348 Effect of propranolol on heart rate and arrhythmias in freely moving mice and isolated hearts of deltaKPQ-SCN5A LQT3 mice

EP Europace ◽  
2005 ◽  
Vol 7 ◽  
pp. 71-71
Keyword(s):  
Heart Rate ◽  
Isolated Hearts ◽  
Freely Moving

Independence of heart rate and circadian period in the golden hamster

1993 ◽  
Vol 264 (2) ◽  
pp. R235-R238
Author(s):  
R. Refinetti ◽  
M. Menaker
Keyword(s):  
Heart Rate ◽  
Cardiac Pacemaker ◽  
Myocardial Cell ◽  
Circadian Oscillation ◽  
Circadian Period ◽  
Isolated Hearts ◽  
Rate Oscillations ◽  
The Mean ◽  
Freely Moving

Cardiac contractions are under the influence of at least two processes of biological timing, one responsible for the mean level of heart rate (oscillations with a frequency of up to several hundred per minute) and another responsible for the circadian rhythm of heart rate (oscillations with a frequency of one per 24 h). To investigate whether the mean level of heart rate is proportional to the frequency of circadian oscillation, we compared the heart rates of normal golden hamsters (circadian period approximately 24 h) and tau-mutant hamsters (circadian period approximately 20 h). Neither in anesthetized preparations nor in freely moving animals was there a difference in heart rate between the two groups despite the 20% difference in circadian period. Thus the mean level of heart rate seems to be independent of the circadian period. It is likely that the tau gene, which affects the frequency of the circadian pacemaker, has no effect on the intrinsic frequency of the cardiac pacemaker. In vitro studies of isolated hearts or myocardial cell cultures are necessary to confirm this inference.

scholarly journals 348 Effect of propranolol on heart rate and arrhythmias in freely moving mice and isolated hearts of deltaKPQ-SCN5A LQT3 mice

EP Europace ◽  
2005 ◽  
Vol 7 (Supplement_1) ◽  
pp. 71-71
Author(s):  
L. Fabritz ◽  
P. Kirchhof ◽  
M. Emmerich ◽  
L. Fortm ller ◽  
G. M nnig ◽  
...  
Keyword(s):  
Heart Rate ◽  
Isolated Hearts ◽  
Freely Moving

Parasympathetic influence on heart rate in euthermic and hibernating ground squirrels.

1995 ◽  
Vol 198 (4) ◽  
pp. 931-937 ◽  
Author(s):  
M B Harris ◽  
W K Milsom
Keyword(s):  
Heart Rate ◽  
Ambient Temperature ◽  
Parasympathetic Nervous System ◽  
Ground Squirrels ◽  
Relative Role ◽  
Body Temperatures ◽  
Inotropic Effects ◽  
Ambient Temperatures ◽  
Isolated Hearts ◽  
C 32

The relative role of the parasympathetic nervous system during deep hibernation is enigmatic. Conflicting hypotheses exist, and both sides draw support from investigations of vagal influence on the heart. Recent studies have shown cardiac chronotropic and inotropic effects of parasympathetic stimulation and inhibition in isolated hearts and anesthetized animals at hibernating body temperatures. No studies, however, have demonstrated such occurrences in undisturbed deeply hibernating animals. The present study documents respiratory-related alterations in heart rate during euthermia and hibernation at ambient temperatures of 15, 10 and 5 degrees C mediated by parasympathetic influence. During quiet wakefulness, euthermic squirrels breathed continuously and exhibited a 29% acceleration in heart rate during inspiration. During deep undisturbed hibernation, at 15, 10 and 5 degrees C ambient temperature, animals exhibited an episodic breathing pattern and body temperatures were slightly above ambient temperature. At each temperature, heart rate during the respiratory episode was greater than that during the apnea. The magnitude of this ventilatory tachycardia decreased with ambient temperature, being 108% at 15 degrees C, 32% at 10 degrees C and 11.5% at 5 degrees C. Animals exposed to 3% CO2 at 5 degrees C, which significantly increased ventilation, still exhibited an 11.7% increase in heart rate during breathing. Thus, the magnitude of the ventilation tachycardia was independent of the level of ventilation, at least over the range studied. Inhibition of vagus nerve conduction at 5 degrees C was achieved using localized nerve block. This led to an increase in apneic heart rate and abolished the ventilatory tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac nicotinic receptors show β-subunit dependent compensatory changes

2021 ◽  
Author(s):  
Katarina Targosova ◽  
Matej Kucera ◽  
Zuzana Kilianova ◽  
Lubica Slobodova ◽  
Kristina Szmicsekova ◽  
...  
Keyword(s):  
Heart Rate ◽  
Muscarinic Receptors ◽  
Nicotinic Receptors ◽  
Isolated Heart ◽  
High Dose ◽  
Β Subunit ◽  
Adrenergic Stimulation ◽  
Relative Expression ◽  
Isolated Hearts ◽  
Heart Functions

