The influence of angiotensin II and cyclic nucleotide second messenger signal transduction on ischemia-reperfusion-induced elevations in microvascular hydraulic permeability

A stable Chinese hamster ovary fibroblast line expressing the rat vascular type 1a angiotensin II (ANG II) receptor was used to study the lipid-derived signal transduction pathways elicited by type 1a ANG II receptor activation. ANG II caused a biphasic and dose-dependent increase in diacylglycerol (DAG) accumulation with an initial peak at 15 s (181 +/- 11% of control, P < 0.02) and a second sustained peak at 5-10 min (214 +/- 10% of control, P < 0.02). The late DAG peak was derived from phosphatidylcholine (PC), and the formation was blocked by ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid. ANG II also increased phosphatidic acid (PA) production nearly fourfold by 7.5 min. In the presence of ethanol, ANG II markedly increased phosphatidylethanol (PEt) formation, indicating activation of phospholipase D (PLD). ANG II was shown to increase the mass of three separate PA species, one of which apparently originated from DAG kinase action on PC-phospholipase C (PLC)-produced DAG, providing evidence for PC-PLC activity. ANG II also formed a third PA species, which originated neither from PLD nor from DAG kinase. These results demonstrate that multiple lipid signals propagated via collateral stimulation of PLC and PLD are generated by specific activation of the vascular type 1a ANG II receptor.

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Myocardial angiotensin II receptor expression and ischemia-reperfusion injury

Vascular Medicine ◽

10.1177/1358836x9800300206 ◽

1998 ◽

Vol 3 (2) ◽

pp. 121-130 ◽

Cited By ~ 32

Author(s):

Baichun Yang ◽

Dayuan Li ◽

M Ian Phillips ◽

Paulette Mehta ◽

Jawahar L Mehta

Keyword(s):

Angiotensin Ii ◽

Reperfusion Injury ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Receptor Expression ◽

Angiotensin Ii Receptor

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Renal endothelial dysfunction and impaired autoregulation after ischemia-reperfusion injury result from excess nitric oxide

AJP Renal Physiology ◽

10.1152/ajprenal.00302.2005 ◽

2006 ◽

Vol 291 (3) ◽

pp. F619-F628 ◽

Cited By ~ 32

Author(s):

Zhengrong Guan ◽

Glenda Gobé ◽

Desley Willgoss ◽

Zoltán H. Endre

Keyword(s):

Nitric Oxide ◽

Renal Failure ◽

Angiotensin Ii ◽

Endothelial Dysfunction ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Artery Occlusion ◽

Tubuloglomerular Feedback ◽

Sprague Dawley ◽

Endothelial Nitric Oxide

Endothelial dysfunction in ischemic acute renal failure (IARF) has been attributed to both direct endothelial injury and to altered endothelial nitric oxide synthase (eNOS) activity, with either maximal upregulation of eNOS or inhibition of eNOS by excess nitric oxide (NO) derived from iNOS. We investigated renal endothelial dysfunction in kidneys from Sprague-Dawley rats by assessing autoregulation and endothelium-dependent vasorelaxation 24 h after unilateral (U) or bilateral (B) renal artery occlusion for 30 (U30, B30) or 60 min (U60, B60) and in sham-operated controls. Although renal failure was induced in all degrees of ischemia, neither endothelial dysfunction nor altered facilitation of autoregulation by 75 pM angiotensin II was detected in U30, U60, or B30 kidneys. Baseline and angiotensin II-facilitated autoregulation were impaired, methacholine EC50 was increased, and endothelium-derived hyperpolarizing factor (EDHF) activity was preserved in B60 kidneys. Increasing angiotensin II concentration restored autoregulation and increased renal vascular resistance (RVR) in B60 kidneys; this facilitated autoregulation, and the increase in RVR was abolished by 100 μM furosemide. Autoregulation was enhanced by Nω-nitro-l-arginine methyl ester. Peri-ischemic inhibition of inducible NOS ameliorated renal failure but did not prevent endothelial dysfunction or impaired autoregulation. There was no significant structural injury to the afferent arterioles with ischemia. These results suggest that tubuloglomerular feedback is preserved in IARF but that excess NO and probably EDHF produce endothelial dysfunction and antagonize autoregulation. The threshold for injury-producing, detectable endothelial dysfunction was higher than for the loss of glomerular filtration rate. Arteriolar endothelial dysfunction after prolonged IARF is predominantly functional rather than structural.

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The roles of protein kinase C and cyclic nucleotide dependent kinase in signal transduction in human interferon γ induction by poly I:poly C

FEBS Letters ◽

10.1016/0014-5793(89)80434-x ◽

1989 ◽

Vol 248 (1-2) ◽

pp. 73-77 ◽

Cited By ~ 7

Author(s):

Motoko Tamura-Nishimura ◽

Shigeru Sasakawa

Keyword(s):

Signal Transduction ◽

Protein Kinase C ◽

Protein Kinase ◽

Cyclic Nucleotide ◽

Interferon Γ ◽

Human Interferon ◽

Kinase C

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The Preventive Effects of Diminazene Aceturate in Renal Ischemia/Reperfusion Injury in Male and Female Rats

Advances in Preventive Medicine ◽

10.1155/2014/740647 ◽

2014 ◽

Vol 2014 ◽

pp. 1-9 ◽

Cited By ~ 14

Author(s):

Maryam Malek ◽

Mehdi Nematbakhsh

Keyword(s):

Angiotensin Ii ◽

Angiotensin Converting Enzyme ◽

Ischemia Reperfusion ◽

Renal Ischemia ◽

Female Rats ◽

Male Rats ◽

Converting Enzyme ◽

Diminazene Aceturate ◽

Male And Female ◽

Male And Female Rats

Background. Angiotensin-converting enzyme 2/angiotensin (1-7)/Mas receptor (ACE2/Ang-1-7/MasR) appears to counteract most of the deleterious actions of angiotensin-converting enzyme/angiotensin II/angiotensin II receptor 1 (ACE/Ang II/AT1R) in renal ischemia/reperfusion (I/R) injury but ACE2 activity and its levels are sexually dimorphic in the kidney. This study was designed to evaluate the effects of activation endogenous ACE2 using the diminazene aceturate (DIZE) in renal I/R injury in male and female rats.Methods. 36 Wistar rats were divided into two groups of male and female and each group distinct to three subgroups (n=6). I/R group was subjected to 45 min of bilateral ischemia and 24 h of reperfusion, while treatment group received DIZE (15 mg/kg/day) for three days before the induction of I/R. The other group was assigned as the sham-operated group.Results. DIZE treatment in male rats caused a significant decrease in blood urea nitrogen (BUN), creatinine, liver functional indices, serum malondialdehyde (MDA), and increase kidney nitrite levels (P<0.05), and in female rats a significant increase in creatinine and decrease serum nitrite levels compared to the I/R group (P<0.05).Conclusions. DIZE may protect the male kidney from renal I/RI through antioxidant activity and elevation of circulating nitrite level.

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