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Pulvirenti, Thekla; Yin, Jianlin; Chaufour, Xavier; McLachlan, Craig S.; Hambly, Brett D.; Bennett, Maxwell R.; Barden, Julian A.

doi:10.1023/a:1010828302936

Cited by 25 publications

(6 citation statements)

References 41 publications

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“…In humans the encoding genes, P2RX4 and P2RX7 , are located within 130 kb of each other on chromosome 12. These genes can be regulated independently: the endothelial expression of P2X 4 receptors in the human aorta is increased following injury; P2X 7 receptor expression is not affected (Pulvirenti et al, 2000). It is possible, however, that these receptors have common promotor elements.…”

Section: Discussionmentioning

confidence: 99%

Effect of P2X4 and P2X7 receptor antagonism on the pressure diuresis relationship in rats

et al. 2013

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Reduced glomerular filtration, hypertension and renal microvascular injury are hallmarks of chronic kidney disease, which has a global prevalence of ~10%. We have shown previously that the Fischer (F344) rat has lower GFR than the Lewis rat, and is more susceptible to renal injury induced by hypertension. In the early stages this injury is limited to the pre-glomerular vasculature. We hypothesized that poor renal hemodynamic function and vulnerability to vascular injury are causally linked and genetically determined. In the present study, normotensive F344 rats had a blunted pressure diuresis relationship, compared with Lewis rats. A kidney microarray was then interrogated using the Endeavour enrichment tool to rank candidate genes for impaired blood pressure control. Two novel candidate genes, P2rx7 and P2rx4, were identified, having a 7− and 3− fold increased expression in F344 rats. Immunohistochemistry localized P2X4 and P2X7 receptor expression to the endothelium of the pre-glomerular vasculature. Expression of both receptors was also found in the renal tubule; however there was no difference in expression profile between strains. Brilliant Blue G (BBG), a relatively selective P2X7 antagonist suitable for use in vivo, was administered to both rat strains. In Lewis rats, BBG had no effect on blood pressure, but increased renal vascular resistance, consistent with inhibition of some basal vasodilatory tone. In F344 rats BBG caused a significant reduction in blood pressure and a decrease in renal vascular resistance, suggesting that P2X7 receptor activation may enhance vasoconstrictor tone in this rat strain. BBG also reduced the pressure diuresis threshold in F344 rats, but did not alter its slope. These preliminary findings suggest a physiological and potential pathophysiological role for P2X7 in controlling renal and/or systemic vascular function, which could in turn affect susceptibility to hypertension-related kidney damage.

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Section: Discussionmentioning

confidence: 99%

Effect of P2X4 and P2X7 receptor antagonism on the pressure diuresis relationship in rats

et al. 2013

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“…Interestingly, a more recent study showed that high shear stress associated with vascular diseases can selectively up-regulate P2Y 2 and P2Y 6 receptors in perfused arterial SMC [101]. P2X 1 and P2X 4 receptors have been shown to be up-regulated in rabbit intimal thickenings [102]. Taken together, these findings strongly suggest that at least some P2 receptor subtypes (most notably P2Y 2 ) are implicated in the development of vascular disease.…”

Section: Modulation Of P2 Receptors In Vascular Injurymentioning

confidence: 99%

P2 receptors in atherosclerosis and postangioplasty restenosis

Seye

Kong

et al. 2006

Purinergic Signalling

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Atherosclerosis is an immunoinflammatory process that involves complex interactions between the vessel wall and blood components and is thought to be initiated by endothelial dysfunction [1–3]. Extracellular nucleotides that are released from a variety of arterial and blood cells [4] can bind to P2 receptors and modulate proliferation and migration of smooth muscle cells (SMC), which is known to be involved in intimal hyperplasia that accompanies atherosclerosis and postangioplasty restenosis [5]. In addition, P2 receptors mediate many other functions, including platelet aggregation, leukocyte adherence, and arterial vasomotoricity. A direct pathological role of P2 receptors is reinforced by recent evidence showing that up-regulation and activation of P2Y2 receptors in rabbit arteries mediates intimal hyperplasia [6]. In addition, up-regulation of functional P2Y receptors also has been demonstrated in the basilar artery of the rat double-hemorrhage model [7] and in coronary arteries of diabetic dyslipidemic pigs [8]. It has been proposed that up-regulation of P2Y receptors may be a potential diagnostic indicator for the early stages of atherosclerosis [9]. Therefore, particular effort must be made to understand the consequences of nucleotide release from cells in the cardiovascular system and the subsequent effects of P2 nucleotide receptor activation in blood vessels, which may reveal novel therapeutic strategies for atherosclerosis and restenosis after angioplasty.

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“…Interestingly, a more recent study showed that high shear stress, associated with vascular diseases, can selectively upregulate P2Y 2 and P2Y 6 receptors in perfused arterial SMC [101]. P2X 1 and P2X 4 receptors have been shown to be upregulated in rabbit intimal thickenings [102]. Taken together, these findings strongly suggest that at least some P2 receptor subtypes (most notably P2Y 2 ) are implicated in the development of vascular disease.…”

Section: Modulation Of P2 Receptors In Vascular Injurymentioning

confidence: 99%

P2 receptors in atherosclerosis and postangioplasty restenosis

Seye

Kong

et al. 2007

Purinergic Signalling

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Atherosclerosis is an immunoinflammatory process that involves complex interactions between the vessel wall and blood components and is thought to be initiated by endothelial dysfunction [Ross (Nature 362:801–09, 1993); Fuster et al. (N Engl J Med 326:242–50, 1992); Davies and Woolf (Br Heart J 69:S3–S11, 1993)]. Extracellular nucleotides that are released from a variety of arterial and blood cells [Di Virgilio and Solini (Br J Pharmacol 135:831–42, 2002)] can bind to P2 receptors and modulate proliferation and migration of smooth muscle cells (SMC), which are known to be involved in intimal hyperplasia that accompanies atherosclerosis and postangioplasty restenosis [Lafont et al. (Circ Res 76:996–002, 1995)]. In addition, P2 receptors mediate many other functions including platelet aggregation, leukocyte adherence, and arterial vasomotricity. A direct pathological role of P2 receptors is reinforced by recent evidence showing that upregulation and activation of P2Y2 receptors in rabbit arteries mediates intimal hyperplasia [Seye et al. (Circulation 106:2720–726, 2002)]. In addition, upregulation of functional P2Y receptors also has been demonstrated in the basilar artery of the rat double-hemorrhage model [Carpenter et al. (Stroke 32:516–22, 2001)] and in coronary artery of diabetic dyslipidemic pigs [Hill et al. (J Vasc Res 38:432–43, 2001)]. It has been proposed that upregulation of P2Y receptors may be a potential diagnostic indicator for the early stages of atherosclerosis [Elmaleh et al. (Proc Natl Acad Sci U S A 95:691–95, 1998)]. Therefore, particular effort must be made to understand the consequences of nucleotide release from cells in the cardiovascular system and the subsequent effects of P2 nucleotide receptor activation in blood vessels, which may reveal novel therapeutic strategies for atherosclerosis and restenosis after angioplasty.

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Untitled

Cited by 25 publications

References 41 publications

Effect of P2X4 and P2X7 receptor antagonism on the pressure diuresis relationship in rats

Effect of P2X4 and P2X7 receptor antagonism on the pressure diuresis relationship in rats

P2 receptors in atherosclerosis and postangioplasty restenosis

P2 receptors in atherosclerosis and postangioplasty restenosis

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