Regiane Miranda-Ferreira

TL;DR: SHR cells have faster and larger catecholamine release responses, explained by more vesicle ready to undergo exocytosis and greater quantal content of vesicles, which could have relevance to further understand the pathogenic mechanisms involved in the development of high blood pressure, as well as in the identification of new drug targets to treat hypertension.

TL;DR: Differences in Ca2+ entry and its subsequent redistribution into the ER and mitochondria are not responsible for the greater secretion seen in SHRs compared with control cells; rather, such differences seem to be due to greater quantal content of spike bursts and to greaterquantal size of individual amperometric events.

TL;DR: The results reveal that in the development of hypertension in diabetic rats, augmentation of circulating ACE activity precedes the sympathetic dysfunction and it seems that the purinergic and noradrenergic neurotransmission is compromised.

TL;DR: Enhanced mitochondrial Ca(2+) cycling may be the basis for the dysfunction of mitochondrial bioenergetics, reported to be present in hypertensive states.

TL;DR: The results suggested that ischemic preconditioning attenuated intestinal dysfunction caused by I and I/R suggested that the jejunal enteric nerves were damaged in the I + SS and the I-R + SS groups, but not inThe IPC groups.