Interplay of Nitric Oxide and Histamine in the Regulation of Coronary Reactive Hyperemia and Coronary Autoregulation

1995 ◽  
pp. 145-149
Author(s):  
M. M. Kostić ◽  
M. R. Petronijević
Keyword(s):  
Nitric Oxide ◽  
Reactive Hyperemia

Effects of regional inhibition of nitric oxide synthesis in intact porcine hearts

1994 ◽  
Vol 266 (4) ◽  
pp. H1516-H1527 ◽  
Author(s):  
K. A. Kirkeboen ◽  
P. A. Naess ◽  
J. Offstad ◽  
A. Ilebekk
Keyword(s):  
Nitric Oxide ◽  
Coronary Flow ◽  
Reactive Hyperemia ◽  
Nitric Oxide Synthesis ◽  
Partial Pressure Of Oxygen ◽  
Doppler Flowmetry ◽  
Flow Response ◽  
Intracoronary Infusion ◽  
Coronary Endothelium

The importance of nitric oxide (NO) in coronary blood flow (CBF) regulation was examined in anesthetized pigs. NO synthesis was inhibited by intracoronary infusion of NG-monomethyl-L-arginine (L-NMMA) or NG-nitro-L-arginine (L-NNA). L-NMMA (30 mumol/min) reduced CBF (Doppler flowmetry) by 16.3% (13.1-20.2%; P < 0.001) and L-NNA (30 mumol/min) by 16.1% (13.9-18.9%; P < 0.001). During NO blockade, myocardial oxygen consumption was unaltered as an increase in oxygen extraction occurred due to a reduced partial pressure of oxygen and oxygen saturation in blood from the anterior interventricular vein. L-Arginine completely reestablished CBF after giving L-NMMA, but not after giving L-NNA. L-NNA reduced the coronary flow response to ADP by 66-83%, whereas the selected dose of L-NMMA did not affect it. The flow response to adenosine was not affected by either L-NMMA or L-NNA. L-NNA reduced reactive hyperemia after occluding the left anterior descending coronary artery for 10 and 30 s but not for 120 s. Our data show that NO produced in the coronary endothelium plays an important role in CBF regulation in vivo, accounting for approximately 16% of CBF and a major part of the flow response to ADP. NO also contributes to reactive hyperemia after brief, but not longer, ischemic periods.

scholarly journals Contribution of Nitric Oxide to Reactive Hyperemia

Hypertension ◽  
1998 ◽  
Vol 32 (1) ◽  
pp. 9-15 ◽  
Author(s):  
Nader Dakak ◽  
Syed Husain ◽  
David Mulcahy ◽  
Neil P. Andrews ◽  
Julio A. Panza ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Hyperemia

Vasodilator responses to adenosine and hyperemia are mediated by A1 and A2 receptors in the cat vascular bed

2002 ◽  
Vol 282 (6) ◽  
pp. R1696-R1709 ◽  
Author(s):  
Trinity J. Bivalacqua ◽  
Hunter C. Champion ◽  
David G. Lambert ◽  
Philip J. Kadowitz
Keyword(s):  
Nitric Oxide ◽  
Reactive Hyperemia ◽  
Phosphodiesterase Inhibitor ◽  
Receptor Antagonists ◽  
Camp Phosphodiesterase ◽  
Nitric Oxide Synthase Inhibitor ◽  
Vascular Bed ◽  
S Period ◽  
Synthase Inhibitor ◽  
Oxide Synthase

