Interplay of the adenosine system and NO in control of renal haemodynamics and excretion: Comparison of normoglycaemic and streptozotocin diabetic rats

Nitric Oxide. 2020 Nov 1:104-105:20-28. doi: 10.1016/j.niox.2020.08.003. Epub 2020 Aug 20.

Abstract

The adenosine (Ado) system may participate in regulation of kidney function in diabetes mellitus (DM), therefore we explored its role and interrelation with NO in the control of renal circulation and excretion in normoglycemic (NG) and streptozotocin-diabetic (DM) rats. Effects of theophylline (Theo), a non-selective Ado receptor antagonist, were examined in anaesthetized NG or in streptozotocin induced diabetic (DM) rats, untreated or after blockade of NO synthesis with l-NAME. We measured arterial blood pressure (MABP), whole kidney blood flow and renal regional flows: cortical and outer- and inner-medullary (IMBF), determined as laser-Doppler fluxes. Renal excretion of water, total solutes and sodium and in situ renal tissue NO signal (selective electrodes) were also determined. Theo experiments disclosed minor baseline vasoconstrictor and vasodilator tone in the kidney of NG and DM rats, respectively. NO blockade increased baseline MABP and decreased renal haemodynamics, similarly in NG and DM rats, indicating comparable vasodilator influence of NO in the two groups. Unexpectedly, in all rats with intact NO synthesis, Ado receptor blockade increased kidney tissue NO. In NO-deficient NG and DM rats, Ado receptor blockade induced comparable renal vasodilatation, suggesting similar vasoconstrictor influence of the Ado system. However, DM rats showed an unexplained association of decreased MABP and IMBF and increased NO signal. Higher baseline renal excretion in DM rats indicated inhibition of renal tubular reabsorption due to the prevalence of natriuretic A2 over antinatriuretic A1 receptors. In conclusion, the experiments provided new insights in functional interrelation of adenosine and NO in normoglycaemia and streptozotocin-diabetes.

Keywords: Adenosine receptors; Hyperglycaemia; Nitric oxide; Renal blood flow; Streptozotocin; l-NAME.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine / metabolism*
  • Animals
  • Arterial Pressure / drug effects
  • Diabetes Mellitus, Experimental / chemically induced
  • Diabetes Mellitus, Experimental / metabolism*
  • Enzyme Inhibitors / pharmacology
  • Kidney / metabolism*
  • Male
  • NG-Nitroarginine Methyl Ester / pharmacology
  • Nitric Oxide / antagonists & inhibitors
  • Nitric Oxide / metabolism*
  • Nitric Oxide Synthase / antagonists & inhibitors
  • Purinergic P1 Receptor Antagonists / pharmacology
  • Rats, Sprague-Dawley
  • Receptor, Adenosine A1 / metabolism
  • Receptors, Adenosine A2 / metabolism
  • Renal Circulation / drug effects*
  • Renal Elimination / drug effects*
  • Streptozocin
  • Theophylline / pharmacology

Substances

  • Enzyme Inhibitors
  • Purinergic P1 Receptor Antagonists
  • Receptor, Adenosine A1
  • Receptors, Adenosine A2
  • Nitric Oxide
  • Streptozocin
  • Theophylline
  • Nitric Oxide Synthase
  • Adenosine
  • NG-Nitroarginine Methyl Ester