Characterization of vascular P2 purinoceptors in the rat isolated perfused kidney

Eltze, Manfrid; Ullrich, Brigitte

doi:10.1016/0014-2999(96)00244-0

Cited by 63 publications

(78 citation statements)

References 40 publications

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“…Functional studies from our laboratory (7,19,20,23) and others (16,46) have established that afferent arterioles express P2X and P2Y receptors. While full characterization of the P2 receptor complement has not been completed, evidence strongly supports the presence of P2X 1 and P2Y 2 receptors on the preglomerular vascular smooth muscle (7, 19-23, 47, 48).…”

Section: Discussionmentioning

confidence: 98%

“…Studies performed in numerous vascular beds have established the relationship between P2X 1 receptor activation and vasoconstriction (7,11,12,15); however, the physiological role of P2X 1 receptors in regulating vascular function remains unclear. Studies suggest that P2 receptors contribute to the regulation of renal microvascular function (1,(7)(8)(9)(10)(16)(17)(18). P2X and P2Y receptors are expressed by preglomerular microvascular smooth muscle (7,8,16,(19)(20)(21)(22)(23), and previous studies implicate P2 receptors in mediating autoregulatory behavior (7-9, 17, 24).…”

Section: Introductionmentioning

confidence: 99%

“…Studies suggest that P2 receptors contribute to the regulation of renal microvascular function (1,(7)(8)(9)(10)(16)(17)(18). P2X and P2Y receptors are expressed by preglomerular microvascular smooth muscle (7,8,16,(19)(20)(21)(22)(23), and previous studies implicate P2 receptors in mediating autoregulatory behavior (7-9, 17, 24). Unfortunately, due to the lack of subtype-specific P2 receptor antagonists, the specific P2 receptor subtype involved in the autoregulatory response has eluded identification.…”

Section: Introductionmentioning

confidence: 99%

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Physiological role for P2X1 receptors in renal microvascular autoregulatory behavior

Inscho¹,

Cook²,

Imig³

et al. 2003

J. Clin. Invest.

146

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This study tests the hypothesis that P2X 1 receptors mediate pressure-induced afferent arteriolar autoregulatory responses. Afferent arterioles from rats and P2X 1 KO mice were examined using the juxtamedullary nephron technique. Arteriolar diameter was measured in response to step increases in renal perfusion pressure (RPP). Autoregulatory adjustments in diameter were measured before and during P2X receptor blockade with NF279 or A 1 receptor blockade with 1,3-dipropyl-8-cyclopentylxanthine (DPCPX). Acute papillectomy or furosemide perfusion was performed to interrupt distal tubular fluid flow past the macula densa, thus minimizing tubuloglomerular feedback-dependent influences on afferent arteriolar function. Under control conditions, arteriolar diameter decreased by 17% and 29% at RPP of 130 and 160 mmHg, respectively. Blockade of P2X 1 receptors with NF279 blocked pressuremediated vasoconstriction, reflecting an attenuated autoregulatory response. The A 1 receptor blocker DPCPX did not alter autoregulatory behavior or the response to ATP. Deletion of P2X 1 receptors in KO mice significantly blunted autoregulatory responses induced by an increase in RPP, and this response was not further impaired by papillectomy or furosemide. WT control mice exhibited typical RPPdependent vasoconstriction that was significantly attenuated by papillectomy. These data provide compelling new evidence indicating that tubuloglomerular feedback signals are coupled to autoregulatory preglomerular vasoconstriction through ATP-mediated activation of P2X 1 receptors.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Physiological role for P2X1 receptors in renal microvascular autoregulatory behavior

Inscho¹,

Cook²,

Imig³

et al. 2003

J. Clin. Invest.

146

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“…Evidence for P2Y and P2X receptors in renal vasculature was found in a pharmacological study assessing nitric oxide (NO) production by Eltze and Ullrich [87]. There is abundant evidence for the expression of multiple P2Y and P2X receptors of vascular endothelium.…”

Section: Nucleotide and Nucleoside Receptor Expression Along The Nephronmentioning

confidence: 99%

Purinergic signaling in the lumen of a normal nephron and in remodeled PKD encapsulated cysts