Hemodynamic responses to adenosine, the A1 receptor agonists N 6-cyclopentyladenosine (CPA) and adenosine amine congener (ADAC), and the A2 receptor agonist 5′-( N-cyclopropyl)-carboxamido-adenosine (CPCA) were investigated in the hindquarter vascular bed of the cat under constant-flow conditions. Injections of adenosine, CPA, ADAC, CPCA, ATP, and adenosine 5′- O-(3-thiotriphosphate) (ATPγS) into the perfusion circuit induced dose-related decreases in perfusion pressure. Vasodilator responses to the A1 agonists were reduced by the A1 receptor antagonists KW-3902 and CGS-15943, whereas responses to CPCA were reduced by the A2 antagonist KF-17837. Vasodilator responses to adenosine were reduced by KW-3902, CGS-15943, and by KF-17837, suggesting a role for both A1 and A2 receptors. Vasodilator responses to ATP and the nonhydrolyzable ATP analog ATPγS were not attenuated by CGS-15943 or KF-17837. After treatment with the nitric oxide synthase inhibitor N ω-nitro-l-arginine methyl ester, the cyclooxygenase inhibitor sodium meclofenamate, or the ATP-dependent K+ (K[Formula: see text]) channel antagonists U-37883A or glibenclamide, responses to adenosine and ATP were not altered. Responses to adenosine, CPA, and CPCA were increased in duration by rolipram, a type 4 cAMP phosphodiesterase inhibitor, but were not altered by zaprinast, a type 5 cGMP phosphodiesterase inhibitor. When blood flow was interrupted for a 30-s period, the magnitude and duration of the reactive vasodilator response were reduced by A1 and A2 receptor antagonists. These data suggest that vasodilator responses to adenosine and the A1and A2 agonists studied are not dependent on the release of cyclooxygenase products, nitric oxide, or the opening of K[Formula: see text] channels in the regional vascular bed of the cat. The present data suggest a role for cAMP in mediating responses to adenosine and suggest that vasodilator responses to adenosine and to reactive hyperemia are mediated in part by A1 and A2 receptors in the hindquarter vascular bed of the cat.

scholarly journals Enhancement of myocardial reactive hyperemia with manganese-superoxide dismutase: role of endothelium-derived nitric oxide

1996 ◽  
Vol 31 (4) ◽  
pp. 537-545 ◽  
Author(s):  
R. Tsunoda ◽  
K. Okumura ◽  
H. Ishizaka ◽  
T. Matsunaga ◽  
T. Tabuchi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Manganese Superoxide Dismutase ◽  
Reactive Hyperemia ◽  
Manganese Superoxide

scholarly journals Cyclooxygenase and nitric oxide synthase dependence of cutaneous reactive hyperemia in humans

2007 ◽  
Vol 293 (1) ◽  
pp. H425-H432 ◽  
Author(s):  
Marvin S. Medow ◽  
Indu Taneja ◽  
Julian M. Stewart
Keyword(s):  
Nitric Oxide ◽  
Peak Flow ◽  
Reactive Hyperemia ◽  
Laser Doppler ◽  
Doppler Flowmetry ◽  
Time To Peak ◽  
Flow Parameters ◽  
Cox Inhibitor ◽  
Cutaneous Circulation ◽  
Synthase Inhibitor

We tested the hypothesis that cyclooxygenases (COXs) or COX products inhibit nitric oxide (NO) synthesis and thereby mask potential effects of NO on reactive hyperemia in the cutaneous circulation. We performed laser-Doppler flowmetry (LDF) with intradermal microdialysis in 12 healthy volunteers aged 19–25 yr. LDF was expressed as the percent cutaneous vascular conduction (%CVC) or as the maximum %CVC (%CVCmax) where CVC is LDF/mean arterial pressure. We tested the effects of the nonisoform-specific NO synthase inhibitor nitro-l-arginine (NLA, 10 mM), the nonspecific COX inhibitor ketorolac (Keto, 10 mM), combined NLA + Keto, and NLA + sodium nitroprusside (SNP, 28 mM) on baseline and reactive hyperemia flow parameters. We also examined the effects of isoproterenol, a β-adrenergic agonist that causes prostaglandin-independent vasodilation to correct for the increase in baseline flow caused by Keto. When delivered directly into the intradermal space, Keto greatly augments all aspects of the laser-Doppler flow response to reactive hyperemia: peak reactive hyperemic flow increased from 41 ± 5 to 77 ± 7%CVCmax, time to peak flow increased from 17 ± 3 to 56 ± 24 s, the area under the reactive hyperemic curve increased from 1,417 ± 326 to 3,376 ± 876%CVCmax·s, and the time constant for the decay of peak flow increased from 100 ± 23 to 821 ± 311 s. NLA greatly attenuates the Keto response despite exerting no effects on baseline LDF or on reactive hyperemia when given alone. Low-dose NLA + SNP duplicates the Keto response. Isoproterenol increased baseline and peak reactive flow. These results suggest that COX inhibition unmasks NO dependence of reactive hyperemia in human cutaneous circulation.

scholarly journals Nitric oxide is not obligatory for radial artery flow-mediated dilation following release of 5 or 10 min distal occlusion

