scholarly journals Dynamics of nitric oxide release in the cardiovascular system.

2003 ◽  
Vol 50 (1) ◽  
pp. 61-68 ◽  
Author(s):  
Aleh Balbatun ◽  
Febee Rophail Louka ◽  
Tadeusz Malinski
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular System ◽  
Critical Role ◽  
Rabbit Heart ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Diagnostic Tools ◽  
No Production ◽  
Ventricular Wall ◽  
No Release

The endothelium plays a critical role in maintaining vascular tone by releasing nitric oxide (NO). Endothelium derived NO diffuses to smooth muscles, triggering their relaxation. The dynamic of NO production is a determining factor in signal transduction. The present studies were designed to elucidate dynamics of NO release from normal and dysfunctional endothelium. The nanosensors (diameter 100-300 nm) exhibiting a response time better than 100 micros and detection limit of 1.0 x 10(-9) mol L(-1) were used for in vitro monitoring of NO release from single endothelial cells from the iliac artery of normotensive (WKY) rats, hypertensive (SHR) rats, and normal and cholesterolemic rabbits. Also, the dynamics and distribution of NO in left ventricular wall of rabbit heart were measured. The rate of NO release was much higher (1200 +/- 50 nmol L(-1) s(-1)) for WKY than for SHR (460 +/- 10 nmol L(-1) s(-1)). Also, the peak NO concentration was about three times higher for WKY than SHR. Similar decrease in the dynamics of NO release was observed for cholesterolemic rabbits. The dynamics of NO release changed dramatically along the wall of rabbit aorta, being highest (0.86 +/- 0.12 micromol L(-1)) for the ascending aorta, and lowest for the iliac aorta (0.48 +/- 0.15 micromol L(-1)). The distribution of NO in the left ventricular wall of rabbit heart was not uniform and varied from 1.23 +/- 0.20 micromol L(-1) (center) to 0.90 +/- 0.15 micromol L(-1) (apex). Both, the maximal concentration and the dynamics of NO release can be useful diagnostic tools in estimating the level of endothelial dysfunction and cardiovascular system efficiency.

Volatile Anesthetics Do Not Alter Bradykinin-induced Release of Nitric Oxide or L-Citrulline in Crystalloid Perfused Guinea Pig Hearts 

1998 ◽  
Vol 89 (2) ◽  
pp. 421-433 ◽  
Author(s):  
Satoshi Fujita ◽  
David L. Roerig ◽  
Wynda W. Chung ◽  
Zeljko J. Bosnjak ◽  
David F. Stowe
Keyword(s):  
Nitric Oxide ◽  
Guinea Pig ◽  
Volatile Anesthetics ◽  
Left Ventricular ◽  
Guanosine Monophosphate ◽  
No Production ◽  
Permeable Membrane ◽  
No Release ◽  
Cgmp Pathway ◽  
Perfused Hearts

Background Nitric oxide (NO) and L-citrulline (L-cit) are released by endothelial NO synthase (eNOS) to induce vasodilation via guanylyl cyclase and cyclic guanosine monophosphate (cGMP). Volatile anesthetics directly reduce vascular muscle tone, but their effects on the eNOS cGMP pathway is controversial. The aim of this study was to examine the effects of anesthetics on bradykinin-induced increases in flow, NO, and L-cit in isolated hearts. Methods Guinea pig hearts were isolated, perfused at 55 mmHg with a crystalloid or erythrocyte perfusate at 37 degrees C, and heart rate, left ventricular pressure, coronary flow (CF), effluent pH, and oxygen tension were monitored. Effluent [NO] was measured by a Clark-type electrode (sensitivity > or = 1 nM = 3 pA) with a selectively permeable membrane. Effluent [L-cit] was measured by chromatography. Before, during, and after exposure to halothane, isoflurane, or sevoflurane, hearts were infused with as much as 100 nM bradykinin to induce increases in CF and effluent release of NO and L-cit. Results In crystalloid-perfused hearts, 10 nm bradykinin produced maximal concentration-dependent increases in CF (87+/-2%), [NO] (24+/-4 nM), NO release (128+/-18 pmol x g(-1) x min(-1)), and [L-cit] (58+/-8 nM). Isoflurane slightly increased CF but not NO. Anesthetics did not alter the bradykinin-induced CF, NO slope relationship, or change [L-cit]. In erythrocyte-perfused hearts, isoflurane also did not alter the bradykinin-induced increase in CF and decrease in percentage of oxygen extracted. Conclusions This is the first study to simultaneously measure CF with bradykinin-induced changes in [NO] and [L-cit] in the presence of halothane, isoflurane, and sevoflurane in intact hearts. The study shows for the first time that volatile anesthetics do not alter the CF to NO relationship and suggests that NO production, NO release, and NO vasodilatory effects mediated by the eNOS cGMP pathway are not significantly affected by anesthetics in crystalloid or erythrocyte-perfused guinea pig hearts.

