RESUMO
Previous studies have shown that individuals with autism spectrum disorder (ASD) demonstrate poorer driving performance than their peers and are less likely to obtain a driver's license. This study aims to examine the relationship between driving performance and executive functioning for novice drivers, with and without ASD, using a driving simulator. Forty-four males (ages 15-23), 17 with ASD and 27 healthy controls, completed paradigms assessing driving skills and executive functioning. ASD drivers demonstrated poorer driving performance overall and the addition of a working memory task resulted in a significant decrement in their performance relative to control drivers. Results suggest that working memory may be a key mechanism underlying difficulties demonstrated by ASD drivers and provides insight for future intervention programs.
Assuntos
Transtorno do Espectro Autista/psicologia , Condução de Veículo/psicologia , Função Executiva , Destreza Motora , Adolescente , Estudos de Casos e Controles , Simulação por Computador , Feminino , Humanos , Masculino , Memória de Curto Prazo , Adulto JovemRESUMO
OBJECTIVES: To identify the receptors by which endothelin-1 (ET-1) increases venomotor tone in hypertension. METHODS: Vascular reactivity to ET-1 and the selective endothelin receptor subtype B (ET(B)) agonist, sarafotoxin 6c (S6c), was studied in mesenteric blood vessels from deoxycorticosterone acetate (DOCA-salt) hypertensive and normotensive control rats. The diameter of small (< or = 280 microm) mesenteric arteries and veins was monitored in vitro using computer-assisted video microscopy. Contractions of mesenteric arteries (< or= 250 microm diameter) were also studied, using a myograph. ET-1 mRNA levels were measured in mesenteric arteries and veins using real-time RT-PCR techniques. RESULTS: ET-1-induced contractions were reduced in arteries of DOCA-salt hypertensive rats compared with those of normotensive control rats; S6c produced negligible contractions in arteries from both groups. ET-1 concentration-responses curves in arteries measured using video microscopy or a myograph were similar. ET-1 and S6c caused veins to contract, and there were no differences between responses to these agonists in tissues from DOCA-salt hypertensive rats or normotensive control rats. Studies using ET(A) and ET(B) receptor antagonists indicated that ET-1-induced venoconstriction was mediated by ET(A) receptors. Potassium chloride concentration-response curves were similar in arteries and veins from normotensive control rats and DOCA-salt hypertensive rats. ET-1 mRNA levels in DOCA-salt hypertensive rat arteries or veins were not different from those in normotensive control rat arteries and veins. CONCLUSIONS: These data indicate that ET-1 reactivity is maintained in mesenteric veins, but not arteries, in DOCA-salt hypertension. Therefore, the sustained increase in venomotor tone mediated by ET(A) receptors that is known to occur in vivo in DOCA-salt hypertensive rats is not caused by direct venoconstriction.