IP3 Mediates Nitric Oxide–Guanosine 3′,5′-Cyclic Monophosphate (NO-cGMP)-Induced Isoflavone Accumulation in Soybean Sprouts under UV-B Radiation

2016 ◽  
Vol 64 (44) ◽  
pp. 8282-8288 ◽  
Author(s):  
Caifeng Jiao ◽  
Pei Wang ◽  
Runqiang Yang ◽  
Lu Tian ◽  
Zhenxin Gu
Keyword(s):  
Nitric Oxide ◽  
Cyclic Monophosphate ◽  
Soybean Sprouts

Heterogeneity in role of endothelium-derived NO in pulmonary arteries and veins of full-term fetal lambs

1995 ◽  
Vol 268 (4) ◽  
pp. H1586-H1592 ◽  
Author(s):  
Y. Gao ◽  
H. Zhou ◽  
J. U. Raj
Keyword(s):  
Nitric Oxide ◽  
Isometric Force ◽  
Pulmonary Veins ◽  
Pulmonary Arteries ◽  
Full Term ◽  
Fourth Generation ◽  
Cyclic Monophosphate ◽  
Arteries And Veins ◽  
Endothelium Dependent Relaxation

Endothelium-derived nitric oxide (EDNO) modulates fetal pulmonary vasoactivity. The role of EDNO in regulation of vasomotor tone in fetal pulmonary arteries vs. that in veins is not known. We have investigated the role of EDNO in the responses of pulmonary arteries and veins of full-term fetal lambs. Fourth-generation pulmonary arterial and venous rings were suspended in organ chambers filled with modified Krebs-Ringer bicarbonate solution (95% O2-5% CO2 at 37 degrees C), and their isometric force was measured. N omega-nitro-L-arginine had no effect on the resting tension of pulmonary arteries with endothelium but caused contraction of pulmonary veins with endothelium. The basal level of intracellular guanosine 3',5'-cyclic monophosphate (cGMP) of pulmonary veins with endothelium was higher than that of arteries with endothelium. In pulmonary arteries, bradykinin, but not acetylcholine, induced endothelium-dependent relaxation and an increase in cGMP content. In pulmonary veins, acetylcholine, but not bradykinin, induced endothelium-dependent relaxation and an increase in cGMP content. Agonist-induced maximal relaxation and increases in cGMP content were smaller in pulmonary arteries than in veins. All these endothelium-dependent responses were abolished by N omega-nitro-L-arginine. In tissues without endothelium, nitric oxide induced significantly less relaxation and less increase in cGMP content in pulmonary arteries than in pulmonary veins. All vessels relaxed similarly to 8-bromoguanosine 3',5'-cyclic monophosphate. Our data suggest that the role of EDNO in modulating tone differs between pulmonary arteries and veins in full-term fetal lambs.(ABSTRACT TRUNCATED AT 250 WORDS)

Hyporesponsiveness to inhaled nitric oxide in isolated, perfused lungs from endotoxin-challenged rats

1996 ◽  
Vol 271 (6) ◽  
pp. L981-L986 ◽  
Author(s):  
A. Holzmann ◽  
K. D. Bloch ◽  
L. S. Sanchez ◽  
G. Filippov ◽  
W. M. Zapol
Keyword(s):  
Nitric Oxide ◽  
Soluble Guanylate Cyclase ◽  
Sepsis Syndrome ◽  
Inhaled Nitric Oxide ◽  
Pulmonary Vasculature ◽  
Cyclic Monophosphate ◽  
Pulmonary Vasodilation ◽  
Lps Challenge ◽  
And Control ◽  
Selective Pulmonary Vasodilation