In anesthetized pigs human chorionic gonadotropin increases myocardial perfusion and function through a β-adrenergic-related pathway and nitric oxide

2013 ◽  
Vol 115 (4) ◽  
pp. 422-435 ◽  
Author(s):  
Elena Grossini ◽  
Daniela Surico ◽  
David A. S. G. Mary ◽  
Claudio Molinari ◽  
Nicola Surico ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cardiac Function ◽  
Coronary Blood Flow ◽  
Chorionic Gonadotropin ◽  
Human Chorionic Gonadotropin ◽  
Left Ventricular ◽  
No Synthase ◽  
No Production ◽  
No Release

Human chorionic gonadotropin (hCG) is not only responsible for numerous pregnancy-related processes, but can affect the cardiovascular system as well. So far, however, information about any direct effect elicited by hCG on cardiac function, perfusion, and the mechanisms involved has remained scarce. Therefore, the present study aimed to determine the primary in vivo effect of hCG on cardiac contractility and coronary blood flow and the involvement of autonomic nervous system and nitric oxide (NO). Moreover, in coronary endothelial cells (CEC), the intracellular pathways involved in the effects of hCG on NO release were also examined. In 25 anesthetized pigs, intracoronary 500 mU/ml hCG infusion at constant heart rate and aortic blood pressure increased coronary blood flow, maximum rate of change of left ventricular systolic pressure, segmental shortening, cardiac output, and coronary NO release ( P < 0.0001). These hemodynamic responses were graded in a further five pigs. Moreover, while blockade of muscarinic cholinoceptors ( n = 5) and of α-adrenoceptors ( n = 5) did not abolish the observed responses, β1-adrenoceptors blocker ( n = 5) prevented the effects of hCG on cardiac function. In addition, β2-adrenoceptors ( n = 5) and NO synthase inhibition ( n = 5) abolished the coronary response and the effect of hCG on NO release. In CEC, hCG induced the phosphorylation of endothelial NO synthase through cAMP/PKA signaling and ERK1/2, Akt, p38 MAPK involvement, which were activated as downstream effectors of β2-adrenoceptor stimulation. In conclusion, in anesthetized pigs, hCG primarily increased cardiac function and perfusion through the involvement of β-adrenoceptors and NO release. Moreover, cAMP/PKA-dependent kinases phosphorylation was found to play a role in eliciting the observed NO production in CEC.

Clinical and Experimental Analysis of 201Thallium Uptake of the Heart

1978 ◽  
Vol 17 (04) ◽  
pp. 142-148
Author(s):  
U. Büll ◽  
S. Bürger ◽  
B. E. Strauer
Keyword(s):  
Oxygen Consumption ◽  
Left Ventricle ◽  
Muscle Mass ◽  
Myocardial Oxygen Consumption ◽  
Animal Experiments ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Ventricular Wall ◽  
Flow Measurements ◽  
Myocardial Flow

