Humoral effects of selective adenosine agonists in spontaneously hypertensive rats

Carla Sala, Angela Monopoli, Cristina Alberti, Carlo Casati, Ennio Ongini, Alberto Zanchetti, Alberto Morganti

Research output: Contribution to journalArticlepeer-review

Abstract

Objective. We studied the dose-response effects of acute administration of the selective A1 adenosine receptor agonist 2-chloro-N6-cyclopentyladenosine (CCPA), the selective A(2A) agonists 2-hexynyl-5'-N-ethylcarboxamidoadenosine (2HE-NECA) and 2-[4-(2-carboxyethyl)phenethylamino]-5'-N-ethylcarboxamidoadenosine (CGS 21680) and the non-selective agonist N-ethylcarboxamidoadenosine (NECA) on plasma renin activity, atrial natriuretic peptide, cyclic guanosine 3',5'-monophosphate (cGMP) and endothelin-1 in spontaneously hypertensive rats. Methods. The drugs were administered intraperitoneally in four doses to conscious rats. Systolic blood pressure and heart rate were measured by the tail-cuff technique. Both humoral and hemodynamic parameters were determined 1 h after dosing in separate sets of animals. Results. All the compounds induced a dose-dependent decrease in systolic blood pressure that was associated with different changes in heart rate. Heart rate was decreased by all doses of CCPA and by the higher doses of the non-selective compound (NECA) and increased by both A(2A) agonists. Plasma renin activity also changed in opposite directions, being decreased increased dose-dependently by 21680 and only moderately by NECA. Plasma natriuretic peptide and cGMP levels increased dependently after CCPA and NECA, but were unaffected by the A(2A) agonists. None of the compounds altered plasma endothelin-1 levels. Conclusions. These results indicate that the renin-suppressive effect of the A1 agonist, which is associated with a cardiodepressant action, may be attributed either to a direct inhibition of renin release or to the concomitant increments in plasma atrial natriuretic peptide and its second messenger, cGMP. In contrast, the renin-stimulating effect of the A(2A) agonists may result either from direct stimulation of renin secretion or from reflex sympathetic activation secondary to the fall in blood pressure.

Original languageEnglish
Pages (from-to)75-79
Number of pages5
JournalJournal of Hypertension
Volume14
Issue number1
Publication statusPublished - 1996

Keywords

  • Adenosine agonists
  • Atrial natriuretic peptide
  • Cyclic guanosine 3',5'-monophosphate
  • Endothelin-1
  • Plasma renin activity
  • Spontaneously hypertensive rats

ASJC Scopus subject areas

  • Endocrinology
  • Internal Medicine

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