2010 ◽  
Vol 298 (1) ◽  
pp. H119-H126 ◽  
Author(s):  
Kyra Pyke ◽  
Daniel J. Green ◽  
Cara Weisbrod ◽  
Matthew Best ◽  
Lawrence Dembo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Shear Rate ◽  
Flow Velocity ◽  
Radial Artery ◽  
Blood Flow Velocity ◽  
Reactive Hyperemia ◽  
Area Under The Curve ◽  
Flow Mediated Dilation ◽  
Significant Difference

This study investigated the nitric oxide (NO) dependence of radial artery (RA) flow-mediated dilation (FMD) in response to three different reactive hyperemia (RH) shear stimulus profiles. Ten healthy males underwent the following three RH trials: 1) 5 min occlusion (5 trial), 2) 10 min occlusion (10 trial), and 3) 10 min occlusion with cuff reinflation at 30 s (10–30 trial). Trials were performed during saline infusion and repeated during NG-monomethyl-l-arginine (l-NMMA) infusion in the brachial artery. RA blood flow velocity was measured with Doppler ultrasound, and B-mode RA images were analyzed using automated edge detection software. Shear rate estimation of shear stress was calculated as the blood flow velocity/vessel diameter. l-NMMA decreased baseline vascular conductance by 35%. l-NMMA infusion did not affect the peak shear rate stimulus ( P = 0.681) or the area under the curve (AUC) of shear rate to peak FMD ( P = 0.088). The AUC was significantly larger in the 10 trial vs. the 10–30 or 5 trial ( P < 0.001). Although percent FMD (%change in diameter) in the 10 trial was larger than that in the 5 trial ( P = 0.035), there was no significant difference in %FMD between the saline and l-NMMA conditions in any trial: 5 trial, 5.62 ± 1.48 vs. 5.63 ± 1.27%; 10 trial, 9.07 ± 1.16 vs. 11.22 ± 2.21%; 10–30 trial, 6.52 ± 1.43 vs. 7.98 ± 1.51% for saline and l-NMMA, respectively ( P = 0.158). We conclude the following: 1) RH following 10 min of occlusion results in an enhanced stimulus and %FMD compared with 5 min of occlusion. 2) When the occlusion cuff is reinflated 30 s postrelease of a 10 min occlusion, it does not result in an enhanced %FMD compared with that which results from RH following 5 min of occlusion. 3) The lack of effect of l-NMMA on FMD suggests that NO may not be obligatory for radial artery FMD in response to either 5 or 10 min of occlusion in healthy volunteers.

Inhibition of Nitric Oxide Synthesis Increases Focal Ischemic Infarction in Rat

1992 ◽  
Vol 12 (5) ◽  
pp. 717-726 ◽  
Author(s):  
Seiji Yamamoto ◽  
Eugene V. Golanov ◽  
Scott B. Berger ◽  
Donald J. Reis
Keyword(s):  
Nitric Oxide ◽  
Reactive Hyperemia ◽  
Competitive Inhibitor ◽  
Lesion Size ◽  
Lesion Volume ◽  
Lesion Formation ◽  
Spontaneously Hypertensive ◽  
Ischemic Infarction ◽  
Platelet Disaggregation

We investigated whether inhibition of nitric oxide (NO) biosynthesis with N-ω-nitro-l-arginine (NNA), a competitive inhibitor of NO synthase (NOS), would modify the volume of the focal ischemic infarction produced by occlusion of the middle cerebral artery (MCA) in spontaneously hypertensive rats. NNA was infused for 1 h (2.4 mg/kg/h) immediately following occlusion of the MCA. NNA increased lesion volume 24 h later by 32% over controls (150.8 ± 16.6 to 199.2 ± 17.4 mm3; p < 0.001, n = 6). This effect was antagonized by co-infusion of l- but not d-arginine. The antihypertensive rilmenidine (0.75 mg/kg) reduced the lesion by 27% (p < 0.05, n = 4). Changes in lesion size were confined to the penumbra. NNA increased arterial pressure (AP) (118 ± 8.9 to 149 ± 16.0 mm Hg; p < 0.01, n = 3) but did not change regional CBF. However, elevation of AP did not change the lesion volume or distribution. We conclude that inhibition of the constitutive form of NOS in vivo increases the volume of focal ischemic infarction as a consequence of reduced NO biosynthesis. The absence of NO availability may extend lesion formation by inhibition of reactive hyperemia, platelet disaggregation, and/or release of neuroprotective neuromodulators in the penumbra, which may counteract and override any of its neurotoxic actions.

