Ca2+ Transients, Contractility, and Inotropic Responses in Rabbit Volume-Overloaded Cardiomyocytes

2000 ◽  
pp. 67-81 ◽  
Author(s):  
Kiyoharu Sakurai ◽  
Hiromi Sugawara ◽  
Tomoo Watanabe ◽  
Shigekazu Nakada ◽  
Hiroyuki Atsumi ◽  
...  
Keyword(s):  
Inotropic Responses

Discrepancies Between Inotropic Responses and β-Adrenoceptor Characteristics After Global Ischemia in Isolated Hearts

1991 ◽  
Vol 18 (5) ◽  
pp. 679-686 ◽  
Author(s):  
Romana van den Ende ◽  
Harry D. Batink ◽  
Martin Pfaffendorf ◽  
Pieter A. van Zwieten
Keyword(s):  
Global Ischemia ◽  
Isolated Hearts ◽  
Inotropic Responses

A simple experimental index for the evaluation of inotropic responses

1987 ◽  
Vol 18 (1) ◽  
pp. 23-29 ◽  
Author(s):  
Samuel H.H. Chan ◽  
B.T. Ong
Keyword(s):  
Inotropic Responses

scholarly journals Dissociation of Chronotropic and Inotropic Responses in the Rat Heart During Sympathetic Stimulation

1999 ◽  
Vol 63 (9) ◽  
pp. 710-717 ◽  
Author(s):  
Norio Onuki ◽  
Hisayuki Takahashi ◽  
Hitoshi Suzuki ◽  
Tomiyoshi Saito ◽  
Kazuhira Maehara ◽  
...  
Keyword(s):  
Rat Heart ◽  
Sympathetic Stimulation ◽  
Inotropic Responses

Hyperthyroidism-induced changes in positive inotropic responses in rats

1992 ◽  
Vol 24 ◽  
pp. 126
Author(s):  
Lindsay Brown ◽  
Gregory Amos ◽  
Catherine Marchant ◽  
Conrad Sernia
Keyword(s):  
Induced Changes ◽  
Inotropic Responses

Positive inotropic responses in cardiac muscles: influence of stimulation frequency and species

1982 ◽  
Vol 60 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Peter K. S. Siegl ◽  
John H. McNeill
Keyword(s):  
Right Ventricular ◽  
Species Difference ◽  
Extracellular Calcium ◽  
Stimulation Frequency ◽  
Force Frequency ◽  
Papillary Muscles ◽  
Drug Induced ◽  
Cardiac Muscles ◽  
Inotropic Responses ◽  
Isolated Rat

Inotropic responses to cumulative additions of methoxaminc (10−7 to 3 × 10−4 M), isoproterenol (10−9 to 10−5 M), or calcium (2 to 32 mM) were measured in isolated rat left atria and papillary muscles and rabbit right ventricular papillary muscles at three stimulation frequencies. Cardiac muscles were incubated in oxygenated Chenoweth–Koelle solution (2 mM calcium) at 37 °C. The basal developed force (BDF) before and maximum developed force (MDF) after challenge with methoxamine and isoproterenol were inversely related to stimulation frequency in rat preparations. BDF was directly related to stimulation rate in rabbit papillary muscles while MDF was independent of the rate. Drug-induced increases in force (MDF – BDF) were independent of stimulation frequency in rat and inversely related to stimulation frequency in rabbit. Responses to calcium were similar to the observed adrenergic responses. Also, force–frequency relationships of the rat and rabbit preparations were not similar in the absence and presence of these agonists. These data show that inotropic responses by rat and rabbit hearts are not affected similarly by stimulation frequency and this may reflect a species difference in the utilization of extracellular calcium for contraction.

Abstract 12677: Impaired Cardiomyocyte Contractility to Angiotensin-(1-12) in a Humanized Angiotensinogen Model of Hypertension

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Yixi Liu ◽  
Heng Jie Cheng ◽  
Xiaoqiang Sun ◽  
Jing Cao ◽  
Zhe Chen ◽  
...  
Keyword(s):  
Contractile Function ◽  
Ang Ii ◽  
Transgenic Rats ◽  
Inotropic Effects ◽  
Cardiomyocyte Contractility ◽  
Inotropic Responses ◽  
Myocyte Contractility ◽  
Agt Gene ◽  
Rat Genome ◽  
Dependent Mechanism

