Acute in vivo analysis of ATP release in rat kidneys in response to changes of renal perfusion pressure

Research output: Contribution to journalArticle

External Institution(s)

  • Medical College of Wisconsin

Details

Original languageEnglish (US)
Article numbere006658
JournalJournal of the American Heart Association
Volume6
Issue number9
StatusPublished - Sep 1 2017
Peer-reviewedYes

Abstract

Background-ATP and derivatives are recognized to be essential agents of paracrine signaling. It was reported that ATP is an important regulator of the pressure-natriuresis mechanism. Information on the sources of ATP, the mechanisms of its release, and its relationship to blood pressure has been limited by the inability to precisely measure dynamic changes in intrarenal ATP levels in vivo. Methods and Results-Newly developed amperometric biosensors were used to assess alterations in cortical ATP concentrations in response to changes in renal perfusion pressure (RPP) in anesthetized Sprague-Dawley rats. RPP was monitored via the carotid artery; ligations around the celiac/superior mesenteric arteries and the distal aorta were used for manipulation of RPP. Biosensors were acutely implanted in the renal cortex for assessment of ATP. Rise of RPP activated diuresis/natriuresis processes, which were associated with elevated ATP. The increases in cortical ATP concentrations were in the physiological range (1-3 μmol/L) and would be capable of activating most of the purinergic receptors. There was a linear correlation with every 1-mm Hg rise in RPP resulting in a 70-nmol/L increase in ATP. Furthermore, this elevation of RPP was accompanied by a 2.5-fold increase in urinary H2O2. Conclusions-Changes in RPP directly correlate with renal sodium excretion and the elevation of cortical ATP. Given the known effects of ATP on regulation of glomerular filtration and tubular transport, the data support a role for ATP release in the rapid natriuretic responses to acute increases in RPP.

    Research areas

  • ATP, Hypertension, Kidney, P2 receptors, Pressure natriuresis, Purinergic signaling, Renal