Hovater

Olteanu

Welty

et al. 2008

Purinergic Signalling

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The nephron is the functional unit of the kidney. Blood and plasma are continually filtered within the glomeruli that begin each nephron. Adenosine 5′ triphosphate (ATP) and its metabolites are freely filtered by each glomerulus and enter the lumen of each nephron beginning at the proximal convoluted tubule (PCT). Flow rate, osmolality, and other mechanical or chemical stimuli for ATP secretion are present in each nephron segment. These ATP-release stimuli are also different in each nephron segment due to water or salt permeability or impermeability along different luminal membranes of the cells that line each nephron segment. Each of the above stimuli can trigger additional ATP release into the lumen of a nephron segment. Each nephron-lining epithelial cell is a potential source of secreted ATP. Together with filtered ATP and its metabolites derived from the glomerulus, secreted ATP and adenosine derived from cells along the nephron are likely the principal two of several nucleotide and nucleoside candidates for renal autocrine and paracrine ligands within the tubular fluid of the nephron. This minireview discusses the first principles of purinergic signaling as they relate to the nephron and the urinary bladder. The review discusses how the lumen of a renal tubule presents an ideal purinergic signaling microenvironment. The review also illustrates how remodeled and encapsulated cysts in autosomal dominant polycystic kidney disease (ADPKD) and remodeled pseudocysts in autosomal recessive PKD (ARPKD) of the renal collecting duct likely create an even more ideal microenvironment for purinergic signaling. Once trapped in these closed microenvironments, purinergic signaling becomes chronic and likely plays a significant epigenetic and detrimental role in the secondary progression of PKD, once the remodeling of the renal tissue has begun. In PKD cystic microenvironments, we argue that normal purinergic signaling within the lumen of the nephron provides detrimental acceleration of ADPKD once remodeling is complete.

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“…14 -18 ATP induces vasoconstriction by activating P2 receptors on preglomerular microvascular smooth muscle cells. 19,20 This vasoconstriction involves activation of P2X and P2Y receptors. It has been established that purinoceptors, especially P2X 1 receptors, play a critical role in mediating pressure-dependent autoregulatory adjustments in afferent arteriolar diameter.…”

mentioning

confidence: 99%

Impaired Ca ²⁺ Signaling Attenuates P2X Receptor–Mediated Vasoconstriction of Afferent Arterioles in Angiotensin II Hypertension

et al. 2005

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Abstract-This study tested the hypothesis that afferent arteriolar responses to purinoceptor activation are attenuated, and Ca 2ϩ signaling mechanisms are responsible for the blunted preglomerular vascular reactivity in angiotensin II (Ang II) hypertension. Experiments determined the effects of ATP, the P2X 1 agonist ␤,␥-methylene ATP or the P2Y agonist UTP on arteriolar diameter using the juxtamedullary nephron technique and on renal myocyte intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ) using single cell fluorescence microscopy. Six or 13 days of Ang II infusion significantly attenuated the vasoconstrictor responses to ATP and ␤,␥-methylene ATP (PϽ0.05). During exposure to ATP (1, 10, and 100 mol/L), afferent diameter declined by 17Ϯ2%, 29Ϯ3%, and 30Ϯ2% in normal control rats and 8Ϯ3%, 7Ϯ3%, and 22Ϯ3% in kidneys of Ang II-infused rats (13 days). Renal myocyte intracellular calcium responses to ATP or ␤,␥-methylene ATP were also decreased in Ang II hypertensive rats. In myocytes of control rats, peak increases in [Ca 2ϩ ] i averaged 107Ϯ21, 170Ϯ38, and 478Ϯ79 nmol/L at ATP concentrations of 1, 10, and 100 mol/L, respectively. Ang II infusion for 13 days decreased the peak responses to ATP (1, 10, and 100 mol/L) to 65Ϯ13, 102Ϯ20, and 367Ϯ73 nmol/L, respectively. The peak increases in [Ca 2ϩ ] i in response to ␤,␥-methylene ATP were also reduced in Ang II hypertensive rats. However, angiotensin hypertension did not change the UTP-mediated vasoconstrictor responses or the myocyte calcium responses to UTP. These results indicate that the impaired autoregulatory response observed in Ang II-dependent hypertension can be attributed to impairment of P2X 1 receptor-mediated signal transduction. (Hypertension. 2005;46:562-568.)

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Characterization of vascular P2 purinoceptors in the rat isolated perfused kidney

Cited by 63 publications

References 40 publications

Physiological role for P2X1 receptors in renal microvascular autoregulatory behavior

Physiological role for P2X1 receptors in renal microvascular autoregulatory behavior

Purinergic signaling in the lumen of a normal nephron and in remodeled PKD encapsulated cysts

Impaired Ca ²⁺ Signaling Attenuates P2X Receptor–Mediated Vasoconstriction of Afferent Arterioles in Angiotensin II Hypertension

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Characterization of vascular P2 purinoceptors in the rat isolated perfused kidney

Cited by 63 publications

References 40 publications

Physiological role for P2X1 receptors in renal microvascular autoregulatory behavior

Physiological role for P2X1 receptors in renal microvascular autoregulatory behavior

Purinergic signaling in the lumen of a normal nephron and in remodeled PKD encapsulated cysts

Impaired Ca 2+ Signaling Attenuates P2X Receptor–Mediated Vasoconstriction of Afferent Arterioles in Angiotensin II Hypertension

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Impaired Ca ²⁺ Signaling Attenuates P2X Receptor–Mediated Vasoconstriction of Afferent Arterioles in Angiotensin II Hypertension