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P2Y2 and renin

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https://www.readbyqxmd.com/read/25154328/regulation-of-na-excretion-and-arterial-blood-pressure-by-purinergic-signalling-intrinsic-to-the-distal-nephron-consequences-and-mechanisms
#1
REVIEW
E Mironova, N Boiko, V Bugaj, V Kucher, J D Stockand
Discretionary control of Na(+) excretion is a key component of the regulation of arterial blood pressure in mammals. Sodium excretion is fine-tuned in the aldosterone-sensitive distal nephron by the activity of the epithelial Na(+) channel (ENaC). Here, ENaC functions as a final effector of the renin-angiotensin-aldosterone system (RAAS) during negative feedback control of blood pressure. Mutations affecting ENaC activity and abnormal regulation of this channel affect blood pressure through pathological changes to Na(+) excretion...
January 2015: Acta Physiologica
https://www.readbyqxmd.com/read/22143248/intrinsic-control-of-sodium-excretion-in-the-distal-nephron-by-inhibitory-purinergic-regulation-of-the-epithelial-na-channel
#2
REVIEW
Glenn M Toney, Volker Vallon, James D Stockand
PURPOSE OF REVIEW: This review summarizes the new evidence for an intrinsic control system in the aldosterone-sensitive distal nephron in which purinergic signaling regulates sodium transport and governs renal sodium excretion. RECENT FINDINGS: Electrophysiological studies identify epithelial Na(+) channels (ENaC) as final effectors of purinergic signaling via P2Y(2) receptors in the distal nephron. Inhibition of ENaC by autocrine/paracrine purinergic signaling reduces sodium reabsorption allowing an appropriately graded pressure-natriuresis response when delivery of sodium to the distal nephron is high...
January 2012: Current Opinion in Nephrology and Hypertension
https://www.readbyqxmd.com/read/17575258/mice-lacking-p2y2-receptors-have-salt-resistant-hypertension-and-facilitated-renal-na-and-water-reabsorption
#3
Timo Rieg, Richard A Bundey, Yu Chen, George Deschenes, Wolfgang Junger, Paul A Insel, Volker Vallon
Extracellular nucleotides (e.g., ATP) regulate many physiological and pathophysiological processes through activation of nucleotide (P2) receptors in the plasma membrane. Here we report that gene-targeted (knockout) mice that lack P2Y2 receptors have salt-resistant arterial hypertension in association with an inverse relationship between salt intake and heart rate, indicating intact baroreceptor function. Knockout mice have multiple alterations in their handling of salt and water: these include suppressed plasma renin and aldosterone concentrations, lower renal expression of the aldosterone-induced epithelial sodium channel alpha-ENaC, greater medullary expression of the Na-K-2Cl-cotransporter NKCC2, and greater furosemide-sensitive Na+ reabsorption in association with greater renal medullary expression of aquaporin-2 and vasopressin-dependent renal cAMP formation and water reabsorption despite similar vasopressin levels compared with wild type...
November 2007: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
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