Example sentences for: butaprost

How can you use “butaprost” in a sentence? Here are some example sentences to help you improve your vocabulary:

  • Incubation of EP 2 -transfected COS1 cells with butaprost free acid produced a concentration-dependent increase in cAMP accumulation with an EC 50 of 480 nM (Fig.

  • This mRNA expression pattern is similar to that of the EP 2 in the mouse [ 5 21 ] . PGE 2 has been reported to stimulate cAMP formation in many tissues, including intestine, microdissected renal tubule segments, and uterus via butaprost sensitive and insensitive receptors [ 14 26 27 28 29 ] . The mRNA expression results are consistent with these functional studies and suggest that the EP 2 receptor plays important roles in mediating PGE2 stimulated cAMP generation in these tissues [ 14 21 26 27 28 29 30 31 32 33 ] .

  • Finally, the EP 2 selective agonist butaprost free acid dose-dependently stimulated cAMP generation in COS-1 cells transfected with the rabbit EP 2 receptor.

  • Cells transfected with the vector alone demonstrated no significant increase in cAMP in response to butaprost free acid.

  • Prostaglandin E 2 is a major cyclooxygenase metabolite of arachidonic acid which exerts diverse effects on vascular smooth muscle tone and epithelial solute transport via G-protein coupled receptors [ 1 2 ] . At least four distinct G-protein coupled PGE 2 receptors have been cloned: the EP 1 , EP 2 , EP 3 , and EP 4 [ 1 ] . Pharmacological studies suggest PGE 2 relaxes vascular smooth muscle through two of these receptors, the EP 2 and EP 4 receptors, which couple to cyclic-AMP generation [ 3 ] . In contrast, PGE 2 constricts other vascular smooth muscle through EP 3 receptors which inhibit cAMP generation via G i or EP 1 receptors which increase Ca 2+mobilization [ 3 ] . Although both EP 2 and EP 4 receptors relax smooth muscle, EP 2 receptors are uniquely sensitive to the agonists butaprost and AH13205 [ 3 4 ] . Previous studies have shown that PGE 2 increases the cAMP concentration in many tissues including kidney, intestine and uterus, but the relative contribution of EP 2 versus EP 4 receptors to these effects is incompletely defined [ 5 6 ] . Recent studies in mice with targeted disruption of these receptors have suggested an important role for EP2 receptor in regulating systemic hemodynamics.


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