期刊
ACTA PHYSIOLOGICA
卷 203, 期 1, 页码 37-45出版社
WILEY
DOI: 10.1111/j.1748-1716.2010.02242.x
关键词
adenosine triphosphate; endothelium; hypertension; neuropeptide Y; nitric oxide; noradrenaline
类别
资金
- United States National Institutes of Health [HL61836, HL60260, NIGMS-GM083036]
- American Heart Association
Noradrenaline, neuropeptide Y and adenosine triphosphate are co-stored in, and co-released from, sympathetic nerves. Each transmitter modulates its own release as well as the release of one another; thus, anything affecting the release of one of these transmitters has consequences for all. Neurotransmission at the sympathetic neurovascular junction is also modulated by non-sympathetic mediators such as angiotensin II, serotonin, histamine, endothelin and prostaglandins through the activation of specific prejunctional receptors. In addition, nitric oxide (NO) has been identified as a modulator of sympathetic neuronal activity, both as a physiological antagonist against the vasoconstrictor actions of the sympathetic neurotransmitters, and also by directly affecting transmitter release. Here, we review the modulation of sympathetic neurovascular transmission by neuronal and non-neuronal mediators with an emphasis on the actions of NO. The consequences for co-transmission are also discussed, particularly in light of hypertensive states where NO availability is diminished.
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