Meng‐Ru ‐R Shen, Joel Linden, Shun‐Sheng ‐S Chen, Sheng‐Nan ‐N Wu*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

33 Scopus citations


1. The effects of adenosine receptor agonists and antagonists on human sperm motility have been studied. Specific binding sites for adenosine and its analogues on human sperm were also investigated. 2. Agonists stimulated human sperm motility in a dose‐dependent manner with a potency order of 5'‐N‐ethylcarboxamidoadenosine (NECA, EC50= 0.3 μmol/L)>2‐[p‐(carboxyethyl)phenylethylamino]‐5'‐N‐ethylcarboxamidoadenosine(CGS‐21680, EC50= 10 μmol/L)> adenosine (EC50= 100 μmol/L). 3. NECA‐stimulated motility was competitively inhibited by various adenosine receptor antagonists. The potency order was 3,7‐dimethy‐l‐propargylxanthine>8‐(p‐sulfophenyl) theophylline > xanthine amino congener. 4. The radioligand [3H]‐NECA bound to sperm membrane in a saturable manner with a Bmax of 21.3 pmol/mg protein and equilibrium Kd of 4 μmol/L. Adenosine agonists and antagonists competed for [3H]‐NECA binding with the same rank order of potency as for the stimulation of human sperm motility. 5. GTPγs inhibited 63% of specific [3H]‐NECA binding with IC50 value of 11 nmol/L. This suggests that the [3H]‐NECA binding sites may be coupled to one or more G proteins. 6. These results indicate the presence of adenosine A2 receptors on human sperm which are responsible for adenosine‐mediated enhancement of sperm motility.

Original languageEnglish
Pages (from-to)527-534
Number of pages8
JournalClinical and Experimental Pharmacology and Physiology
Issue number7-8
StatePublished - 08 1993
Externally publishedYes


  • adenosine
  • receptor
  • sperm motility.


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