Endothelial nitric oxide synthase is predominantly involved in angiotensin II modulation of renal vascular resistance and norepinephrine release

摘要

In contrast to the important impact of NO in regulation of renal blood flow, not much is known about its role in modulating presynaptic neurotransmitter release (9). New studies suggested an important role of NO in modulating presynaptic sympathetic neurotransmitter release, whereas NO generated by angiotensin II increased norepinephrine release in mice kidneys and rat atrium (7, 28, 31). However, it is still unclear which isoform of NOS is generating presynaptic active NO. Thus, the aims of our study were 1) to assess the predominant NOS responsible for generating NO and counteracting angiotensin H-induced changes in pressor response in mice kidney; and 2) to confirm the important role of NO in modulating renal neurotransmitter release and investigate the NO synthase responsible for generating the presynaptic active NO. To perform experiments studying effects assigned to either eNOS or nNOS, we investigated kidneys of mice that are homozygous (-/-) for disruption of the eNOS or nNOS gene.