
Maliheh Nobakht ◽  
...  

The mechanism of action of lithium, an effective treatment for bipolar disease, is still unknown. In this study, the mesenteric vascular beds of control rats and rats that were chronically treated with lithium were prepared by the McGregor method, and the mesenteric vascular bed vasorelaxation responses were examined. NADPH-diaphorase histochemistry was used to determine the activity of NOS (nitric oxide synthase) in mesenteric vascular beds. We demonstrated that ACh-induced vasorelaxation increased in the mesenteric vascular bed of rats treated with lithium. Acute Nο-nitro-l-arginine methyl ester (l-NAME) administration in the medium blocked ACh-induced vasorelaxation in the control group more effectively than in lithium-treated rats, while the vasorelaxant response to sodium nitroprusside, a NO donor, was not different between lithium-treated and control groups. Acute aminoguanidine administration blocked ACh-induced vasorelaxation of lithium-treated rats, but had no effect in the control rats. Furthermore, NOS activity, determined by NADPH-diaphorase staining, was significantly greater in the mesenteric vascular beds from chronic lithium-treated rats than in those from control rats. These data suggest that the enhanced ACh-induced endothelium-derived vasorelaxation in rat mesenteric bed from chronic lithium-treated rats might be associated with increased NOS activity, likely via iNOS. Simultaneous acute l-NAME and indomethacin administration suggests the possible upregulation of EDHF (endothelium-derived hyperpolarizing factor) in lithium-treated rats.


2005 ◽  
Vol 514 (2-3) ◽  
pp. 183-189 ◽  
Author(s):  
Amir Ali Borhani ◽  
Golbahar Houshmand ◽  
Morteza Samini ◽  
Khodadad Namiranian ◽  
Amir Reza Hajrasouliha ◽  
...  

2002 ◽  
Vol 283 (3) ◽  
pp. G587-G594 ◽  
Author(s):  
M. A. Potenza ◽  
O. A. Botrugno ◽  
M. A. De Salvia ◽  
G. Lerro ◽  
C. Nacci ◽  
...  

Expression of constitutive and inducible cyclooxygenase (COX-1 and COX-2, respectively) and the role of prostanoids were investigated in the aorta and mesenteric vascular bed (MVB) from the portal vein-ligated rat (PVL) as a model of portal hypertension. Functional experiments were carried out in MVB from PVL and sham-operated rats in the absence or presence of the nonselective COX inhibitor indomethacin or the selective inhibitors of COX-1 (SC-560) or COX-2 (NS-398). Western blots of COX-1 and COX-2 proteins were evaluated in aorta and MVB, and PGI2 production by enzyme immunoassay of 6-keto-PGF1α was evaluated in the aorta. In the presence of functional endothelium, decreased contraction to norepinephrine (NE) and increased vasodilatation to ACh were observed in MVB from PVL. Exposure of MVB to indomethacin, SC-560, or NS-398 reversed the hyporeactivity to NE and the increased endothelial vasodilatation to ACh in PVL, with NS-398 being more potent than the other two inhibitors. Upregulation of COX-1 and COX-2 expressions was detected in aorta and MVB from PVL portal hypertensive rats, and increased production of 6-keto-PGF1α was observed in aorta from portal hypertensive rats. These results suggest that generation of endothelial vasodilator prostanoids, from COX-1 and COX-2 isoforms, accounts for the increased mesenteric blood flow in portal hypertension.


1977 ◽  
Vol 53 (3) ◽  
pp. 233-239 ◽  
Author(s):  
K. Kondo ◽  
M. S. Manku ◽  
D. F. Horrobin ◽  
R. Boucher ◽  
J. Genest

1. In the perfused rat mesenteric vascular bed, the effects of angiotensin II, cortisol and prostaglandin E2 on the vascular responses to noradrenaline or potassium chloride were studied. 2. Angiotensin II in subpressor concentrations potentiated the vasoconstrictor response to noradrenaline and potassium chloride. This effect of angiotensin II was inhibited in the presence of indomethacin and prostaglandin E2. 3. Cortisol in physiological concentrations inhibited the potentiating effect of angiotensin II. 4. Prostaglandin E2 enhanced the vasoconstrictor response to noradrenaline. This effect was not abolished by cortisol. 5. These results suggest that some actions of angiotensin II and cortisol in vivo are mediated by the regulation of prostaglandin synthesis or release.


2016 ◽  
Vol 94 (11) ◽  
pp. 1227-1236 ◽  
Author(s):  
Angélica K. Bernardelli ◽  
Rita de C.V. de A.F. Da Silva ◽  
Thiago Corrêa ◽  
José Eduardo Da Silva-Santos

We evaluated the effects of phenylephrine, norepinephrine, angiotensin II, and vasopressin in mesenteric, renal, carotid, and tail arteries, and in perfused mesenteric vascular bed from rats subjected to the cecal ligation and puncture (CLP) model of sepsis. Phenylephrine and angiotensin II were less efficacious in mesenteric arteries from the CLP 6 h and CLP 18 h groups than in preparations from non-septic animals, but no differences were found for norepinephrine and vasopressin between the preparations. In renal arteries, none of the vasoconstrictors had impaired activity in the CLP groups. Nonetheless, carotid arteries from the CLP 18 h group presented reduced reactivity to all vasoconstrictors tested, but only phenylephrine and norepinephrine had their effects reduced in carotid arteries from the CLP 6 h group. Despite the reduced responsiveness to phenylephrine, tail arteries from septic rats were hyperreactive to vasopressin and norepinephrine at 6 h and 18 h after the CLP surgery, respectively. The mesenteric vascular bed from CLP groups was hyporeactive to phenylephrine, norepinephrine, and angiotensin II, but not to vasopressin. The vascular contractility in sepsis varies from the well-described refractoriness, to unaltered or even hyperresponsiveness to vasoconstrictors, depending on the vessel, the vasoactive agent, and the time period evaluated.


1994 ◽  
Vol 1 ◽  
pp. 426
Author(s):  
L.A. Szirmai ◽  
E. Monos ◽  
W.J. Stekiel ◽  
J.H. Lombard

2007 ◽  
Vol 46 (2) ◽  
pp. 97-104 ◽  
Author(s):  
A.P.M. Rocha ◽  
L.C.R.M. Carvalho ◽  
M.A.V. Sousa ◽  
S.V.F. Madeira ◽  
P.J.C. Sousa ◽  
...  

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