Inhaled nitric oxide (iNO) causes selective pulmonary vasodilation and improves oxygenation in patients with the adult respiratory distress syndrome (ARDS). Approximately 30% of ARDS patients fail to respond to iNO. Because sepsis syndrome often accompanies a decreased response to iNO, we investigated NO responsiveness in isolated, perfused lungs from rats exposed to lipopolysaccharide (LPS). Eighteen hours after intraperitoneal injection of 0.5 mg/kg LPS, rat lungs were isolated, perfused, and preconstricted with U-46619. Ventilation with 0.4, 4, and 40 parts per million by volume NO vasodilated LPS-pretreated lungs 75, 47, and 42% less than control lungs (P < 0.01 value differs at each concentration). The diminished vasodilatory response to iNO was associated with decreased NO-stimulated guanosine 3',5'-cyclic monophosphate (cGMP) release into the perfusate. Soluble guanylate cyclase activity did not differ in lung extracts from LPS-pretreated and control rats. LPS increased pulmonary cGMP-phosphodiesterase (PDE) activity by 40%. The PDE-sensitive cGMP analogue 8-bromoguanosine 3',5'-cyclic monophosphate vasodilated lungs from LPS-pretreated rats less than lungs from control rats. In contrast, the PDE-insensitive 8-para-chlorophenylthioguanosine 3',5'-cyclic monophosphate vasodilated lungs equally from both groups. After LPS challenge, the rat pulmonary vasculature becomes hyporesponsive to iNO. Hyporesponsiveness to iNO appears partly attributable to increased pulmonary cGMP-PDE activity.

Nitric oxide donors reduce the rise in reperfusion-induced intestinal mucosal permeability

1993 ◽  
Vol 265 (1) ◽  
pp. G189-G195 ◽  
Author(s):  
D. Payne ◽  
P. Kubes
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Ischemia Reperfusion ◽  
Intestinal Blood Flow ◽  
Mucosal Barrier ◽  
Barrier Dysfunction ◽  
Mucosal Permeability ◽  
Cyclic Monophosphate ◽  
Barrier Disruption ◽  
51Cr Edta

Recent data have demonstrated that inhibition of nitric oxide synthesis exacerbated the mucosal injury associated with reperfusion of the postischemic intestine. In this study, using a feline 1-h intestinal ischemia followed by reperfusion model, we tested the possibility that exogenous sources of nitric oxide may prevent the reperfusion-induced mucosal barrier disruption and examined the mechanisms involved. Mucosal barrier integrity was assessed by determining 51Cr-EDTA clearance from blood to lumen. Intestinal blood flow and resistance were also determined. Reperfusion after 1 h of ischemia significantly increased 51Cr-EDTA clearance (0.05 +/- 0.01 to 0.35 +/- 0.07 ml.min-1.100 g-1) and decreased intestinal blood flow by 50%. Exogenous sources of nitric oxide including SIN-1, CAS-754, and nitroprusside as well as exogenous L-arginine all reduced reperfusion-induced mucosal barrier dysfunction without improving intestinal blood flow. Inhibition of endogenous nitric oxide with NG-nitro-L-arginine methyl ester between 1 and 2 h of reperfusion further augmented the rise in mucosal permeability associated with ischemia-reperfusion. Addition of the permeable analogue of guanosine 3',5'-cyclic monophosphate, 8-bromoguanosine 3',5'-cyclic monophosphate, improved reperfusion-induced intestinal blood flow significantly but did not provide protection against mucosal barrier disruption associated with the first hour of ischemia-reperfusion. Exogenous sources of nitric oxide can reduce reperfusion-induced mucosal barrier dysfunction independent of alterations in intestinal blood flow.

Reciprocal regulation by putatively nitroxidergic and adrenergic nerves of monkey and dog temporal arterial tone

1991 ◽  
Vol 261 (6) ◽  
pp. H1740-H1745 ◽  
Author(s):  
N. Toda ◽  
T. Okamura
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Electrical Stimulation ◽  
Superficial Temporal Artery ◽  
Temporal Artery ◽  
Synthesis Inhibitor ◽  
Reciprocal Regulation ◽  
Cyclic Monophosphate ◽  
Prostaglandin F2 Alpha ◽  
Arterial Tone

In monkey and dog superficial temporal artery strips denuded of the endothelium, transmural electrical stimulation and nicotine produced a contraction that was abolished by phentolamine and potentiated by NG-nitro-L-arginine (L-NNA), a nitric oxide (NO) synthesis inhibitor. The potentiation was reversed by L-arginine but not by its D-enantiomer. The arteries treated with phentolamine and contracted with prostaglandin F2 alpha responded to the electrical stimulation and nicotine with relaxations that were abolished by tetrodotoxin and hexamethonium, respectively, and were markedly inhibited by L-NNA but not by D-NNA, atropine, and timolol. The L-NNA-induced inhibition was reversed by L-arginine. Nicotine increased the level of guanosine 3',5'-cyclic monophosphate in the monkey arteries; the increment was prevented by L-NNA. It is concluded that the monkey and dog temporal arterial tone appears to be reciprocally regulated by adrenergic vasoconstrictor and nonadrenergic noncholinergic vasodilator nerves. The neurogenic relaxation would be mediated by NO that is possibly released from the vasodilator nerve and transmits information to smooth muscle; therefore the nerve may be called "nitroxidergic."

