scholarly journals Exercise-induced pulmonary vasoconstriction during combined blockade of nitric oxide synthase and beta adrenergic receptors.

1994 ◽  
Vol 93 (2) ◽  
pp. 677-683 ◽  
Author(s):  
D W Kane ◽  
T Tesauro ◽  
T Koizumi ◽  
R Gupta ◽  
J H Newman
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Adrenergic Receptors ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Pulmonary Vasoconstriction ◽  
Exercise Induced ◽  
Oxide Synthase

Abstract 15295: Molecular Mechanism of Chronic Sildenafil-Caused Regression of Heart Failure: Effects on the Express of Cardiac SR Ca2+-ATPase, Subtype of β-Adrenergic Receptors and Nitric Oxide Synthase Isoforms

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Heng-Jie Cheng ◽  
Tiankai Li ◽  
Che Ping Cheng
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Adrenergic Receptors ◽  
Left Ventricular ◽  
Male Rats ◽  
Protein Levels ◽  
Myocyte Function ◽  
Oxide Synthase ◽  
Β Adrenergic Receptors

Background: Sildenafil (SIL), a selective inhibitor of PDE5 has been shown to exert profound beneficial effects in heart failure (HF). Recently we further found that SIL caused regression of cardiac dysfunction in a rat model with isoproterenol (ISO)-induced progressive HF. However, the molecular basis is unclear. We hypothesized that reversal of HF-induced detrimental alterations on the expressions of cardiac SR Ca 2+ -ATPase (SERCA2a), β-adrenergic receptors (AR) and nitric oxide synthase (NOS) isoforms by SIL may play a key role for its salutary role in HF. Methods: Left ventricular (LV) and myocyte function and the protein levels of myocyte β 1 - and β 3 - AR, SERCA2a, phospholamban (PLB) and three NOS were simultaneously evaluated in 3 groups of male rats (6/group): HF , 3 months (M) after receiving ISO (170 mg/kg sq for 2 days); HF/SIL , 2 M after receiving ISO, SIL (70 μg/kg/day sq via mini pump) was initiated and given for 1 M; and Controls (C). Results: Compared with controls, ISO-treated rats progressed to severe HF at 3 M after ISO followed by significantly decreased LV contractility (E ES , HF: 0.7 vs C: 1.2 mmHg/μl) and slowed LV relaxation, reductions in the peak velocity of myocyte shortening (77 vs 136 μm/sec), relengthening (62 vs 104 μm/sec) and [Ca 2+ ] iT (0.15 vs 0.24) accompanied by a diminished myocyte inotropic response to β-AR agonist, ISO (10 -8 M). These abnormalities were associated with concomitant significant decreases in myocyte protein levels of β 1 -AR (0.23 vs 0.64), SERCA2a (0.46 vs 0.80), PLB Ser16 /PLB ratio (0.24 vs 0.40) and eNOS (0.28 vs 0.46), but significantly increases in protein levels of β 3 -AR (0.29 vs 0.10) and iNOS (0.18 vs 0.08) with relatively unchanged nNOS. Chronic SIL prevented the HF-induced decreases in LV and myocyte contraction, relaxation, peak [Ca 2+ ] iT , and restored normal myocyte contractile response to ISO stimulation. With SIL, protein levels of myocyte β 1 - and β 3 -AR, SERCA2a were restored close to control values, but eNOS was significantly elevated than controls (0.77). Conclusions: Chronic SIL prevents HF-caused downregulation of cardiac β 1 -AR and reverse contrast changes between iNOS and β 3 -AR with SERCA 2a and eNOS expression, leading to the preservation of LV and myocyte function, [Ca 2+ ] iT , and β-adrenergic reserve.

scholarly journals The role of nitric oxide synthase in exercise induced changes in endothelial progenitor cell number

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Patrick Nicholas Colleran ◽  
Miles A. Tanner ◽  
Shena L. Latcham ◽  
Sara L. Collier ◽  
M. Harold Laughlin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Cell Number ◽  
Endothelial Progenitor ◽  
Exercise Induced ◽  
Induced Changes ◽  
Oxide Synthase

IL-1 inhibits beta-adrenergic control of cardiac calcium current: role of L-arginine/nitric oxide pathway

1994 ◽  
Vol 267 (5) ◽  
pp. H1753-H1758 ◽  
Author(s):  
G. J. Rozanski ◽  
R. C. Witt
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Ventricular Myocytes ◽  
Interleukin 1 ◽  
Cell Voltage ◽  
Cellular Mechanisms ◽  
Beta Adrenergic ◽  
Nitric Oxide Synthase Inhibitor ◽  
Adrenergic Control ◽  
Oxide Synthase

Modulation of the beta-adrenergic control of cardiac L-type Ca2+ current (Ica) by human recombinant interleukin-1 beta (IL-1) was examined in adult guinea pig ventricular myocytes using the whole cell voltage-clamp technique. ICa was elicited in Cs(+)-loaded myocytes by depolarizing pulses from a holding potential of -40 mV. Isoproterenol (0.01 and 1 microM) exposed to myocytes pretreated with 1 ng/ml IL-1 evoked a significantly smaller increase in ICa density compared with control cells. This IL-1-mediated decrease in beta-responsiveness was usually observed with pretreatment periods of > 1 h and varied as a function of the L-arginine concentration of the pretreatment medium. In addition, it was prevented by 1) IL-1 receptor antagonist, 2) substituting D-arginine for L-arginine, or 3) incubating cells with the nitric oxide synthase inhibitor NG-monomethyl-L-arginine. Thus the present data illustrate that IL-1 significantly alters the beta-adrenergic control of cardiac Ca2+ channels by cellular mechanisms that involve the activation of nitric oxide synthase. These mechanisms may play a role in altering ventricular function during cytokine-mediated inflammatory processes affecting the heart.

EXERCISE-INDUCED NITRIC OXIDE SYNTHASE GENE EXPRESSION

1998 ◽  
Vol 30 (Supplement) ◽  
pp. 144
Author(s):  
C. C. Lin ◽  
T. L. Lin ◽  
S. M. Yu ◽  
S. S. Hsieh
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Exercise Induced ◽  
Oxide Synthase

Pulmonary Vasoconstriction and Hypertension in Mice With Targeted Disruption of the Endothelial Nitric Oxide Synthase (NOS 3) Gene

1997 ◽  
Vol 81 (1) ◽  
pp. 34-41 ◽  
Author(s):  
Wolfgang Steudel ◽  
Fumito Ichinose ◽  
Paul L. Huang ◽  
William E. Hurford ◽  
Rosemary C. Jones ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Targeted Disruption ◽  
Pulmonary Vasoconstriction ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide
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