scholarly journals Extract from leaf of Psidium guajava L depresses the guinea pig atrial contractility by interfering with potassium and calcium channels

2009 ◽  
Vol 45 (3) ◽  
pp. 483-489
Author(s):  
Antonio Nei Santana Gondim ◽  
Vanda Rodrigues de Oliveira ◽  
Sellyanna Domeny dos Santos ◽  
Bagnólia Araújo da Silva ◽  
Carla Maria Lins de Vasconcelos ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Cardiac Tissue ◽  
Negative Inotropic Effect ◽  
Psidium Guajava ◽  
Inotropic Effect ◽  
Myocardial Cells ◽  
Action Mechanism ◽  
Aqueous Fraction ◽  
Effect Curve ◽  
The Right

The negative inotropic effect of aqueous fraction (AqF) obtained from the acetic extract of Psidium guajava L leaf was investigated on the guinea pig left atrium. Myocardial force was measured isometrically (27 ± 0.1 ºC, 2 Hz). AqF (100 μg/ml) reduced contractility of about 85 ± 9.4 % (n = 4, p < 0.001, Fcalc = 51.70, F(0.01; 4; 21) = 5.09, EC50 = 14.28 ± 3 μg/mL) in a concentration-dependent fashion. This effect was reduced by 20 mM of tetraethylammonium (TEA), increasing EC50 to 50 ± 7 μg/ml (n = 4, p < 0.001, Fcalc = 282.13; F(0.01; 21; 66) = 2.36). AqF (100 μg/ml) shifted to the right the CaCl2 concentration-effect curve, increasing the EC50 from 2170 ± 112 to 2690 ± 132 μM (n = 3, p < 0.001, Fcalc = 220.80 ; F(0.01; 29; 60) = 2.19). L-NAME (100 μM) did not modify the AqF inotropic effect (n = 3, p > 0.05) sugesting that the oxide nitric pathway did not participate of the action mechanism of AqF. We can conclude that AqF depresses the atrial contractile by reducing the calcium entry in myocardial cells and also by openenig potassium channels of cardiac tissue.

Functional and autoradiographic characterization of dopamine D2-like receptors in the guinea pig heart

2002 ◽  
Vol 80 (6) ◽  
pp. 578-587 ◽  
Author(s):  
María de Jesús Gómez ◽  
Guy Rousseau ◽  
Réginald Nadeau ◽  
Roberto Berra ◽  
Gonzalo Flores ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Western Blot ◽  
Dopamine Receptors ◽  
Negative Inotropic Effect ◽  
Cyclase Activity ◽  
Inotropic Effect ◽  
Receptor Subtypes ◽  
Guinea Pig Heart ◽  
Additional Information ◽  
The Right

Dopamine receptors include the D1- (D1 and D5 subtypes) and D2-like (D2, D3, and D4 subtypes) families. D1-like receptors are positively and D2-like receptors negatively coupled to the adenylyl cyclase. Dopamine D2-like (D4 subtype) receptors have been identified in human and rat hearts. However the presence of D2 and D3 receptor subtypes is unclear. Furthermore, their role in cardiac functions is unknown. By autoradiographic studies of guinea pig hearts, we identified D3 and D4 receptors, using the selective radioligands [3H]-7-OH-DPAT and [3H]emonapride (YM-09151-2 plus raclopride). Western blot analysis confirmed D3 and D4 receptors in the right and left ventricle of the same species. Selective agonists of D3 and D4 receptors (±)-7-OH-DPAT and PD 168 077 (10–9 to 10–5 M, respectively) induced a significant negative chronotropic and inotropic effect in the isolated guinea pig heart preparation. Negative inotropic effect induced by PD 168 077 was associated with an inhibition in cyclase activity. No changes in cyclase activity were found with (±)-7-OH-DPAT. The aim of this study is to support the presence of D3 and D4 receptors in the heart. Although our results suggest that D3 and D4 receptors are functionally active in the heart, we need additional information with an antagonist and an agonist of improved potency and selectivity to understand the respective roles of D3 and D4 receptors in the cardiac functions.Key words: Dopamine receptors (D2, D3, D4 subtypes), autoradiography, Western blot, cAMP, heart.

