Species differences in responses to hyperosmolality and D600 in cat and rat heart

1978 ◽  
Vol 235 (3) ◽  
pp. H276-H280 ◽  
Author(s):  
J. T. Willerson ◽  
S. Wheelan ◽  
R. C. Adcock ◽  
G. H. Templeton ◽  
K. Wildenthal
Keyword(s):  
Cardiac Muscle ◽  
Rat Heart ◽  
Cardiac Contractility ◽  
Extracellular Calcium ◽  
Inotropic Effect ◽  
Inotropic Effects ◽  
Positive Effects ◽  
Positive Effect ◽  
Cat Heart ◽  
Isolated Rat

The direct inotropic effect of hypertonic mannitol was compared in isolated rat and cat papillary muscles. The inotropic effects of paired electrical stimulation and D600 were also evaluated in the same species. At extracellular calcium concentrations of 2.5 mM, hypertonic mannitol (25--100 mosmol/kg H2O above normal) depressed contractility in isolated rat myocardium; hyperosmolality exerted a positive effect only when extracellular Ca2+ was low (e.g., 0.3 mM). Paired pacing exerted a small but significant inotropic effect in rat heart when extracellular Ca2+ was 2.5 mM, and a larger effect at lower Ca2+. As previously noted, hypertonic mannitol and paired pacing both produced significant positive effects in isolated cat heart at an extracellular Ca2+ concentration of 2.5 mM. D600 exerted less of a depressant effect on contractility in rat than in cat heart at concentrations of 10(-6)--10(-7) M. The data suggest that 1) in contrast to results in cat heart, the positive inotropic effect of hyperosmolality in isolated rat cardiac muscle is apparent only when extracellular calcium concentration is reduced; 2) the inotropic effect of paired pacing in rat heart is greatest at low Ca2+ levels, but persists to a lesser degree at extracellular calcium concentrations of 2.5 mM; and 3) D600-inhibitable calcium channels appear to be relatively less important in the maintenance of cardiac contractility in rat than in cat cardiac muscle.

scholarly journals Coronary vasodilation and positive inotropism by urocortin in the isolated rat heart

2001 ◽  
Vol 169 (1) ◽  
pp. 177-183 ◽  
Author(s):  
K Terui ◽  
A Higashiyama ◽  
N Horiba ◽  
KI Furukawa ◽  
S Motomura ◽  
...  
Keyword(s):  
Rat Heart ◽  
Isolated Rat Heart ◽  
Coronary Vasodilation ◽  
Duration Of Action ◽  
Inotropic Effects ◽  
Vasodilator Effect ◽  
Cardiac Effects ◽  
Positive Inotropic Effects ◽  
Isolated Rat

Corticotropin-releasing factor (CRF) has a coronary vasodilator effect and a positive inotropic effect on the isolated rat heart. Recently, expression of CRF receptor type 2 (CRF-R2) has been demonstrated in the heart. In addition, urocortin (Ucn), a new member of the CRF family, has been reported to have much greater affinity for CRF-R2 than CRF. It is suggested that the cardiac effects of Ucn may be more potent than those of CRF. We compared the effect of Ucn with that of CRF on isolated rat heart. The effects of Ucn were then analyzed to determine whether these effects were mediated by CRF receptors and/or any other mediators under the following conditions: perfusion buffer containing (1) alpha-helical CRF 9-41, (2) indomethacin, (3) N(G)-nitro-l -arginine methylester and (4) propranolol. Ucn exhibited a greater effect with a longer duration of action than CRF. Indomethacin significantly attenuated the vasodilator effects of Ucn (P<0.05). CRF receptor antagonist diminished both coronary vasodilation and the positive inotropic effects of Ucn (P<0.05). These results suggest that the cardiac effects of Ucn may be mediated by a CRF receptor, and prostaglandins may be involved in the vasodilator effect.

Roselle Polyphenols Exert Potent Negative Inotropic Effects via Modulation of Intracellular Calcium Regulatory Channels in Isolated Rat Heart

2016 ◽  
Vol 17 (3) ◽  
pp. 251-259 ◽  
Author(s):  
Yi-Cheng Lim ◽  
Siti Balkis Budin ◽  
Faizah Othman ◽  
Jalifah Latip ◽  
Satirah Zainalabidin
Keyword(s):  
Intracellular Calcium ◽  
Rat Heart ◽  
Isolated Rat Heart ◽  
Inotropic Effects ◽  
Negative Inotropic Effects ◽  
Isolated Rat

