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

Modulation of positive inotropy and metabolic coronary dilatation by myocardial α-adrenoceptors

1985 ◽  
Vol 63 (12) ◽  
pp. 1513-1521 ◽  
Author(s):  
Bruce J. Youngson ◽  
Jaime Talesnik
Keyword(s):  
Calcium Chloride ◽  
Blood Supply ◽  
Sympathetic Stimulation ◽  
Inotropic Action ◽  
Ischaemic Damage ◽  
Rat Hearts ◽  
Coronary Vasodilatation ◽  
Dependent Inhibition ◽  
Adrenoceptor Agonists ◽  
Inotropic Responses

Cardiac hyperactivity and its consequent metabolically induced coronary vasodilatation (MCD) were studied in isolated, perfused, electrically paced rat hearts. The α-adrenoceptor agonists, phenylephrine and methoxamine, produced a concentration-dependent inhibition of the inotropic responses to noradrenaline, dobutamine, isoprenaline, tyramine, and glucagon, while relatively potentiating their MCD reactions. This inhibition was unrelated to the α-agonists' known inotropic action and was not affected by catecholamine depletion of the heart. Withdrawal of the α-agonists or administration of the α-adrenoceptor antagonists phentolamine, phenoxybenzamine, or prazosin returned the inotropic and MCD reactions to normal. Neither the MCD response to electrically induced tachycardia nor the inotropic reactions produced by calcium chloride were affected by α-adrenoceptor agonists or antagonists. Alone, α-adrenoceptor antagonists were shown to potentiate the inotropic responses to noradrenaline and isoprenaline while the MCD was relatively diminished. The responses to glucagon were unaltered by α-antagonists. We postulate that myocardial reactivity to sympathetic stimulation can be modulated through α-adrenoceptors by the inhibition of processes that mediate cardiostimulation at post-β-adrenoceptor sites, together with facilitation of those leading up to MCD. Accordingly, this modulation would act to prevent ischaemic damage to the heart by acting to limit the inotropic responses to increasing sympathetic stimulation while maximizing the blood supply to the myocardium.

Heart rate as a determinant of the decay rate of the cardiac inotropic response to sympathetic nervous activity

1983 ◽  
Vol 61 (11) ◽  
pp. 1374-1381 ◽  
Author(s):  
Yukitaka Masuda ◽  
Matthew N. Levy
Keyword(s):  
Heart Rate ◽  
Sinus Rhythm ◽  
Nervous Activity ◽  
Ventricular Myocardium ◽  
Sympathetic Nervous Activity ◽  
Inotropic Response ◽  
Sympathetic Stimulation ◽  
Junctional Rhythm ◽  
Decay Times ◽  
Inotropic Responses

The cardiac responses to sympathetic nerve stimulation were measured in a series of open-chest, anesthetized dogs. In half the animals, the hearts were in a sinus rhythm; in the remaining animals, the hearts were in an atrioventricular (AV) junctional rhythm. Cocaine markedly prolonged the decay times of the chronotropic responses after cessation of sympathetic stimulation, regardless of the type of rhythm. The decay times of the inotropic responses were only slightly prolonged by cocaine in animals with a sinus rhythm, but the prolongations were pronounced in animals with an AV junctional rhythm. The lower basal heart rate appeared to be more responsible for the greater decay times of the inotropic responses in the animals with an AV junctional rhythm than in those with a sinus rhythm. In a second series of dogs, complete heart block was produced, cocaine was given, AND the hearts were paced at four different frequencies. The mean decay time of the inotropic response to sympathetic stimulation varied inversely AND substantially with the pacing frequency. The change in contraction frequency probably affects the rate of neurotransmitter dissipation from the ventricular myocardium, by altering either the coronary blood flow or the massaging action of the cardiac contractions.

scholarly journals α1A and α1B-adrenoceptor mediated inotropic responses in rat heart

1999 ◽  
Vol 79 ◽  
pp. 175
Author(s):  
Hitomi Otani ◽  
Katsuyuki Mishima ◽  
Hiroshi Kawasaki ◽  
Chiyoko Inagaki
Keyword(s):  
Rat Heart ◽  
Inotropic Responses

Pertussis toxin-sensitive and -insensitive mechanisms of α1-adrenoceptor-mediated inotropic responses in rat heart

2001 ◽  
Vol 419 (2-3) ◽  
pp. 249-252 ◽  
Author(s):  
Hitomi Otani ◽  
Akihiro Oshiro ◽  
Masahiro Yagi ◽  
Chiyoko Inagaki
Keyword(s):  
Pertussis Toxin ◽  
Rat Heart ◽  
Inotropic Responses

Non-classical regulation of β1- and β2-adrenoceptor-mediated inotropic responses in rat heart ventricle by the G protein Gi

2014 ◽  
Vol 387 (12) ◽  
pp. 1177-1186 ◽  
Author(s):  
Caroline Bull Melsom ◽  
Rizwan Iqbal Hussain ◽  
Øivind Ørstavik ◽  
Jan Magnus Aronsen ◽  
Ivar Sjaastad ◽  
...  
Keyword(s):  
G Protein ◽  
Rat Heart ◽  
Heart Ventricle ◽  
Inotropic Responses

Thyroid hormone modulates inotropic responses, α-adrenoceptor density and catecholamine concentrations in the rat heart

1996 ◽  
Vol 354 (6) ◽  
pp. 755-764 ◽  
Author(s):  
J. Zwaveling ◽  
H. D. Batink ◽  
E. A. Winkler Prins ◽  
M. Pfaffendorf ◽  
P. A. van Zwieten ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Rat Heart ◽  
Inotropic Responses

Rigorous swim training impairs mitochondrial function in post-ischaemic rat heart

1997 ◽  
Vol 160 (1) ◽  
pp. 139-148
Author(s):  
S.B. LEICHTWEIS ◽  
C. LEEUWENBURGH ◽  
D. J. PARMELEE ◽  
R. FIEBIG ◽  
L. L. JI
Keyword(s):  
Mitochondrial Function ◽  
Rat Heart
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