Calcium channels and excitation–contraction coupling in cardiac cells. II. A pharmacological study of the biphasic contraction in guinea-pig papillary muscle

1987 ◽  
Vol 65 (9) ◽  
pp. 1832-1839 ◽  
Author(s):  
E. Honoré ◽  
M. M. Adamantidis ◽  
B. A. Dupuis ◽  
C. E. Challice ◽  
P. Guilbault
Keyword(s):  
Guinea Pig ◽  
Papillary Muscle ◽  
Positive Inotropic Effect ◽  
Pharmacological Study ◽  
Negative Inotropic Effect ◽  
Cardiac Cells ◽  
Inotropic Effect ◽  
Free Solution ◽  
Contraction Coupling ◽  
Rich Solution

Biphasic contractions were obtained in guinea-pig papillary muscle by inducing partial depolarization in K+-rich solution (17 mM) in the presence of 0.3 μM isoproterenol. Mn2+ ions inhibited the two components of contraction in a similar way. Nifedipine and particularly Cd2+ ions specifically inhibited the second component of contraction. Isoproterenol and BAY K 8644 markedly increased the amplitude of the second component (P2) of contraction. Nevertheless, a moderate positive inotropic effect of isoproterenol was found on the first component (P1) of contraction when excitability was restored by 0.2 mM Ba instead of isoproterenol. Acetylcholine and hypoxia decreased the amplitude of the second component of contraction to a greater extent. In the presence of digoxin or Na+-free solution, P1was strongly increased. When sarcoplasmic reticular function was hindered by 1 mM caffeine or in the presence of Ca2+-free Sr2+ solution, digoxin always induced a negative inotropic effect on P2. Inversely in these conditions the transient positive inotropic effect of Na+-free solution was strongly reduced. These results are consistent with the hypothesis that the late component of contraction is triggered by the slow inward Ca2+ current and that the early component is due to Ca2+ release from the sarcoplasmic reticulum.

scholarly journals Potentiation of the negative inotropic effect of adenosine on guinea pig atria by cinepazide.

1980 ◽  
Vol 30 ◽  
pp. 133
Author(s):  
Hideki Moritoki ◽  
Shinji Fujita ◽  
Masao lakei ◽  
Yukio Ishida ◽  
Akira Akashi
Keyword(s):  
Guinea Pig ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Guinea Pig Atria

Role of cyclooxygenase in ventricular effects of adrenomedullin: is adrenomedullin a double-edged sword in sepsis?

2004 ◽  
Vol 286 (3) ◽  
pp. H1034-H1042 ◽  
Author(s):  
Shivani Mittra ◽  
Jean-Marc Hyvelin ◽  
Qixian Shan ◽  
Fai Tang ◽  
Jean-Pierre Bourreau
Keyword(s):  
Cardiac Tissue ◽  
Ventricular Myocytes ◽  
Marked Decrease ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Prolonged Incubation ◽  
Cell Contractility ◽  
Rat Ventricular Myocytes ◽  
Cell Shortening ◽  
Cox Inhibitor