Studies were carried out in order to determine the factors influencing myocardial 201T1 uptake. A total of 158 patients was examined with regard to both 201T1 uptake and the assessment of left ventricular and coronary function (e. g. quantitative ventriculography, coronary arteriography, coronary blood flow measurements). Moreover, 42 animal experiments (closed chest cat) were performed. The results demonstrate that:1) 201T1 uptake in the normal and hypertrophied human heart is linearly correlated with the muscle mass of the left ventricle (LVMM);2) 201T1 uptake is enhanced in the inner (subendocardial) layer and is decreased in the outer (subepicardial) layer of the left ventricular wall. The 201T1 uptake of the right ventricle is 40% lower in comparison to the left ventricle;3) the basic correlation between 201T1 uptake and LVMM is influenced by alterations of both myocardial flow and myocardial oxygen consumption; and4) inotropic interventions (isoproterenol, calcium, norepinephrine) as well as coronary dilatation (dipyridamole) may considerably augment 201T1 uptake in accordance with changes in myocardial oxygen consumption and/or myocardial flow.It is concluded that myocardial 201T1 uptake is determined by multiple factors. The major determinants have been shown to include (i) muscle mass, (ii) myocardial flow and (iii) myocardial oxygen consumption. The clinical data obtained from patient groups with normal ventricular function, with coronary artery disease, with left ventricular wall motion abnormalities and with different degree of left ventricular hypertrophy are correlated with quantitated myocardial 201T1 uptake.

Echocardiographic Quantification of Regional Left Ventricular Wall Motion With Color Kinesis

Circulation ◽  
1996 ◽  
Vol 93 (10) ◽  
pp. 1877-1885 ◽  
Author(s):  
Roberto M. Lang ◽  
Philippe Vignon ◽  
Lynn Weinert ◽  
James Bednarz ◽  
Claudia Korcarz ◽  
...  
Keyword(s):  
Wall Motion ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Ventricular Wall ◽  
Left Ventricular Wall Motion ◽  
Color Kinesis ◽  
Ventricular Wall Motion

Decrease in ambient [Cl-] stimulates nitric oxide release from cultured rat mesangial cells

1994 ◽  
Vol 267 (1) ◽  
pp. F190-F195 ◽  
Author(s):  
H. Tsukahara ◽  
Y. Krivenko ◽  
L. C. Moore ◽  
M. S. Goligorsky
Keyword(s):  
Nitric Oxide ◽  
Mesangial Cells ◽  
Ionic Composition ◽  
Juxtaglomerular Apparatus ◽  
Cytosolic Calcium ◽  
No Synthase ◽  
Tubuloglomerular Feedback ◽  
No Production ◽  
Rapid Reduction ◽  
No Release

It has been hypothesized that fluctuations of the ionic composition in the interstitium of juxtaglomerular apparatus (JGA) modulate the function of extraglomerular mesangial cells (MC), thereby participating in tubuloglomerular feedback (TGF) signal transmission. We examined the effects of isosmotic reductions in ambient sodium concentration ([Na+]) and [Cl-] on cytosolic calcium concentration ([Ca2+]i) in cultured rat MC. Rapid reduction of [Na+] or [Cl-] in the bath induced a concentration-dependent rise in [Ca2+]i. MC are much more sensitive to decreases in ambient [Cl-] than to [Na+]; a decrease in [Cl-] as small as 14 mM was sufficient to elicit a detectable [Ca2]i response. These observations suggest that MC can be readily stimulated by modest perturbations of extracellular [Cl-]. Next, we examined whether activation of MC by lowered ambient [Cl-] influences cellular nitric oxide (NO) production. Using an amperometric NO sensor, we found that a 13 mM decrease in ambient [Cl-] caused a rapid, Ca2+/calmodulin-dependent rise in NO release from MC. This response was not inhibitable by dexamethasone, indicating the involvement of the constitutive rather than the inducible type of NO synthase in MC. In addition, the NO release was blunted by indomethacin pretreatment, suggesting that a metabolite(s) of cyclooxygenase regulates the activation of NO synthase in MC. Our findings that small perturbations in external [Cl-] stimulate MC to release NO, a highly diffusible and rapidly acting vasodilator, provide a possible mechanism to explain the transmission of the signal for the TGF response within the JGA.

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