Renal Vascular Reactivity to P&lt;sub&gt;2&lt;/sub&gt;-Purinoceptor Activation in Spontaneously Hypertensive Rats

Fernández, Óscar; Wangensteen, Rosemary; Osuna, Antonio; Vargas, Félix

doi:10.1159/000028346

Cited by 20 publications

(11 citation statements)

References 20 publications

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“…In contrast, ATP causes vasodilatation when baseline renal vascular resistance is high. This reflects P2Y-mediated production of NO [86]. More recent data have shown vasoactive actions of P2X4 and/or P2X7 in the rat renal artery [242].…”

Section: Physiological Responses In the Glomerulus And Renal Vasculaturementioning

confidence: 72%

Purinergic signalling in the kidney in health and disease

Burnstock

Evans

Bailey

2013

Purinergic Signalling

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The involvement of purinergic signalling in kidney physiology and pathophysiology is rapidly gaining recognition and this is a comprehensive review of early and recent publications in the field. Purinergic signalling involvement is described in several important intrarenal regulatory mechanisms, including tuboglomerular feedback, the autoregulatory response of the glomerular and extraglomerular microcirculation and the control of renin release. Furthermore, purinergic signalling influences water and electrolyte transport in all segments of the renal tubule. Reports about purine-and pyrimidine-mediated actions in diseases of the kidney, including polycystic kidney disease, nephritis, diabetes, hypertension and nephrotoxicant injury are covered and possible purinergic therapeutic strategies discussed.

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Section: Physiological Responses In the Glomerulus And Renal Vasculaturementioning

confidence: 72%

Purinergic signalling in the kidney in health and disease

Burnstock

Evans

Bailey

2013

Purinergic Signalling

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“…For obvious ethical reasons, these investigations are not possible in normotensive individuals. However, in a hypertensive animal model (spontaneously hypertensive rat), purinergic reactivity and nitric-oxide-induced vasodilatation were well preserved [28]. Secondly, the study design allowed only one infusion procedure per patient.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of adenosine-induced renal vasodilatation in hypertensive patients

Wierema

Houben

Postma³

et al. 2005

Journal of Hypertension

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“…In those experiments in which ATP caused an increase in [Ca 2ϩ ] i , a second ATP application led to nearly an identical response (Ͼ95%) if there was Ն15 min between ATP applications. Shorter time intervals between applications resulted in smaller increases in [Ca 2ϩ ] i , presumably the result of receptor desen- sitization (16,32). For the studies shown in Figure 2A, a control ATP-mediated increase in [Ca 2ϩ ] i was first obtained, followed by adenosine, ATP, UTP, ADP, or 2Mes-ATP administered in a random order.…”

Section: Statistical Analysesmentioning

confidence: 94%

Purinergic Receptor Signaling at the Basolateral Membrane of Macula Densa Cells

Liu¹,

Bell²,

Peti‐Peterdi³

et al. 2002

Journal of the American Society of Nephrology

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Abstract. Purinergic receptors are important in the regulation of renal hemodynamics; therefore, this study sought to determine if such receptors influence macula densa cell function. Isolated glomeruli containing macula densa cells, with and without the cortical thick ascending limb, were loaded with the Ca 2ϩ sensitive indicators, Fura Red (confocal microscopy) or fura 2 (conventional video image analysis). Studies were performed on an inverted microscope in a chamber with a flowthrough perfusion system. Changes in cytosolic calcium concentration ([Ca 2ϩ ] i ) from exposed macula densa plaques were assessed upon addition of adenosine, ATP, UTP, ADP, or 2-methylthio-ATP (2-MeS-ATP) for 2 min added to the bathing solution. The tubuloglomerular feedback (TGF) mechanism is a very important regulator of renal hemodynamics. This mechanism operates as a negative feedback loop, sensing changes in distal nephron fluid flow rate by detecting flow-dependent alterations in luminal sodium chloride concentration ([NaCl]) at the macula densa. Signals are then sent by the macula densa cells, which contract the afferent arteriole, thereby adjusting the level of GFR and renal blood flow (1-3). Furthermore, macula densa cells can also influence release of renin from the granular cells in the afferent arteriole (4). The primary mechanism by which the macula densa cells detect changes in [NaCl] is through an apically located Na:2Cl:K cotransport mechanism (5,6). It has also been found that the sensitivity of this TGF mechanism can be reset by a large number of different factors. For instance, renal interstitial pressure and angiotensin II are potent regulators of TGF sensitivity (7,8). Nitric oxide, prostaglandin, thromboxanes, and many other local factors and hormones can also influence the sensitivity of the TGF mechanism (9). The site(s) at which all these factors exert their influence is not well understood. One possibility is that modulation of TGF can occur at the level of the macula densa cells, and it is therefore of particular interest to investigate the receptors expressed by macula densa cells and what effects occur in these cells with receptor activation. For instance, it has recently been reported that macula densa cells possess AT 1 receptors for angiotensin II and that activation of these receptors increases sodium-proton exchange of the apical NHE2 isoform (10 -12).Purinergic receptors have been identified as playing a large role within the juxtaglomerular apparatus (13). These receptors are activated by extracellular purines (adenosine, ADP, and ATP) and pyrimidines (UDP and UTP) and are important signaling molecules that mediate various biologic effects in the kidney. They may serve as paracrine regulators of renal microvascular resistance (14,15) and may modulate mesangial cell contraction, alter epithelial ion transport, and influence the TGF mechanism (16 -20) via cell surface receptors for purines.There are two main families of purine receptors: adenosine or P1 receptors and P2 receptors, the latter recogni...

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Renal Vascular Reactivity to P<sub>2</sub>-Purinoceptor Activation in Spontaneously Hypertensive Rats

Cited by 20 publications

References 20 publications

Purinergic signalling in the kidney in health and disease

Purinergic signalling in the kidney in health and disease

Mechanisms of adenosine-induced renal vasodilatation in hypertensive patients

Purinergic Receptor Signaling at the Basolateral Membrane of Macula Densa Cells

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