Nitric oxide-induced microvascular permeability alterations: a regulatory role for cGMP

1993 ◽  
Vol 265 (6) ◽  
pp. H1909-H1915 ◽  
Author(s):  
P. Kubes
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Guanylate Cyclase ◽  
Microvascular Permeability ◽  
Independent Effect ◽  
No Donor ◽  
Cyclic Monophosphate ◽  
Protein Clearance ◽  
Guanylate Cyclase Activation ◽  
Permeability Alterations

This study evaluated the physiological effects of compounds that alter guanosine 3',5'-cyclic monophosphate (cGMP) on the increase in vascular protein clearance induced by nitric oxide (NO) synthesis inhibition in the feline small intestine. A lymphatic vessel draining the small bowel was cannulated; vascular protein clearance and intestinal blood flow were measured. N omega-nitro-L-arginine methyl ester (L-NAME), the NO inhibitor, was infused (0.5 mumol/min) into the superior mesenteric artery. Vascular protein clearance increased approximately 4.6-fold, whereas blood flow decreased to 50% of control. Elevation of cGMP by 1) cytosolic guanylate cyclase activation with a NO donor (SIN 1) or 2) a cGMP analogue, 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP) completely prevented the rise in microvascular permeability associated with L-NAME. Moreover, these compounds reduced (almost 90%) baseline vascular protein clearance, whereas inhibition of cytosolic guanylate cyclase with methylene blue significantly increased this parameter. Atrial natriuretic factor (ANF) has been reported to increase tissue cGMP levels and microvascular permeability. In this study, ANF did indeed increase intestinal microvascular permeability however this occurred independent of changes in intestinal cGMP levels. These data support a role for cGMP associated with NO-induced microvascular permeability alterations and raise the possibility that ANF has a cGMP-independent effect on microvascular permeability within the intestine.

cGMP mediates the desensitization to bradykinin in isolated canine coronary arteries

1995 ◽  
Vol 268 (2) ◽  
pp. H865-H870 ◽  
Author(s):  
L. Olmos ◽  
J. V. Mombouli ◽  
S. Illiano ◽  
P. M. Vanhoutte
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Coronary Arteries ◽  
No Synthase ◽  
Cyclic Monophosphate ◽  
Prostaglandin F2 Alpha ◽  
Relaxation Curves ◽  
Synthase Inhibitor ◽  
The Right ◽  
Selective Impairment

The relaxation to bradykinin in canine coronary arteries is mediated by endothelium-derived nitric oxide (NO) and hyperpolarizing factor (EDHF). Desensitization to the kinin was induced by incubation of canine coronary arteries with endothelium with 10(-8) M bradykinin for 30 min. After washout, tissues were contracted with prostaglandin F2 alpha, and concentration-relaxation curves to bradykinin were obtained in control and desensitized arteries treated with indomethacin. After desensitization, there was a shift to the right of the concentration-relaxation curves to bradykinin. However, the elevation in guanosine 3',5'-cyclic monophosphate (cGMP) levels evoked by bradykinin was similar in both groups of tissues. The curves to bradykinin obtained in the presence of NG-nitro-L-arginine (an NO synthase inhibitor) were depressed, whereas those obtained in arteries contracted with potassium (to eliminate the EDHF-mediated relaxation) were not affected by the desensitization. Addition of NG-nitro-L-arginine, oxyhemoglobin, or methylene blue before the desensitization procedure preserved, whereas 3-morpholinosydnonimine (SIN-1, a donor of NO) and 8-bromoguanosine 3',5'-cyclic monophosphate impaired, the EDHF-mediated relaxation to bradykinin. Thus the selective impairment of the EDHF-dependent relaxation to bradykinin may be mediated by NO, acting mainly through increased production of cGMP.

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