Adrenomedullin (ADM) is upregulated in cardiac tissue under various pathophysiological conditions. However, the direct inotropic effect of ADM on normal and compromised cardiomyocytes is not clear. In rat ventricular myocytes, ADM produced an initial (<30 min) increase in cell shortening and Ca2+ transient and, on prolonged incubation (>1 h), a marked decrease in cell shortening and Ca2+ transient. Both effects were sensitive to inhibition by the ADM antagonist ADM-(22–52). The increase and decrease in cell shortening and Ca2+ transient were attenuated by pretreatment with indomethacin [a nonspecific cyclooxygenase (COX) inhibitor], nimesulide and SC-236 (specific COX-2 inhibitors), and tranylcypromine (a prostacyclin synthase inhibitor); SQ-29548 (a thromboxane receptor antagonist) was without effect. Cells isolated from LPS-treated rats that were in the late, hypodynamic phase of septic shock also showed a marked decrease in cell shortening and Ca2+ transient. Because ADM is overexpressed in sepsis, we repeated the above protocol in cells isolated from LPS-treated rats. At 4 h after LPS injection, ADM levels markedly increased in plasma, ventricles, and freshly isolated ventricular myocytes. Decreases in cell shortening and Ca2+ transient in LPS-treated cells were reversed by pretreatment with ADM-(22–52). Anti-ADM (rat) IgG also reversed the decrease in cell shortening and other parameters of cell kinetics. Indomethacin, SC-236, and tranylcypromine restored cell contractility and the decrease in Ca2+ transient, whereas SQ-29548 had no effect, implying that prostacyclin played a role in both effects. However, with regard to cell-shortening kinetics, indomethacin and SQ-29548 decreased the amount of time taken by the cells to return to baseline, whereas SC-236 and tranylcypromine did not, implying that not only prostacyclin, but also thromboxane, is involved. The results indicate that ADM interacts with COX to yield prostanoids, which mediate its negative inotropic effect in LPS-treated rat ventricular myocytes.

The Negative Inotropic Effect of β3-Adrenoceptor Stimulation in the Beating Guinea Pig Heart

2000 ◽  
Vol 35 (5) ◽  
pp. 786-790 ◽  
Author(s):  
Tetsuya Kitamura ◽  
Katsuya Onishi ◽  
Kaoru Dohi ◽  
Tsutomu Okinaka ◽  
Naoki Isaka ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Guinea Pig Heart

scholarly journals Negative Inotropic Effect of Diazepam in Isolated Guinea Pig Heart.

2001 ◽  
Vol 63 (2) ◽  
pp. 135-143 ◽  
Author(s):  
Yukio HARA ◽  
Hiroe KOBAYASHI ◽  
Satomi OOSHIRO ◽  
Keisuke FUTAMURA ◽  
Takeshi NISHINO ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Guinea Pig Heart

Mechanism of the negative inotropic effect of adenosine in guinea pig atrial myocytes

1994 ◽  
Vol 267 (6) ◽  
pp. H2420-H2429
Author(s):  
D. Wang ◽  
L. Belardinelli
Keyword(s):  
Guinea Pig ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Dependent Manner ◽  
Atrial Myocytes ◽  
Patch Clamp Technique ◽  
Concentration Dependent Manner ◽  
Whole Cell Patch Clamp ◽  
K Current ◽  
Highly Correlated

The ionic basis of the negative inotropic effect of adenosine on guinea pig atrial myocytes was studied. Membrane potentials and currents were measured using a whole cell patch-clamp technique. The contractility was assessed by video quantitation of cell twitch amplitude. Adenosine shortened action potential duration [measured at 90% repolarization (APD90)] and decreased twitch amplitude in a concentration-dependent manner. The maximal effects of adenosine (100 microM) were to reduce APD90 from 102 +/- 14 to 34 +/- 8 ms (n = 11) and twitch amplitude from 4.3 +/- 0.9 to 1.5 +/- 0.4 microns (n = 8). The concentration of adenosine that caused one-half of the maximal reductions of twitch amplitude and of APD90 was 0.6 microM. Reductions in APD90 and in twitch amplitude were parallel and highly correlated (r = 0.98). Decreases in twitch amplitude by adenosine could be mimicked by application of voltage-clamp pulses with durations similar to the durations of action potentials in the presence of adenosine. Clamp pulse could reverse adenosine-induced but not cadmium chloride-induced decreases in twitch amplitude. Adenosine activated the inwardly rectifying K+ current (IK,Ado), but did not significantly decrease the L-type Ca2+ current (ICa,L). Adenosine reduced the effects of BAY K 8644 on APD90 and twitch amplitude but did not attenuate the BAY K-induced increase in ICa,L. The effects of adenosine on APD90 and twitch amplitude could be reversed after activation of IK,Ado was inhibited by intracellular application of cesium and tetraethylammonium chloride.(ABSTRACT TRUNCATED AT 250 WORDS)

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