Nitric oxide up-regulates the expression of calcium-dependent potassium channels in the supraoptic nuclei and neural lobe of rats following dehydration

2006 ◽  
Vol 404 (1-2) ◽  
pp. 50-55 ◽  
Author(s):  
Massako Kadekaro ◽  
Guangxiao Su ◽  
Rong Chu ◽  
Yongzhong Lei ◽  
Junfa Li ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Potassium Channels ◽  
Neural Lobe ◽  
Calcium Dependent ◽  
Supraoptic Nuclei

Enhanced role of potassium channels in relaxations to acetylcholine in hypercholesterolemic rabbit carotid artery

1994 ◽  
Vol 266 (5) ◽  
pp. H2061-H2067 ◽  
Author(s):  
S. Najibi ◽  
C. L. Cowan ◽  
J. J. Palacino ◽  
R. A. Cohen
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Carotid Artery ◽  
Potassium Channels ◽  
Abdominal Aorta ◽  
Combined Treatment ◽  
Rabbit Carotid Artery ◽  
Calcium Dependent ◽  
Endothelium Dependent Relaxation

The effect of hypercholesterolemia for 10 wk on endothelium-dependent relaxations to acetylcholine was studied in isolated rings of rabbit carotid artery and abdominal aorta contracted with phenylephrine or elevated potassium. In these arteries obtained from hypercholesterolemic rabbits, endothelium-dependent relaxations to acetylcholine were not significantly different from those of normal rabbits. In normal and hypercholesterolemic arteries, partial relaxation persisted in the presence of NG-nitro-L-arginine methyl ester (L-NAME), which blocked acetylcholine-induced increases in arterial guanosine 3',5'-cyclic monophosphate (cGMP). Combined treatment with L-NAME and the calcium-dependent potassium-channel inhibitor, charybdotoxin, blocked relaxations in both groups, suggesting that L-NAME-resistant relaxations are mediated by an endothelium-derived hyperpolarizing factor. Charybdotoxin alone or depolarizing potassium had no significant effect on normal carotid artery or normal and hypercholesterolemic abdominal aorta but significantly inhibited relaxations of the carotid artery from cholesterol-fed rabbits. The enhanced role of calcium-dependent potassium channels and the hyperpolarizing factor in relaxation of the hypercholesterolemic carotid artery suggested by these results was likely related to the fact that acetylcholine failed to stimulate cGMP only in that artery. These data suggest that endothelium-dependent relaxation in these rabbit arteries is mediated by nitric oxide-cGMP-dependent and -independent mechanisms. In hypercholesterolemia, the contribution of nitric oxide-cGMP in the carotid artery is reduced, but a hyperpolarizing factor and calcium-dependent potassium channels maintain normal acetylcholine-induced relaxation.

Nitric oxide directly activates calcium-dependent potassium channels in vascular smooth muscle

Nature ◽  
1994 ◽  
Vol 368 (6474) ◽  
pp. 850-853 ◽  
Author(s):  
Victoria M. Bolotina ◽  
Soheil Najibi ◽  
James J. Palacino ◽  
Patrick J. Pagano ◽  
Richard A. Cohen
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Potassium Channels ◽  
Vascular Smooth Muscle ◽  
Calcium Dependent

Calcium-activated potassium channels and nitric oxide coregulate estrogen-induced vasodilation

2000 ◽  
Vol 279 (1) ◽  
pp. H319-H328 ◽  
Author(s):  
Charles R. Rosenfeld ◽  
Richard E. White ◽  
Tim Roy ◽  
Blair E. Cox
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Potassium Channels ◽  
Uterine Artery ◽  
Single Channel ◽  
Open Probability ◽  
Calcium Dependent ◽  
Calcium Activated Potassium Channels ◽  
Artery Flow ◽  
Oxide Synthase