Inotropic effects of ejection are myocardial properties

1994 ◽  
Vol 266 (3) ◽  
pp. H1202-H1213 ◽  
Author(s):  
P. P. De Tombe ◽  
W. C. Little
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Negative Effects ◽  
Inotropic Effects ◽  
Contraction Duration ◽  
Loading System ◽  
Positive Effect ◽  
Isolated Rat

Recent studies in isolated and in vivo canine hearts have suggested that the left ventricular end-systolic pressure (LVPes) of ejecting beats is the net result of a balance between positive and negative effects of ejection. At present, it is unknown whether these ejection effects are merely a ventricular chamber property or represent a fundamental myocardial property. Accordingly, we examined the effects of ejection in eight isolated rat cardiac trabeculae at the sarcomere level. We approximated in situ sarcomere shortening patterns using an iterative computer loading system. Six isovolumic contractions were compared with four ejecting contractions. The superfusing solution contained either 0.7 mM Ca2+ or 0.65 mM Sr2+ plus 0.15 mM Ca2+. With Ca2+, simulated LVPes ("LVP"es) of ejecting contractions was significantly lower than isovolumic "LVP"es (-5.3 +/- 5.6%), whereas with Sr2+, ejecting "LVP"es was significantly higher than isovolumic "LVP"es (+4.5 +/- 7.5%). Contraction duration and time to end systole were markedly prolonged in ejecting vs. isovolumic contractions with either Ca2+ or Sr2+. As a consequence, comparison of simulated LVP between ejecting and isovolumic beats throughout the contraction, i.e., at the same simulated LVV and time, revealed only a positive effect of ejection with either Ca2+ (+18.8 +/- 5.5%) or Sr2+ (+23.4 +/-9.3%). We conclude that both positive and negative effects of ejection are basic myocardial properties.

scholarly journals sGCα1 mediates the negative inotropic effects of NO in cardiac myocytes independent of changes in calcium handling

2011 ◽  
Vol 301 (1) ◽  
pp. H157-H163 ◽  
Author(s):  
Sharon M. Cawley ◽  
Starsha Kolodziej ◽  
Fumito Ichinose ◽  
Peter Brouckaert ◽  
Emmanuel S. Buys ◽  
...  
Keyword(s):  
Cardiac Myocytes ◽  
Soluble Guanylate Cyclase ◽  
Contractile Function ◽  
Cardiac Contractility ◽  
Left Ventricular ◽  
Calcium Handling ◽  
Inotropic Effect ◽  
Inotropic Effects ◽  
Spermine Nonoate ◽  
Brl 37344

In the heart, nitric oxide (NO) modulates contractile function; however, the mechanisms responsible for this effect are incompletely understood. NO can elicit effects via a variety of mechanisms including S-nitrosylation and stimulation of cGMP synthesis by soluble guanylate cyclase (sGC). sGC is a heterodimer comprised of a β1- and an α1- or α2-subunit. sGCα1β1 is the predominant isoform in the heart. To characterize the role of sGC in the regulation of cardiac contractile function by NO, we compared left ventricular cardiac myocytes (CM) isolated from adult mice deficient in the sGC α1-subunit (sGCα1−/−) and from wild-type (WT) mice. Sarcomere shortening under basal conditions was less in sGCα1−/− CM than in WT CM. To activate endogenous NO synthesis from NO synthase 3, CM were incubated with the β3-adrenergic receptor (β3-AR) agonist BRL 37344. BRL 37344 decreased cardiac contractility in WT CM but not in sGCα1−/− myocytes. Administration of spermine NONOate, an NO donor compound, did not affect sarcomeric shortening in CM of either genotype; however, in the presence of isoproterenol, addition of spermine NONOate reduced sarcomere shortening in WT but not in sGCα1−/− CM. Neither BRL 37344 nor spermine NONOate altered calcium handling in CM of either genotype. These findings suggest that sGCα1 exerts a positive inotropic effect under basal conditions, as well as mediates the negative inotropic effect of β3-AR signaling. Additionally, our work demonstrates that sGCα1β1 is required for NO to depress β1/β2-AR-stimulated cardiac contractility and that this modulation is independent of changes in calcium handling.

