Acidosis Counteracts the Negative Inotropic Effect of K+on Ventricular Muscle Strips from the ToadBufo marinus

2004 ◽  
Vol 77 (2) ◽  
pp. 223-231 ◽  
Author(s):  
Johnnie Bremholm Andersen ◽  
Hans Gesser ◽  
Tobias Wang
Keyword(s):  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Ventricular Muscle

Negative Inotropic Effect of Ketamine in Rabbit Ventricular Muscle

1990 ◽  
Vol 71 (3) ◽  
pp. 275???278 ◽  
Author(s):  
Ben F. Rusy ◽  
John K. Amuzu ◽  
Hemmo A. Bosscher ◽  
David Redon ◽  
Hirochika Komai
Keyword(s):  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Ventricular Muscle ◽  
Rabbit Ventricular Muscle

Effect of ryanodine on cardiac muscle

1963 ◽  
Vol 204 (6) ◽  
pp. 975-978 ◽  
Author(s):  
Winifred G. Nayler
Keyword(s):  
Cardiac Muscle ◽  
Ethylenediaminetetraacetic Acid ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Ventricular Muscle ◽  
Tyrode Solution

Ryanodine (1 x 10–8 m) exerted a negative inotropic effect on toad ventricular muscle. The amplitude of contractions recorded from ryanodine-depressed ventricles were enhanced by raising the rate of stimulation, by increasing the extracellular Ca++ concentration, and by the addition of caffeine. The negative inotropic effect of ryanodine was reversed following perfusion with Tyrode solution containing 4 mm ethylenediaminetetraacetic acid.

Negative Inotropic Effect of Basic Fibroblast Growth Factor on Adult Rat Cardiac Myocyte

Circulation ◽  
1997 ◽  
Vol 96 (8) ◽  
pp. 2501-2504 ◽  
Author(s):  
Yuji Ishibashi ◽  
Yoshitoshi Urabe ◽  
Hiroyuki Tsutsui ◽  
Shintaro Kinugawa ◽  
Masaru Sugimachi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Cardiac Myocyte ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Fibroblast Growth ◽  
Adult Rat

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.

Cholinergic stimulation modulates negative inotropic effect of cocaine on ferret ventricular myocardium

1996 ◽  
Vol 270 (2) ◽  
pp. H678-H684
Author(s):  
L. Miao ◽  
Z. Qiu ◽  
J. P. Morgan
Keyword(s):  
Response Curve ◽  
Negative Inotropic Effect ◽  
Ventricular Myocardium ◽  
Inotropic Effect ◽  
Dependent Manner ◽  
Cholinergic Stimulation ◽  
Concentration Dependent Manner ◽  
Cell Shortening ◽  
Inotropic State ◽  
Concentration Response Curve

We tested the hypothesis that the negative inotropic effect (NIE) of cocaine is mediated, at least in part, by cholinergic stimulation and can be correlated with the degree of adenosine 3',5'-cyclic monophosphate (cAMP) dependency of the inotropic state. Cardiac myocytes were isolated from left ventricles of ferrets and loaded with the fluorescent Ca2+ indicator indo 1. Cells were placed in physiological solution containing 2.0 mM Ca2+ and stimulated at 0.5 Hz and 30 degrees C. Cocaine decreased peak cell shortening and peak intracellular Ca2+ in a concentration-dependent manner (10(-8)-10(-4) M). The concentration-response curve of cocaine was shifted significantly downward compared with those of lidocaine and procaine in the same range of concentrations. Atropine (10(-6) M) shifted the concentration-response curve of cocaine, but not those of lidocaine and procaine, rightward, with a pA2 value (7.66) similar to that obtained with carbachol (7.99). With prior addition of isoproterenol (ISO, 10(-8) M) or increased Ca2+ (4.0 mM) to increase cell shortening to the same degree (approximately 60%), cocaine and carbachol decreased contractility to a significantly greater extent in ISO-stimulated myocytes. To clarify whether these treatments changed responsiveness of the contractile elements to Ca2+, the effect of 2,3-butanedione monoxime, an agent that interferes with the interaction of myosin and actin, was tested with previous addition of ISO or increased Ca2+, and no differential effect occurred. Therefore, we postulate that 1) the NIE of cocaine on myocytes is caused by decreased Ca2+ availability; 2) this effect is due to specific stimulation of cholinergic receptors in addition to other direct myocardial (probably local anesthetic) effects; and 3) the NIE correlates with the level of cAMP dependence of the inotropic state.

Gαi-biased apelin analog protects against isoproterenol-induced myocardial dysfunction in rats

2021 ◽  
Vol 320 (4) ◽  
pp. H1646-H1656
Author(s):  
David Coquerel ◽  
Eugénie Delile ◽  
Lauralyne Dumont ◽  
Frédéric Chagnon ◽  
Alexandre Murza ◽  
...  
Keyword(s):  
Cardiovascular Diseases ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Myocardial Dysfunction ◽  
Negative Inotropic Effect ◽  
Left Ventricular ◽  
Inotropic Effect ◽  
Camp Production ◽  
Data Point

By using more potent Gαi-biased APJ agonists that strongly inhibit cAMP production, these data point to the negative inotropic effect of APJ-mediated Gαi signaling in the heart and highlight the potential protective impact of APJ-dependent Gαi signaling in cardiovascular diseases associated with left ventricular hypertrophy.

Sign in / Sign up

Export Citation Format

Share Document