Angiotensin II and Nitric Oxide Interaction

Gasparo, Marc de

doi:10.1007/1-4020-7960-5_12

Cited by 28 publications

(36 citation statements)

References 121 publications

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“…In mammalian cells, a major source of ROS derives from the membrane-bound NAD(P)H oxidase system, which exists in nonphagocytic cells of the vascular wall such as fibroblasts, vascular smooth muscle cells and endothelial cells (19). Increased ROS generation can induce cell inflammation (20,21).…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II stimulates MCP-1 production in rat glomerular endothelial cells via NAD(P)H oxidase-dependent nuclear factor-kappa B signaling

Pan

Yang

Cheng

2009

Braz J Med Biol Res

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Angiotensin II (Ang II) plays a crucial role in the pathogenesis of renal diseases. The objective of the present study was to investigate the possible inflammatory effect of Ang II on glomerular endothelial cells and the underlying mechanism. We isolated and characterized primary cultures of rat glomerular endothelial cells (GECs) and observed that Ang II induced the synthesis of monocyte chemoattractant protein-1 (MCP-1) in GECs as demonstrated by Western blot. Ang II stimulation, at concentrations ranging from 0.1 to 10 μm, of rat GECs induced a rapid increase in the generation of reactive oxygen species as indicated by laser fluoroscopy. The level of p47 phox protein, an NAD(P)H oxidase subunit, was also increased by Ang II treatment. These effects of Ang II on GECs were all reduced by diphenyleneiodonium (1.0 μm), an NAD(P)H oxidase inhibitor. Ang II stimulation also promoted the activation of nuclear factor-kappa B (NF-κB). Telmisartan (1.0 μm), an AT 1 receptor blocker, blocked all the effects of Ang II on rat GECs. These data suggest that the inhibition of NAD(P)H oxidase-dependent NF-κB signaling reduces the increase in MCP-1 production by GECs induced by Ang II. This may provide a mechanistic basis for the benefits of selective AT 1 blockade in dealing with chronic renal disease.

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Section: Discussionmentioning

confidence: 99%

Angiotensin II stimulates MCP-1 production in rat glomerular endothelial cells via NAD(P)H oxidase-dependent nuclear factor-kappa B signaling

Pan

Yang

Cheng

2009

Braz J Med Biol Res

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“…Ang II elicits its actions via two distinct receptors: the AT1 and Ang II type 2 receptors (AT2) (22). Although the AT2 receptor is usually expressed at low density in adults, it is upregulated in pathological states such as vascular injury, salt depletion, heart failure, or cardiac hypertrophy (23). Pharmacological studies indicate that there is crosstalk between AT1 and AT2 receptors and stimulation of the AT2 receptor opposes the effect of the AT1.…”

Section: Oxidative Stress Asmentioning

confidence: 99%

“…Pharmacological studies indicate that there is crosstalk between AT1 and AT2 receptors and stimulation of the AT2 receptor opposes the effect of the AT1. Whereas stimulation of the AT1 receptor leads to cellular growth, angiogenesis, and vasoconstriction, AT2 receptor stimulation causes opposite effects, antiproliferation, anti-angiogenesis, and vasodilation (23). Thus, AT1 and AT2 receptors are ideal candidates for maintaining a proper balance between the vasodilator agent NO and ROS.…”

Section: Oxidative Stress Asmentioning

confidence: 99%

Possible Role of Oxidative Stress in the Pathogenesis of Hypertension

2008

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Recently oxidative stress has been proposed as the cause of hypertension. An imbalance in superoxide and nitric oxide production may account for reduced vasodilation, which in turn can favor the development of hypertension. In vitro and in human studies support this hypothesis. The supplementation of antioxidants, particularly in the form of fresh fruit and vegetables, reduces blood pressure, supporting a role for free radicals in hypertension.Diabetes Care 31 (Suppl. 2):S181-S184, 2008

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“…For example, exposures to angiotensin II (Ang II) 17,18 and corticosterone 19 influence intracellular signal transduction pathways and gene transcription for hours beyond the period of exposure.…”

