Natriuretic peptides like NO facilitate cardiac vagal neurotransmission and bradycardia via a cGMP pathway
Natriuretic peptides like NO facilitate cardiac vagal neurotransmission and bradycardia via a cGMP pathway
复制标题
DOI：
10.1152/ajpheart.2001.281.6.h2318
复制
发表时间：
2001-12-01
影响因子：
4.8
通讯作者：
Paterson, DJ
中科院分区：
文献类型：
--
作者：
Herring, N;Zaman, JAB;Paterson, DJ
我们测试了这样一个假设，即与cGMP产生偶联的利钠肽受体（NPR）通过增强乙酰胆碱释放和迷走神经诱导的心动过缓以类似于一氧化氮（NO）的方式起作用。在离体豚鼠心房-右迷走神经制备物中评价酶抑制剂和通道阻滞剂对心房利钠肽（ANP）、脑源性利钠肽（BNP）和C型利钠肽（CNP）作用的影响。RT-PCR证实豚鼠窦房结组织中存在NPR B和A受体mRNA。BNP和CNP显著升高（P
We tested the hypothesis that natriuretic peptide receptors (NPRs) that are coupled to cGMP production act in a similar way to nitric oxide (NO) by enhancing acetylcholine release and vagal-induced bradycardia. The effects of enzyme inhibitors and channel blockers on the action of atrial natriuretic peptide (ANP), brain-derived natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) were evaluated in isolated guinea pig atrial-right vagal nerve preparations. RT-PCR confirmed the presence NPR B and A receptor mRNA in guinea pig sinoatrial node tissue. BNP and CNP significantly (P