Adenosine receptors in the cardiovascular system

Olsson, Ray A.

doi:10.1002/(sici)1098-2299(199611/12)39:3/4<301::aid-ddr9>3.0.co;2-v

Cited by 30 publications

(18 citation statements)

References 72 publications

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“…Thus, it is possible that 10 µM CPA is interacting with A 2 receptors expressed by the mouse microvasculature; however, currently there are no data documenting the expression profiles for adenosine receptors in mouse kidney. It is also possible that the dilation reflects activation of other vasodilatory mechanisms such as stimulation of K channels (53)(54)(55).…”

Section: Discussionmentioning

confidence: 99%

Physiological role for P2X1 receptors in renal microvascular autoregulatory behavior

Ew¹,

Cook²,

Jd³

et al. 2003

J. Clin. Invest.

165

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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: 99%

Physiological role for P2X1 receptors in renal microvascular autoregulatory behavior

Ew¹,

Cook²,

Jd³

et al. 2003

J. Clin. Invest.

165

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“…Purinoceptors are divided into two major families (2,4,9,(37)(38)(39)(40)(41)(42)(43)(44)(45)(46). Extracellular adenosine exerts its effects through activation of G protein-coupled, P1 receptors, which are broadly divided into four major subtypes (A1, A2A, A2B and A3 receptors) (9,(41)(42)(43)(44)47).…”

Section: Receptors and Intracellular Signalingmentioning

confidence: 99%

“…Extracellular adenosine exerts its effects through activation of G protein-coupled, P1 receptors, which are broadly divided into four major subtypes (A1, A2A, A2B and A3 receptors) (9,(41)(42)(43)(44)47). A1 receptors evoke vasoconstriction by inhibiting adenylate cyclase activity, thereby reducing cAMP generation in vascular smooth muscle.…”

Section: Receptors and Intracellular Signalingmentioning

confidence: 99%

Role of Interstitial ATP and Adenosine in the Regulation of Renal Hemodynamics and Microvascular Function

2004

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“…Adenosine traditionally signals through modulation of intracellular cAMP levels 16, 17. Activation of A 1 receptors suppresses cAMP formation and A 2 receptor activation increases cAMP production.…”

Section: Signaling Mechanismsmentioning

confidence: 99%

Mysteries of Renal Autoregulation

Inscho

2009

Hypertension

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A utoregulation is an important renal regulatory mechanism that provides an important protective role in glomerular hemodynamics. 1 The phenomenon of autoregulatory behavior has been recognized for many decades, but a clear understanding of the underlying mechanisms involved in mediating resistance adjustments remains to be established. As illustrated in Figure 1, pressure-mediated autoregulatory behavior operates by recognizing a change in renal perfusion pressure, or renal vascular transmural pressure, and initiating induction of autoregulatory resistance changes intended to stabilize renal blood flow and/or glomerular filtration rate. The net result is that renal blood flow and glomerular filtration rate remain relatively stable over a wide range of renal perfusion pressures. Autoregulatory behavior is exquisitely sensitive in healthy normal kidneys but significantly less efficient in pathological settings, such as diabetes mellitus and some forms of hypertension. Complete loss of autoregulatory control results in renal blood flow that behaves more passively, thus increasing variability and rendering flow more directly determined by renal perfusion pressure. 1,2 Whole kidney autoregulation reflects regulatory input from the myogenic and tubuloglomerular feedback mechanisms at the very least. [3][4][5][6][7] Recently, contributions of a third and possibly a fourth mechanism have been suggested. 6,7 Consequently, with continued study, the mechanisms underlying renal autoregulatory resistance adjustments are slowly becoming clearer. In addition to the P1 receptor hypothesis put forth to explain signal transduction for tubuloglomerular feedback-dependent resistance changes, we have explored the hypothesis that pressure-mediated autoregulatory responses are mediated by extracellular ATP and activation of P2X 1 receptors. 3,8,9 Conclusive identification of the signaling molecules that mediate autoregulation remains a point of debate, but it appears clear that the release of a purine-based moiety is required for autoregulatory adjustments in afferent arteriolar resistance. 3-5,8 -10 This review tries to focus on the new and current questions that need resolution regarding the P2 receptor hypothesis and how the tubuloglomerular feedback (TGF) system overlaps with those questions. For a more detailed discussion and review of the mechanisms of TGF and myogenic contributions to autoregulatory behavior, the reader is referred to several recent and excellent reviews that dwell more on the relative contributions of both systems to overall autoregulation.

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Adenosine receptors in the cardiovascular system

Cited by 30 publications

References 72 publications

Physiological role for P2X1 receptors in renal microvascular autoregulatory behavior

Physiological role for P2X1 receptors in renal microvascular autoregulatory behavior

Role of Interstitial ATP and Adenosine in the Regulation of Renal Hemodynamics and Microvascular Function

Mysteries of Renal Autoregulation

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