Nitric oxide and cardiovascular control

Calver, Alison; Collier, Joe; Vallance, Patrick

doi:10.1113/expphysiol.1993.sp003687

Cited by 167 publications

(116 citation statements)

References 127 publications

(197 reference statements)

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“…The vasodilatation induced by moxonidine was almost totally blocked by central L-NAME, while the bradycardia was not affected; this suggests that different central mechanisms are activated by moxonidine to induce vasodilatation and bradycardia. It is well accepted that NO either peripherally or centrally has an important role in the maintenance of blood pressure (Calver et al, 1993;Zanzinger et al, 1995;Liu et al, 1996). Inhibition of peripheral NOS results in increased arterial pressure, an indication that NO produced at its basal rate by the vascular endothelium causes vasodilatation (Rees et al, 1989).…”

Section: Ts Moreira Et Al Moxonidine-induced Hypotension: Possible mentioning

confidence: 99%

Central blockade of nitric oxide synthesis reduces moxonidine‐induced hypotension

Moreira

Takakura

Menani

et al. 2004

British J Pharmacology

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1 Nitric oxide (NO) and a 2 -adrenoceptor and imidazoline agonists such as moxonidine may act centrally to inhibit sympathetic activity and decrease arterial pressure. 2 In the present study, we investigated the effects of pretreatment with L-NAME (NO synthesis inhibitor), injected into the 4th ventricle (4th V) or intravenously (i.v.), on the hypotension, bradycardia and vasodilatation induced by moxonidine injected into the 4th V in normotensive rats. 3 Male Wistar rats with a stainless steel cannula implanted into the 4th V and anaesthetized with urethane were used. Blood flows were recorded by use of miniature pulsed Doppler flow probes implanted around the renal, superior mesenteric and low abdominal aorta. 4 Moxonidine (20 nmol), injected into the 4th V, reduced the mean arterial pressure (À4273 mmHg), heart rate (À2277 bpm) and renal (À62715%), mesenteric (À4178%) and hindquarter (À5078%) vascular resistances. 5 Pretreatment with L-NAME (10 nmol into the 4th V) almost abolished central moxonidineinduced hypotension (À1073 mmHg) and renal (À1074%), mesenteric (À1174%) and hindquarter (À1376%) vascular resistance reduction, but did not affect the bradycardia (À1878 bpm). 6 The results indicate that central NO mechanisms are involved in the vasodilatation and hypotension, but not in the bradycardia, induced by central moxonidine in normotensive rats.

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Section: Ts Moreira Et Al Moxonidine-induced Hypotension: Possible mentioning

confidence: 99%

Central blockade of nitric oxide synthesis reduces moxonidine‐induced hypotension

Moreira

Takakura

Menani

et al. 2004

British J Pharmacology

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“…The effects of NO differ depending on the rate, duration, place of production, and the nature of the target molecules. Under physiological conditions, cNOS generate low levels of NO which have direct regulatory effects (e.g., neurotransmission and the regulation of blood vessels) [18,19] . In contrast, iNOS generates high levels of NO which mediates antimicrobial and antitumoral activities [19] .…”

Section: No and Ibdmentioning

confidence: 99%

“…Under physiological conditions, cNOS generate low levels of NO which have direct regulatory effects (e.g., neurotransmission and the regulation of blood vessels) [18,19] . In contrast, iNOS generates high levels of NO which mediates antimicrobial and antitumoral activities [19] . This isoform was first isolated in murine macrophages and was subsequently found in several other cell types, including epithelial cells, hepatocytes, endothelial cells, and fibroblasts.…”

Section: No and Ibdmentioning

confidence: 99%

Overview of cytokines and nitric oxide involvement in immuno-pathogenesis of inflammatory bowel diseases

Soufli

Toumi

Rafa

et al. 2016

WJGPT

289

193

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“…Inducible NOS-dependent peroxynitrite production has been recently implicated in the pathophysiology of atherosclerosis [5,6] hypercholesterolaemia [7], hypertension [8], septic shock [9] and diabetes mellitus [7].…”

mentioning

confidence: 99%

Evidence for iNOS-dependent peroxynitrite production in diabetic platelets

et al. 1999

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Nitric oxide (NO), an important mediator of both physiological and pathological processes [1], is derived from l-arginine by a family of enzymes termed NO synthases [2]. At least three isoforms of NO synthase (NOS) have been detected. Of these, endothelial (eNOS) and neuronal (nNOS) enzymes are constitutive and regulated by Ca 2+ /calmodulin. The inducible NOS (iNOS) originally detected in macrophages and in the endothelium is produced in response to cytokines and cellular debris of microbial origin. This inducible form can produce 10-to 50-fold more NO than the constitutive NOS. In addition, Diabetologia (1999) Abstract Aims/hypothesis. The aim of the present study was twofold. Firstly, to determine whether diabetic platelets produce more peroxynitrite than normal platelets and secondly to correlate the peroxynitrite production with the intraplatelet induction of the inducible isoform of nitric oxide-synthase. Methods. Intraplatelet peroxynitrite production was monitored with dichlorofluorescin acetate with a combination of confocal microscopy and steady-state fluorescence. The platelets were probed for the induction of the inducible-nitric oxide-synthase by western immunoblotting.Results. In the presence of extracellular l-arginine (100 mmol/l), platelets from subjects with Type I (insulin-dependent) diabetes displayed about 5 times higher fluorescence than those from control subjects. To determine whether inducible-nitric oxide-synthase was the source of peroxynitrite, dichlorofluorescein production was quantified as a function of larginine as well as nitric oxide-synthase inhibitors, in platelets from control subjects, subjects with Type I diabetes and subjects with Type II (non-insulin-dependent) diabetes mellitus. Platelets from subjects with Type I yielded about sevenfold and those from Type II about threefold larger amounts of l-arginine/nitric oxide-synthase-dependent dichlorofluorescein fluorescence than those from control subjects. The platelets were then immunologically probed for inducible-nitric oxide-synthase, which has previously been implicated in peroxynitrite production and detected in megakaryocytes of subjects with coronary heart disease. Western immunoblots of intraplatelet proteins indicated that the inducible-nitric oxide-synthase was absent in control subjects. Platelets from both Type I and Type II diabetic subjects, however, contained inducible-nitric oxide-synthase. Conclusion/interpretation. Inducible-nitric oxide-synthase-derived peroxynitrite is a source of platelet damage in diabetes. [Diabetologia (1999) 42: 539± 544]

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Nitric oxide and cardiovascular control

Cited by 167 publications

References 127 publications

Central blockade of nitric oxide synthesis reduces moxonidine‐induced hypotension

Central blockade of nitric oxide synthesis reduces moxonidine‐induced hypotension

Overview of cytokines and nitric oxide involvement in immuno-pathogenesis of inflammatory bowel diseases

Evidence for iNOS-dependent peroxynitrite production in diabetic platelets

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