Inhibitory effect of organotin compounds on rat neuronal nitric oxide synthase through interaction with calmodulin

2004 ◽  
Vol 324 (1) ◽  
pp. 178-185 ◽  
Author(s):  
Koji Ohashi ◽  
Shiro Kominami ◽  
Takeshi Yamazaki ◽  
Shigeru Ohta ◽  
Shigeyuki Kitamura
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Inhibitory Effect ◽  
Organotin Compounds ◽  
Oxide Synthase

Relationship between structure and inhibitory effect of arginine analogues on neuronal nitric oxide synthase activity

1996 ◽  
Vol 21 (10) ◽  
pp. 1187-1192 ◽  
Author(s):  
Isao Yokoi ◽  
Yukiko Namba ◽  
Hideaki Kabuto ◽  
Kazunori Inada ◽  
Motoyuki Iida ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Inhibitory Effect ◽  
Oxide Synthase ◽  
Nitric Oxide Synthase Activity

scholarly journals Neuronal nitric oxide synthase regulation of calcium cycling in ventricular cardiomyocytes is independent of Cav1.2 channel modulation under basal conditions

2019 ◽  
Vol 472 (1) ◽  
pp. 61-74 ◽  
Author(s):  
Janine Ebner ◽  
Michal Cagalinec ◽  
Helmut Kubista ◽  
Hannes Todt ◽  
Petra L. Szabo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Single Channel ◽  
Neuronal Nitric Oxide Synthase ◽  
Inhibitory Effect ◽  
Open Probability ◽  
No Donor ◽  
Ventricular Cardiomyocytes ◽  
Nos Inhibitors ◽  
Oxide Synthase

AbstractNeuronal nitric oxide synthase (nNOS) is considered a regulator of Cav1.2 L-type Ca2+ channels and downstream Ca2+ cycling in the heart. The commonest view is that nitric oxide (NO), generated by nNOS activity in cardiomyocytes, reduces the currents through Cav1.2 channels. This gives rise to a diminished Ca2+ release from the sarcoplasmic reticulum, and finally reduced contractility. Here, we report that nNOS inhibitor substances significantly increase intracellular Ca2+ transients in ventricular cardiomyocytes derived from adult mouse and rat hearts. This is consistent with an inhibitory effect of nNOS/NO activity on Ca2+ cycling and contractility. Whole cell currents through L-type Ca2+ channels in rodent myocytes, on the other hand, were not substantially affected by the application of various NOS inhibitors, or application of a NO donor substance. Moreover, the presence of NO donors had no effect on the single-channel open probability of purified human Cav1.2 channel protein reconstituted in artificial liposomes. These results indicate that nNOS/NO activity does not directly modify Cav1.2 channel function. We conclude that—against the currently prevailing view—basal Cav1.2 channel activity in ventricular cardiomyocytes is not substantially regulated by nNOS activity and NO. Hence, nNOS/NO inhibition of Ca2+ cycling and contractility occurs independently of direct regulation of Cav1.2 channels by NO.

Inhibitory effect of melatonin on nitric oxide synthase in rat enteric nervous system

2001 ◽  
Vol 120 (5) ◽  
pp. A176-A176
Author(s):  
P KOPPITZ ◽  
M STORR ◽  
D SAUR ◽  
M KURJAK ◽  
H ALLESCHER
Keyword(s):  
Nitric Oxide ◽  
Nervous System ◽  
Nitric Oxide Synthase ◽  
Enteric Nervous System ◽  
Inhibitory Effect ◽  
Oxide Synthase
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