Section: Discussionmentioning

confidence: 99%

Voltage-Dependent Calcium Currents Are Enhanced in Nucleus of the Solitary Tract Neurons Isolated From Renal Wrap Hypertensive Rats

2007

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Abstract-The nucleus of the solitary tract (NTS) is the central site of termination of baroreceptor afferents. We hypothesize that changes occur in voltage-gated calcium channels (VGCCs) within NTS neurons as a consequence of hypertension. Whole-cell patch-clamp recordings were obtained from adult normotensive (109Ϯ2 mm Hg; nϭ6 from 6 sham-operated and 31 nonsurgically treated) and hypertensive (158Ϯ6 mm Hg; nϭ24) rats. In some experiments, 4-(4-[dihexadecylamino]styryl)-N-methylpyridinium iodide was applied to the aortic nerve to visualize NTS neurons receiving baroreceptor synaptic contacts. Ba 2ϩ currents (500 ms; Ϫ80 mV prepotential; 500 ms voltage steps in 5-mV increments to ϩ15mV) peaked between Ϫ20 and Ϫ10 mV and were blocked by 100 m of Cd 2ϩ . Peak VGCCs were not different comparing non-4-(4-[dihexadecylamino]styryl)-N-methylpyridinium iodide-labeled and 4-(4-[dihexadecylamino]styryl)-N-methylpyridinium iodide-labeled NTS neurons in hypertensive and normotensive rats. The peak VGCC was significantly greater in cells from hypertensive compared with normotensive rats for both non-DiA-labeled (Pϭ0.02) and DiA-labeled (Pϭ0.04) neurons. To separate high-voltage activated (HVA) and low-voltage activated (LVA) components of VGCCs, voltage ramps (Ϫ110 mV to ϩ30 mV over 50 ms) were applied from a holding potential of Ϫ60 mV (LVA channels inactivated) and a holding potential of Ϫ100 mV (both LVA and HVA currents activated). HVA currents were subtracted from HVAϩLVA currents to yield the LVA current. Peak LVA currents were not different between hypertensive (8.9Ϯ0.8 pA/pF) and normotensive (7.8Ϯ0.6 pA/pF) groups of NTS neurons (Pϭ0.27). These results demonstrate that 4 weeks of renal wrap hypertension induce an increase in Ca T he arterial baroreceptor reflex plays an indispensable role in integrated cardiovascular regulation. Baroreceptors are stretch receptors located in systemic arteries, and they transmit information to the central nervous system regarding the level of blood pressure. The central nervous system integrates this information and initiates changes in heart rate and peripheral resistance in an attempt to maintain blood pressure within normal limits. The first central synapse of the baroreflex arc is in the medullary nucleus of the solitary tract (NTS); therefore, NTS neurons play a key role in cardiovascular regulation.We have reported previously that ligand-gated and voltagegated ion channels in NTS neurons receiving arterial baroreceptor afferent inputs undergo adaptive changes in chronic hypertension. In renal wrap hypertension, NTS neuronal sensitivity to activation of ␥-aminobutyric acid type A receptors is reduced, 1,2 whereas sensitivity to activation of ␥-aminobutyric acid type B receptors is enhanced. 1 Voltagegated, transient outward potassium currents are reduced in NTS neurons in chronic renal wrap hypertension. 3 These alterations are viewed as adaptations in response to hypertension and could modify baroreflex regulation of sympathetic nerve discharge and heart rate in hypertension. 4...

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Angiotensin II and Nitric Oxide Interaction

Cited by 28 publications

References 121 publications

Angiotensin II stimulates MCP-1 production in rat glomerular endothelial cells via NAD(P)H oxidase-dependent nuclear factor-kappa B signaling

Angiotensin II stimulates MCP-1 production in rat glomerular endothelial cells via NAD(P)H oxidase-dependent nuclear factor-kappa B signaling

Possible Role of Oxidative Stress in the Pathogenesis of Hypertension

Voltage-Dependent Calcium Currents Are Enhanced in Nucleus of the Solitary Tract Neurons Isolated From Renal Wrap Hypertensive Rats

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