Background: Angiotensin-(1-12) [Ang-(1-12)] is a chymase-dependent source for Angiotensin II (Ang II) inotropic activity that may be impaired in a model of sustained hypertension with high cardiac Ang II content due to insertion of the human angiotensinogen (AGT) gene in the rat genome. Accordingly, we evaluated the effects of Ang-(1-12) and Ang II on myocyte contractility and [Ca 2+ ] i regulation in 9 adult male transgenic rats expressing the human AGT gene [TGR(hAGT)L1623)] and 9 SD controls. Methods: We compared LV myocyte contraction, relaxation and [Ca 2+ ] i transient ([Ca 2+ ] iT ) responses to Ang-(1-12) (4x10 -6 M) and Ang II (10 -6 M) in freshly isolated LV myocytes. Results: Myocyte contraction (dL/dt max , 109.6 vs 127.9 μm/s), relaxation (dR/dt max , 95.3 vs 107.5 μm/s) and [Ca 2+ ] iT (0.15 vs 0.24) were depressed in TGR(hAGT)L1623 rats compared to SD controls. Moreover, cell contractile and [Ca 2+ ] iT responses following exposure to Ang-(1-12) or Ang II were markedly blunted. In SD myocytes, versus baseline, Ang II or Ang-(1-12) superfusion produced significant increases in dL/dt max [Ang II: 44% vs Ang-(1-12): 34%], dR/dt max (33% vs 26%) and [Ca 2+ ] iT (31% vs 25%). Importantly, the magnitude of the responses to the two agents in TGR(hAGT)L1623 myocytes was significantly reduced. Versus the changes in SD myocytes, Ang-(1-12) caused significantly less increases in dL/dt max (22%), dR/dt max (16%) and [Ca 2+ ] iT (15%) in TGR(hAGT)L1623 myocytes . Ang II also caused similar significantly attenuated increases in dL/dt max (27%), dR/dt max (25%) and [Ca 2+ ] iT (23%). The Ang-(1-12)-induced inotropic effects were completely prevented in the presence of the inhibitory cAMP analog, Rp-cAMPS (10 –4 M, 2 hours) in both SD and TGR(hAGT)L1623 myocytes, but were further augmented only intransgenic rats after incubation of myocytes with the G i inhibitor, pertussis toxin (PTX, 2 μg/ml, 36°C, 5 hours). Conclusions: Ang-(1-12) stimulates LV myocyte contractile function and [Ca 2+ ] iT in both SD and TGR(hAGT)L1623 rats. Furthermore, we now show that the blunted inotropic responses to Ang-(1-12) and Ang II in rats expressing the human AGT gene is mediated through a cAMP-dependent mechanism that is coupled to both stimulatory G and inhibitory PTX-sensitive G proteins.

Differential pre- and postsynaptic effects of desipramine on cardiac sympathetic nerve terminals in RHF

2002 ◽  
Vol 283 (5) ◽  
pp. H1863-H1872 ◽  
Author(s):  
Chang-Seng Liang ◽  
Yoshihiro Himura ◽  
Michihiro Kashiki ◽  
Suzanne Y. Stevens
Keyword(s):  
Sympathetic Nerve ◽  
Glyoxylic Acid ◽  
Nerve Endings ◽  
Immunocytochemical Staining ◽  
Receptor Density ◽  
Cardiac Sympathetic Nerve ◽  
Uptake Inhibition ◽  
Uptake Activity ◽  
Β Receptor ◽  
Inotropic Responses

Right heart failure (RHF) is characterized by chamber-specific reductions of myocardial norepinephrine (NE) reuptake, β-receptor density, and profiles of cardiac sympathetic nerve ending neurotransmitters. To study the functional linkage between NE uptake and the pre- and postsynaptic changes, we administered desipramine (225 mg/day), a NE uptake inhibitor, to dogs with RHF produced by tricuspid avulsion and progressive pulmonary constriction or sham-operated dogs for 6 wk. Animals receiving no desipramine were studied as controls. We measured myocardial NE uptake activity using [3H]NE, β-receptor density by [125I]iodocyanopindolol, inotropic responses to dobutamine, and noradrenergic terminal neurotransmitter profiles by glyoxylic acid-induced histofluorescence for catecholamines, and immunocytochemical staining for tyrosine hydroxylase and neuropeptide Y. Desipramine decreased myocardial NE uptake activity and had no effect on the resting hemodynamics in both RHF and sham animals but decreased myocardial β-adrenoceptor density and β-adrenergic inotropic responses in both ventricles of the RHF animals. However, desipramine treatment prevented the reduction of sympathetic neurotransmitter profiles in the failing heart. Our results indicate that NE uptake inhibition facilitates the reduction of myocardial β-adrenoceptor density and β-adrenergic subsensitivity in RHF, probably by increasing interstitial NE concentrations, but protects the cardiac noradrenergic nerve endings from damage, probably via blockade of NE-derived neurotoxic metabolites into the nerve endings.

Atrioventricular responses of canine heart following chronic unilateral vagotomy

1987 ◽  
Vol 253 (2) ◽  
pp. H394-H401 ◽  
Author(s):  
D. V. Priola ◽  
C. Anagnostelis ◽  
C. Sanchez-Wilson ◽  
T. M. Blomquist
Keyword(s):  
Frequency Response ◽  
Control Mechanisms ◽  
Canine Heart ◽  
Response Curves ◽  
Group Iii ◽  
Group I ◽  
Group Ii ◽  
The Right ◽  
Inotropic Responses ◽  
Intrinsic Cardiac Nerves

The intrinsic cardiac nerves (ICN) have been shown to develop supersensitivity to nicotine (NIC) following complete extrinsic cardiac denervation. The present experiments were performed to delineate the pattern of ICN distribution in the heart by examining the pattern of NIC supersensitivity after unilateral vagotomy (VGX). Thirty-eight dogs were placed on cardiopulmonary bypass and inotropy evaluated by means of isovolumic pressures from fluid-filled balloons placed in the atria and ventricles. The animals were divided into three groups: group I, sham-operated controls; group II, animals studied 1–2 wk after VGX; and group III, animals studied 8–12 wk after VGX. Chronotropic and inotropic responses were evaluated in terms of NIC and acetylcholine (ACh) dose-response curves as well as frequency-response curves to stimulation of the intact vagus nerve (0.5–30 Hz). No change in NIC sensitivity was observed in group II, and vagal frequency-response curves were identical to group I. In group III dogs, both the right atrium and right ventricle showed significant increases in NIC sensitivity after left vagotomy. All group III animals showed right-shifted frequency-response curves. We conclude that nicotinic supersensitivity of the ICN and inotropic unresponsiveness to vagal stimulation occur but are slow in developing (70–130 days); and preganglionic sprouting does not appear to play a functional role in the adjustment of cardiac control mechanisms to unilateral vagotomy.

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