Interaction Between Negative Inotropic Effects of Halothane and Nifedipine in the Isolated Rat Heart

1983 ◽  
Vol 5 (4) ◽  
pp. 592-597 ◽  
Author(s):  
Alistair G. Marshall ◽  
Igor Kissin ◽  
J. G. Reves ◽  
Edwin L. Bradley ◽  
Eugene H. Blackstone
Keyword(s):  
Rat Heart ◽  
Isolated Rat Heart ◽  
Inotropic Effects ◽  
Negative Inotropic Effects ◽  
Isolated Rat

Effects of Desflurane in Senescent Rat Myocardium

2006 ◽  
Vol 105 (5) ◽  
pp. 961-967 ◽  
Author(s):  
Sandrine Rozenberg ◽  
Sophie Besse ◽  
Julien Amour ◽  
Benoît Vivien ◽  
Benoît Tavernier ◽  
...  
Keyword(s):  
Negative Inotropic Effect ◽  
Left Ventricular ◽  
Inotropic Effect ◽  
Shortening Velocity ◽  
Adult Rats ◽  
Inotropic Effects ◽  
Beta Adrenoceptor ◽  
Low Load ◽  
Positive Effect ◽  
Negative Inotropic Effects

Background The myocardial negative inotropic effects of desflurane are less pronounced than those of other halogenated anesthetics, partly because of intramyocardial catecholamine store release. However, the effects of desflurane on aging myocardium are unknown, whereas aging is known to be associated with an attenuation of catecholamine responsiveness. Methods The effects of desflurane (1.9-9.3 vol%) were studied in left ventricular papillary muscle of adult and senescent rats (29 degrees C; 0.5 mm Ca; stimulation frequency 12 pulses/min). The inotropic effects were compared under low and high loads, using the maximum unloaded shortening velocity and maximum isometric active force, and without or with alpha- and beta-adrenoceptor blockade. Results Desflurane induced a moderate positive inotropic effect in adult rats but a negative inotropic effect in senescent rats. After alpha- and beta-adrenoceptor blockade, desflurane induced a comparable negative inotropic effect in adult and senescent rats. No lusitropic effect under low load was observed, whereas desflurane induced a slight but significant positive lusitropic effect under high load similar between the two groups of rats. This positive effect was abolished by adrenoceptor blockade. Conclusion The authors' study suggests that desflurane does not induce significant intramyocardial catecholamine release in senescent myocardium, a result that should be integrated in the well-known alteration in the catecholamine response during aging.

Adenosine attenuation of catecholamine-enhanced contractility of rat heart in vivo

1991 ◽  
Vol 260 (5) ◽  
pp. H1635-H1639 ◽  
Author(s):  
F. D. Romano ◽  
T. S. Naimi ◽  
J. G. Dobson
Keyword(s):  
Rat Heart ◽  
Receptor Agonist ◽  
Jugular Vein ◽  
Cardiac Contractility ◽  
Physiological Role ◽  
Inotropic Effects ◽  
Adenosine A1 ◽  
Positive Inotropic Effects ◽  
A1 Receptor

The antiadrenergic action of adenosine was examined in open- and closed-chest preparations of anesthetized rats. The positive inotropic effects of a jugular vein infusion of either isoproterenol or epinephrine were attenuated by phenylisopropyladenosine, an adenosine A1-receptor agonist. 1,3-Dipropyl,8-cyclopentylxanthine, a specific A1-receptor antagonist, inhibited the action of phenylisopropyladenosine. The results indicate that adenosine receptor-mediated mechanisms are functional in the blood-perfused rodent heart and support the possibility of a physiological role for adenosine in modulating cardiac contractility.

scholarly journals Evaluation of Negative Inotropic Effects of a Isoquinoline Alkaloid N-14

2021 ◽  
Vol 4 (3) ◽  
pp. 01-05
Author(s):  
Inoyat Jumayev
Keyword(s):  
Muscle Contraction ◽  
Papillary Muscle ◽  
Heart Muscle ◽  
Rat Heart ◽  
Cyclopiazonic Acid ◽  
Negative Inotropic Effect ◽  
Isoquinoline Alkaloid ◽  
Inotropic Effect ◽  
Inotropic Effects ◽  
Negative Inotropic Effects

In studies, the alkaloid 1-(2-Chloro-4,5-methylenedioxyphenyl)-2-hydroxyethyl-6,7-dimethoxy-1,2,3,4-tetrahydroisoquinoline (N-14) had a negative inotropic effect on the activity of the papillary muscle contraction of the rat heart detected. Ca2+ ions from SR play an important role in the process of contraction of the heart muscle. With this in mind, the negative inotropic effect of the N-14 alkaloid was investigated with the modification of the accumulation processes of Ca2+ ions to SR. To clarify this, we examined the effects of the alkaloid being studied on SERCA2a and RyR2. To do this, the inhibitor of SERCA2a - cyclopiazonic acid (CPA) and RyR activator caffeine, which provide the accumulation of Ca2+ ions in SR, were used.

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