Amazonian trees have limited capacity to acclimate plant hydraulic properties in response to long‐term drought

This is the author accepted manuscript. The final version is available from Wiley via the DOI in this recordThe fate of tropical forests under future climate change is dependent on the capacity of their trees to adjust to drier conditions. The capacity of trees to withstand drought is likely to be determined by traits associated with their hydraulic systems. However, data on whether tropical trees can adjust hydraulic traits when experiencing drought remain rare. We measured plant hydraulic traits (e.g. hydraulic conductivity and embolism resistance) and plant hydraulic system status (e.g. leaf water potential, native embolism and safety margin) on >150 trees from 12 genera (36 species) and spanning a stem size range from 14 to 68 cm diameter at breast height (DBH) at the world's only long‐running tropical forest drought experiment. Hydraulic traits showed no adjustment following 15 years of experimentally imposed moisture deficit. This failure to adjust resulted in these drought‐stressed trees experiencing significantly lower leaf water potentials, and higher, but variable, levels of native embolism in the branches. This result suggests that hydraulic damage caused by elevated levels of embolism is likely to be one of the key drivers of drought‐induced mortality following long‐term soil moisture deficit. We demonstrate that some hydraulic traits changed with tree size, however, the direction and magnitude of the change was controlled by taxonomic identity. Our results suggest that Amazonian trees, both small and large, have limited capacity to acclimate their hydraulic systems to future droughts, potentially making them more at risk of drought‐induced mortality.Natural Environment Research Council (NERC)Brazilian Higher Education Coordination Agency (CAPES)Royal SocietyEuropean Union FP7ARCFAPESP/Microsof

Phentolamine relaxes human corpus cavernosum by a nonadrenergic mechanism activating ATP-sensitive K+ channel

To investigate the pharmacodynamics of phentolamine in human corpus cavernosum (HCC) with special attention to the role of the K+ channels. Strips of HCC precontracted with nonadrenergic stimuli and kept in isometric organ bath immersed in a modified Krebs - Henseleit solution enriched with guanethidine and indomethacine were used in order to study the mechanism of the phentolamine-induced relaxation. Phentolamine caused relaxation (approximate to50%) in HCC strips precontracted with K+ 40 mM. This effect was not blocked by tetrodotoxin ( 1 muM) (54.6 +/- 4.6 vs 48.9 +/- 6.4%) or (atropine ( 10 muM) (52.7 +/- 6.5 vs 58.6 +/- 5.6%). However, this relaxation was significantly attenuated by L-NAME (100 muM) (59.7 +/- 5.8 vs 27.8 +/- 7.1%; P<0.05; n = 8) and ODQ (100 &mu;M) (62.7 +/- 5.1 vs 26.8 +/- 3.9%; P<0.05; n = 8). Charybdotoxin and apamin (K-Ca-channel blockers) did not affect the phentolamine relaxations (54.6 +/- 4.6 vs 59.3 +/- 5.2%). Glibenclamide (100 muM), an inhibitor of K-ATP-channel, caused a significant inhibition (56.7 +/- 6.3 vs 11.3 +/- 2.3%; P<0.05; n = 8) of the phentolamine-induced relaxation. In addition, the association of glibenclamide and L-NAME almost abolished the phentolamine-mediated relaxation (54.6 +/-5.6 vs 5.7 +/- 1.4%; P<0.05; n = 8). The results suggest that phentolamine relaxes HCC by a nonadrenergic noncholinergic mechanism dependent on nitric oxide synthase activity and activation of K-ATP-channel.171273