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Although 5HT 2A  receptors mediate contractions of normal arteries to serotonin (5HT), in some cardiovascular diseases, other receptor subtypes contribute to the marked increase in serotonin contractions. We hypothesized that enhanced contractions of arteries from diabetics to 5HT are mediated by an increased contribution from multiple 5HT receptor subtypes. We compared responses to selective 5HT receptor agonists and expression of 5HT receptor isoforms (5HT 1B , 5HT 2A , and 5HT 2B ) in aorta from nondiabetic (ND) compared to type 2 diabetic mice (DB, BKS.Cg- Dock7    m  +/+ Lepr db  /J). 5HT, 5HT 2A  (TCB2 and BRL54443), and 5HT 2B  (norfenfluramine and BW723C86) receptor agonists produced concentration-dependent contractions of ND arteries that were markedly increased in DB arteries. Neither ND nor DB arteries contracted to a 5HT 1B  receptor agonist. MDL11939, a 5HT 2A  receptor antagonist, and LY272015, a 5HT 2B  receptor antagonist, reduced contractions of arteries from DB to 5HT more than ND. Expression of 5HT 1B , 5HT 2A , and 5HT 2B  receptor subtypes was similar in ND and DB. Inhibition of rho kinase decreased contractions to 5HT and 5HT 2A  and 5HT 2B  receptor agonists in ND and DB. We conclude that in contrast to other cardiovascular diseases, enhanced contraction of arteries from diabetics to 5HT is not due to a change in expression of multiple 5HT receptor subtypes.

experimental diabetes research

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5HT2Aand5HT2