Nitric oxide synthase (NOS) contributes to estradiol-17β (E2β)-induced uterine vasodilation, but additional mechanisms are involved, and the cellular pathways remain unclear. We determined if 1) uterine artery myocytes express potassium channels, 2) E2β activates these channels, and 3) channel blockade plus NOS inhibition alters E2β-induced uterine vasodilation. Studies of cell-attached patches identified a 107 ± 7 pS calcium-dependent potassium channel (BKCa) in uterine artery myocytes that rapidly increased single-channel open probability 70-fold ( P < 0.05) after exposure to 100 nM E2β through an apparent cGMP-dependent mechanism. In ovariectomized nonpregnant ewes ( n = 11) with uterine artery flow probes and catheters, local BKCa blockade with tetraethylammonium (TEA; 0.05–0.6 mM) dose dependently inhibited E2β-induced uterine vasodilation ( n = 37, R = 0.77, P < 0.0001), with maximum inhibition averaging 67 ± 11%. Mean arterial pressure (MAP) and E2β-induced increases ( P ≤ 0.001) in heart rate (13%) and contralateral uterine blood flow (UBF, ∼5-fold) were unaffected. Local NOS inhibition plus BKCa blockade, using submaximal doses of nitro-l-arginine methyl ester (5 mg/ml) and TEA (0.3 mM), did not alter basal UBF but completely inhibited ipsilateral E2β-induced uterine vasodilation without affecting MAP and E2β-induced increases in contralateral UBF and heart rate. Acute E2β-mediated uterine vasodilation involves rapid activation of uterine artery BKCa and NOS, and the pathway for their interaction appears to include activation of guanylyl cyclase.

scholarly journals Quercetin relaxes human gastric smooth muscles directly through ATP‐sensitive potassium channels and not depending on the nitric oxide pathway

2021 ◽  
Author(s):  
Beata Modzelewska ◽  
Krzysztof Drygalski ◽  
Tomasz Kleszczewski ◽  
Andrzej Chomentowski ◽  
Krzysztof Koryciński ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Potassium Channels ◽  
Smooth Muscles ◽  
Nitric Oxide Pathway

Hypovolemia upregulates the expression of neuronal nitric oxide synthase gene in the paraventricular and supraoptic nuclei of rats

1998 ◽  
Vol 790 (1-2) ◽  
pp. 25-32 ◽  
Author(s):  
Yoichi Ueta ◽  
Andrew Levy ◽  
Stafford L. Lightman ◽  
Yuko Hara ◽  
Ryota Serino ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Supraoptic Nuclei

scholarly journals Dissection of a Hypoxia-induced, Nitric Oxide–mediated Signaling Cascade

2009 ◽  
Vol 20 (18) ◽  
pp. 4083-4090 ◽  
Author(s):  
Pascale F. Dijkers ◽  
Patrick H. O'Farrell
Keyword(s):  
Nitric Oxide ◽  
Signal Transduction ◽  
Signaling Cascade ◽  
S2 Cells ◽  
Signal Transduction System ◽  
Signaling Systems ◽  
Calcium Dependent ◽  
Drosophila S2 Cells ◽  
Oxide Synthase ◽  
Multiple Signaling

Befitting oxygen's key role in life's processes, hypoxia engages multiple signaling systems that evoke pervasive adaptations. Using surrogate genetics in a powerful biological model, we dissect a poorly understood hypoxia-sensing and signal transduction system. Hypoxia triggers NO-dependent accumulation of cyclic GMP and translocation of cytoplasmic GFP-Relish (an NFκB/Rel transcription factor) to the nucleus in Drosophila S2 cells. An enzyme capable of eliminating NO interrupted signaling specifically when it was targeted to the mitochondria, arguing for a mitochondrial NO signal. Long pretreatment with an inhibitor of nitric oxide synthase (NOS), L-NAME, blocked signaling. However, addition shortly before hypoxia was without effect, suggesting that signaling is supported by the prior action of NOS and is independent of NOS action during hypoxia. We implicated the glutathione adduct, GSNO, as a signaling mediator by showing that overexpression of the cytoplasmic enzyme catalyzing its destruction, GSNOR, blocks signaling, whereas knockdown of this activity caused reporter translocation in the absence of hypoxia. In downstream steps, cGMP accumulated, and calcium-dependent signaling was subsequently activated via cGMP-dependent channels. These findings reveal the use of unconventional steps in an NO pathway involved in sensing hypoxia and initiating signaling.

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