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3. Mechanical removal of the endothelium did not significantly (P= 0.06) increase the pD2 for 5-HT; however, the maximal responses were significantly greater at 22��C (Fig. 3A and Table 2). The magnitude of the increase in the maximal response to 5-HT after cooling was greater in endothelium-denuded vessels (22��C, 269.2 �� 26% DKS versus 30��C, 172.2 �� 20% DKS; n= 6; Fig. 3A) compared with endothelium-intact vessels (22��C, 217.0 �� 19% DKS versus 30��C, 169.8 �� 19% DKS; n= 6). However, the absolute values for the maximal response at each temperature were not statistically significant when intact and denuded arteries were compared. Treatment with the combination of l-NAME (300 ��m) plus ibuprofen (10 ��m) caused a significant check details (P Montelukast Sodium 35.0 �� 10% DKS) and 22��C (control, 11.0 �� 4.3% DKS versus?l-NAME/ibuprofen, 78.5 �� 27% DKS). However, there was no significant (P= 0.14) difference in the contraction evoked by l-NAME/ibuprofen between temperatures. The concentration�Cresponse curves to 5-HT were similar in the presence of l-NAME/ibuprofen at both 30 and 22��C (Fig. 3B and Table 2). In untreated vessels, the response to CCh was also similar (P= 0.50) at both temperatures (Fig. 4A). In contrast, the l-NAME + ibuprofen-resistant response was significantly reduced in cooled vessels. When the arteries were precontracted with phenylephrine (10 ��m), the response to CCh at the two temperatures was again not significantly different (P= 0.77). However, under phenylephrine-induced tone, the l-NAME + ibuprofen-resistant response was of a similar magnitude at both temperatures (Fig. 4B). This study assessed the in vitro reactivity of isolated equine small lamellar arteries, enabling the effects of vasoconstrictor and vasodilator agents to be compared at two different temperatures. The response of the small lamellar arteries was characterized by a cooling-induced inhibition of the contractile machinery, as demonstrated by the reduction of the peak height response to DKS (118 mm KCl) and a reduction of the ��-adrenoceptor-mediated response. In contrast, the response to 5-HT was enhanced by cooling. Moreover, the cooling-enhanced effect of 5-HT was augmented when the endothelium EPZ6438 was denuded, suggesting a potential modulating role of the endothelium in these arteries. Physiologically, inhibition of cooling-enhanced contraction by the endothelium in the small lamellar arteries may help to maintain the blood flow to the digit by preventing changes in vascular resistance. Nevertheless, the response evoked by 5-HT was still enhanced by cooling to some extent, even in the presence of a functional endothelium, suggesting that the activation of 5-HT receptors and their downstream cellular signals may be more resistant to the ��stress�� caused by reductions in temperature than other receptor systems.