l-NAME-treatment alters ectonucleotidase activities in kidney membranes of rats

Abstract

The general increase in ATP hydrolysis and in ecto-5'-nucleotidase activity suggests a rise in renal adenosine levels and in renal autoregulatory responses in order to protect the kidney against the threat presented by hypertension.

Effect of dietary supplementation of ginger and turmeric rhizomes on ectonucleotidases, adenosine deaminase and acetylcholinesterase activities in synaptosomes from the cerebral cortex of hypertensive rats

“…This result is in agreement with previously described studied by Balbinott et al (2005). Also, many authors have reported the ability of the arginine analog, L-NAME, to induce systemic arterial hypertension (Furstenau et al, 2008(Furstenau et al, , 2010Cardoso et al, 2012Cardoso et al, , 2014, which probably occurs due to the capacity of L-NAME to inhibit the production of nitric oxide, a well known vasodilator molecule, by blocking nitric oxide synthase (NOS) activity (Moncada et al, 1991). However, dietary supplementation with both rhizomes and treatment with a positive control drug (atenolol) caused a significant reduction of SBP in the hypertensive rats (Fig.…”

“…Alterations in the activities of this enzyme complex have been verified in various studies in hypertensive patients (Schetinger et al, 2007;Lunkes et al, 2009;Bagattini et al, 2011;Cardoso et al, 2012). Regarding L-NAME-induced hypertension in rats, it has recently been demonstrated that ectonucleotidase activities are altered in these enzyme activities in different tissues (Furstenau et al, 2008(Furstenau et al, , 2010Cardoso et al, 2012). Nevertheless, our study report for the first time, to the best of our knowledge, alterations of ectonucleotidase activities in cerebral cortex synaptosomes in L-NAME-induced hypertensive rats.…”

“…The chronic inhibition of NO produces volumedependent elevation of blood pressure and its physiological and pathological characteristics resemble essential hypertension (Lerman et al, 2005;Cardoso et al, 2012Cardoso et al, , 2014. Several studies have administered in vivo an inhibitor of nitric oxide biosynthesis, the N-nitro-L-arginine methyl ester hydrochloride (L-NAME), which is an L-arginine analog, to induce hypertension in rats (Furstenau et al, 2008(Furstenau et al, , 2010Cardoso et al, 2012Cardoso et al, , 2014. The brain especially the cerebral cortex is a major target of the deleterious effects of hypertension and is responsible for a large portion of the related mortality and morbidity (Dahlof, 2007;Toth et al, 2015).…”

Purinergic Signaling and Blood Vessels in Health and Disease

“…A 2A receptor knockout mice had increased proliferation of endothelial cells and increased smooth muscle hypertrophy and collagen deposition in the pulmonary arteries and increased wall area thickness and smooth muscle actin immunoreactivity in the pulmonary resistance vessels, suggesting that adenosine, acting at A 2A receptors, is an important regulatory mechanism to protect against development of pulmonary arterial hypertension . Increased ATP hydrolysis by ectonucleotidases resulting in an accumulation of adenosine in the kidney of hypertensive animals has been reported (Fürstenau et al, 2010).…”

Purinergic signalling in the kidney in health and disease

“…ATP-induced hypotension is associated with alteration of sympathetic nerve activity mediated through vagal afferent pathways [366]. It has been reported that there is an increase in ATP hydrolysis resulting from an increase in ecto-5′-nucleotidase activity and accumulation of adenosine in the kidney of hypertensive animals [96]. A high salt diet given to Ang II hypertensive rats significantly impairs autoregulation of rat juxtamedullary afferent arterioles, which is associated with a decline in afferent arteriolar reactivity to ATP mediated by P2X1 receptors [154].…”