Nicotinic receptors (NR) play an important role in the cholinergic regulation of heart functions, and converging evidence suggests a diverse repertoire of NR subunits in the heart. A recent hypothesis about the plasticity of β NR subunits suggests that β2 and β4 subunits may substitute for each other. In our study, we assessed the hypothetical β subunit interchangeability in the heart at the level of mRNA. Using two mutant mice strains lacking β2 or β4 NR subunits, we examined the relative expression of NR subunits and other key cholinergic molecules. We investigated the physiology of isolated hearts perfused by Langendorff's method at basal conditions and after cholinergic and/or adrenergic stimulation. Lack of β2 NR subunit was accompanied with decreased relative expression of β4 and α3 subunits. No other cholinergic changes were observed at the level of mRNA, except for increased M3 and decreased M4 muscarinic receptors. Isolated hearts lacking β2 NR subunit showed different dynamics in heart rate response to indirect cholinergic stimulation. In hearts lacking β4 NR subunit, increased levels of β2 subunits were observed together with decreased mRNA for acetylcholine-synthetizing enzyme and M1 and M4 muscarinic receptors. Changes in the expression levels in β4-/- hearts were associated with increased basal heart rate and impaired response to a high dose of acetylcholine upon adrenergic stimulation. In support of the proposed plasticity of cardiac NRs, our results confirmed subunit-dependent compensatory changes to missing cardiac NRs subunits with consequences on isolated heart physiology.

scholarly journals Effect of L-glutamate injected into the hypothalamus on blood pressure and heart rate in freely moving rats

1982 ◽  
Vol 32 ◽  
pp. 268
Author(s):  
Shizuo Nakamura ◽  
Hisashi Ohta ◽  
Shigenori Watanabe ◽  
Showa Ueki
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Freely Moving Rats ◽  
Freely Moving

Hemodynamic effects of posterior hypothalamic injection of neuropeptide Y in awake rats

1991 ◽  
Vol 261 (3) ◽  
pp. H814-H824 ◽  
Author(s):  
J. R. Martin ◽  
M. M. Knuepfer ◽  
T. C. Westfall
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Neuropeptide Y ◽  
Cardiovascular System ◽  
Peripheral Resistance ◽  
Hypothalamic Nucleus ◽  
Initial Increase ◽  
System Control ◽  
Posterior Hypothalamic Nucleus ◽  
Freely Moving

Unilateral microinjection of neuropeptide Y (NPY) into the posterior hypothalamic nucleus was previously found to evoke a sympathoexcitatory-mediated increase in mean arterial pressure (MAP) in urethan-anesthetized rats. In this study, the effect of unilateral injection of NPY into the posterior hypothalamic nucleus on the cardiovascular system of conscious, freely moving rats was determined. Microinjection of NPY (0.2-2.4 nmol) or the cholinergic agonist carbachol (0.5-5.5 nmol) resulted in concentration-dependent increases in MAP. Pretreatment of animals with 7.5 mg/kg iv of the ganglionic blocker pentolinium resulted in a blockade of the increase in MAP evoked by microinjection of NPY (2.4 nmol) or carbachol (3.3 nmol). Despite their similarity of effects on MAP, NPY and carbachol evoked different changes in heart rate. NPY increased heart rate, whereas carbachol evoked a biphasic change in heart rate that consisted of an initial increase followed by a decrease. In addition, carbachol caused increases in both hindquarter and mesenteric vascular resistances, whereas NPY caused a short-lasting increase in mesenteric resistance and a tendency toward an increase in hindquarter resistance. Both NPY and carbachol increased total peripheral resistance while NPY decreased stroke volume. Cardiac output was not significantly affected by either NPY or carbachol, although NPY had a tendency to decrease cardiac output. These results suggest that microinjection of NPY or carbachol into the posterior hypothalamic nucleus of conscious rats evokes an increase in MAP primarily as a result of sympathoexcitation and that NPY and carbachol selectively affect autonomic nervous system control of the cardiovascular system.

Chronic heart rate reduction remodels ion channel transcripts in the mouse sinoatrial node but not in the ventricle

2006 ◽  
Vol 24 (1) ◽  
pp. 4-12 ◽  
Author(s):  
Anne-Laure Leoni ◽  
Céline Marionneau ◽  
Sophie Demolombe ◽  
Sabrina Le Bouter ◽  
Matteo E. Mangoni ◽  
...  
Keyword(s):  
Heart Rate ◽  
Ion Channel ◽  
Clustering Analysis ◽  
Connexin 43 ◽  
Sinoatrial Node ◽  
Rt Pcr ◽  
Cardiac Electrical Activity ◽  
Channel Expression ◽  
Freely Moving ◽  
Α Subunits

We investigated the effects of chronic and moderate heart rate (HR) reduction on ion channel expression in the mouse sinoatrial node (SAN) and ventricle. Ten-week-old male C57BL/6 mice were treated twice daily with either vehicle or ivabradine at 5 mg/kg given orally during 3 wk. The effects of HR reduction on cardiac electrical activity were investigated in anesthetized mice with serial ECGs and in freely moving mice with telemetric recordings. With the use of high-throughput real-time RT-PCR, the expression of 68 ion channel subunits was evaluated in the SAN and ventricle at the end of the treatment period. In conscious mice, ivabradine induced a mean 16% HR reduction over a 24-h period that was sustained over the 3-wk administration. Other ECG parameters were not modified. Two-way hierarchical clustering analysis of gene expression revealed a separation of ventricles from SANs but no discrimination between treated and untreated ventricles, indicating that HR reduction per se induced limited remodeling in this tissue. In contrast, SAN samples clustered in two groups depending on the treatment. In the SAN from ivabradine-treated mice, the expression of nine ion channel subunits, including Navβ1 (−25%), Cav3.1 (−29%), Kir6.1 (−28%), Kvβ2 (−41%), and Kvβ3 (−30%), was significantly decreased. Eight genes were significantly upregulated, including K+ channel α-subunits (Kv1.1, +30%; Kir2.1, +29%; Kir3.1, +41%), hyperpolarization-activated cation channels (HCN2, +24%; HCN4, +52%), and connexin 43 (+26%). We conclude that reducing HR induces a complex remodeling of ion channel expression in the SAN but has little impact on ion channel transcripts in the ventricle.

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