scholarly journals Standard therapy potentiation of patients with Stable Angina FC III with concomitant Hypertension through nitric oxide donator L-arginine administration

2018 ◽  
pp. 83-86
Author(s):  
N. V. Zozuliak ◽  
Z. V. Zozuliak ◽  
V. Ye. Neiko ◽  
I. B. Romash ◽  
I. R. Romash ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Stable Angina ◽  
Standard Therapy ◽  
Therapy Group ◽  
Reactive Hyperemia ◽  
Antioxidant Properties ◽  
Stiffness Index ◽  
Standard Therapy Group ◽  
Oxidation Stress ◽  
Group I

The purpose of the study was to improve treatment of patients with Stable Angina  functional class III (FC) with concomitant arterial hypertension (AH) through a combination of standard therapy with L-arginine. There were examined63 patients with Stable Angina III FK with AH. All patients in the clinic were analyzedby the test with reactive hyperemia, were measured levels of cardio-ankle vascular index, pulse wave velocity, aortic stiffness index and the thickness of the complex "intima-media". It has been established that in studied patients with L-arginine significantly improves endothelium dependent vasodilatation, presumably due to the supply of substrate for the synthesis of nitric oxide, as well as due to antioxidant properties, which prevents the excessive formation of toxic peroxynitrite in conditions of high oxidation stress. Endothelial-independent vasodilation in the standard therapy group was significantly lowered, while in the L-arginine group, the incidence of changes was unreliable, which may indicate a decrease in sensitivity to nitrates in Group I. Thus, the inclusion to antianginal and antihypertensive therapyof L-arginine is more pronouncedaffects subclinical parameters of arterial rigidity, than in the background of treatment with standard therapy.

Postischemic vasodilation in human forearm is dependent on endothelium-derived nitric oxide

1996 ◽  
Vol 270 (4) ◽  
pp. H1435-H1440 ◽  
Author(s):  
I. T. Meredith ◽  
K. E. Currie ◽  
T. J. Anderson ◽  
M. A. Roddy ◽  
P. Ganz ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Dose Response ◽  
Supply And Demand ◽  
Reactive Hyperemia ◽  
Normal Subjects ◽  
Response Relationship ◽  
Dose Response Relationship ◽  
Time Curve ◽  
Nitric Oxide Synthase Inhibitor ◽  
Hyperemic Flow

Although endothelium-derived nitric oxide contributes to basal vascular tone, little is known about its role in regulating blood flow during changes in metabolic supply and demand. We examined the contribution of endothelium-derived nitric oxide to reactive hyperemia in the forearm of 20 normal subjects (12 women, 8 men) aged 27 +/- 4 yr (means +/- SD), using the nitric oxide synthase inhibitor, NG-monomethyl-L-arginine (L-NMMA). Forearm ischemia was induced by suprasystolic blood pressure cuff inflation for 5 min, and the subsequent hyperemic flow was recorded for 5 min using venous occlusion strain-gauge plethysmography. The efficacy of nitric oxide blockade was tested by comparing the dose-response relationship to the endothelium-dependent agonist, acetylcholine (3, 10, and 30 mg/min), before and after intra-arterial infusion of up to 2,000 mg/min of L-NMMA. L-NMMA produced a significant downward and rightward shift in the dose-response relationship to acetylcholine and a 39% reduction in response to the maximum dose (P < 0.001). In the presence of L-NMMA, peak hyperemic flow was reduced 16% (26.5 +/- 2.1 to 22.3 +/- 1.5 ml.min-1.100 ml of forearm-1, P < 0.03), and the minimum forearm vascular resistance was increased 22.8% (3.5 +/- 0.3 to 4.3 +/- 0.4 mmHg.ml-1.min.100 ml, P < 0.02). Total hyperemia, calculated from the area under the flow vs. time curve, at 1 and 5 min after cuff release was 17 and 23% less, respectively (13.6 +/- 1.2 vs. 11.3 +/- 1.1 and 31.8 +/- 2.7 vs. 24.6 +/- 1.8 ml/100 ml, P < 0.002), following L-NMMA. These data suggest that endothelium-derived nitric oxide plays a role in both reactive hyperemia and in the maintenance of the hyperemic response following ischemia in the forearm.

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