Effects of Angiotensin II on Nitric Oxide Generation in Proliferating and Quiescent Rat Coronary Microvascular Endothelial Cells

Abstract

phospholipases C and D or protein kinase C (2). These transducers in turn regulate the expression of several growth factors, including platelet-derived growth factor and basic fibroblast growth factor (3). In contrast, AT2 is expressed in a few adult tissues, such as heart and kidney tissues, at low levels, and its activation has been implicated in growth inhibitory and/or proapoptotic effects as a result of stimulation of tyrosine phosphatase(s) (4). The results of recent studies suggest that co-stimulation of the AT2 receptor along with blockade of the AT1 receptor by either Ang II receptor blockers or angiotensin converting enzyme inhibitors (ACEIs) increases nitric oxide (NO) release and causes some

Nitric oxide synthase and NAD(P)H oxidase modulate coronary endothelial cell growth

“…Similar increases in these parameters have recently been reported in rat CMEC and aortic endothelial cells in which the effects of angiotensin II on NO production and eNOS mRNA/protein expressions were investigated in relation to the state of cell growth [20,31]. However, in the current study no marked difference was observed in iNOS activity between growing and quiescent rat CMEC in contrast to elevation in eNOS activity.…”

“…However, the current data as to the effects of NO on endothelial cell growth are rather contradictory in that both growth-stimulating [3,10] and growth-inhibiting effects have been reported [27][28][29]. Besides, the effects of endothelial cell growth on the activity and expression of NAD(P)H oxidase remains to be fully elucidated, although the correlation between cell growth and enzymatic regulation of eNOS has recently been well-documented [20]. The present study was therefore designed to investigate the reciprocal relationship between coronary endothelial cell growth and the concurrent expression and activity of the enzymes, namely, eNOS and NAD(P)H oxidase that are associated with the regulation of endothelial cell redox state.…”

“…Hybridizations were performed overnight with [ 32 P]-dCTP-random-prime-labeled eNOS or GAPDH cDNA probes that were prepared as previously described [20]. The filters were then washed to a final stringency of 0.1 x SSPE / 0.1% SDS at 65 o C and exposed to KODAK X-100 XAR film (Sigma) with intensifying screens at -80 o C. Quantification of autoradiograms was performed by densitometry, and values for eNOS were normalized to those of GAPDH.…”

Interaction of Endothelial Nitric Oxide and Angiotensin in the Circulation

“…Losartan had no effect on basal ovarian blood flow in rats but blocked the ANG II-induced flow reduction, and, in contrast, the AT 2 receptor antagonist PD123319 increased ovarian basal blood flow and failed to reverse the effect of exogenous ANG II, indicating that under physiological conditions, ovarian blood flow of the rat is negatively regulated by ANG II through AT 2 receptors (Mitsube et al, 2003). Bayraktutan and Ulker (2003) suggested that ANG II stimulates NO production in rat coronary microvascular endothelial cells in both an AT 1 -and AT 2 -receptorregulated manner. Heinemann et al (1997) noted that intravenous injections of ANG II increased blood pressure, which was accompanied by a decrease in blood flow through the superior mesenteric artery and an increase in femoral blood flow, possibly due to vasodilatation; telmisartan prevented all of the hemodynamic responses, and the ANG II-evoked femoral vasodilatation was suppressed by L-NAME.…”

Differential mechanisms of angiotensin II and PDGF-BB on migration and proliferation of coronary artery smooth muscle cells

“…Indeed, the combinations of either atherogen with mevastatin, apocynin or losartan have led to reduced enzymatic activities compared to sole Ang II or PDGF-BB treatments. In this context, our previous studies have shown using endothelial cells that Ang II increases eNOS activity via concomitant involvement of its type 1 and type 2 receptor subtypes and also enhances cell proliferation and NADPH oxidase which are attenuated by MnTBAP, apocynin or antisense p22-phox (a pivotal subunit of NADPH oxidase) cDNA treatments [32][33][34]. [12].…”