Effects of Chronicβ-Adrenergic Receptor Stimulation in Mice

Kudej, Raymond K.; Iwase, Mitsunori; Uechi, Masami; Vatner, Dorothy E.; Oka, Naoki; Ishikawa, Yoshihiro; Shannon, Richard P.; Bishop, Sanford P.; Vatner, Stephen F.

doi:10.1006/jmcc.1997.0508

Cited by 104 publications

(91 citation statements)

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“…In most animals, ISO induces subendocardial fibrosis and increases the collagen volume of the heart, 23,24 but in the present study the ISO-induced fibrosis was less than 6% of the total cardiac area in both genotypes on the 7th day. It has been reported that chronic ISO infusion induces considerably less connective tissue in mice than in other animals 25 and therefore a reduction in the size of cardiac myocytes rather than in the extent of cardiac fibrosis would be responsible for the attenuation of cardiac hypertrophy in eNOS-Tg mice.…”

Section: Discussionmentioning

confidence: 98%

Overexpression of Endothelial Nitric Oxide Synthase Attenuates Cardiac Hypertrophy Induced by Chronic Isoproterenol Infusion.

Ozaki

Kawashima

Yamashita

et al. 2002

Circ J

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Section: Discussionmentioning

confidence: 98%

Overexpression of Endothelial Nitric Oxide Synthase Attenuates Cardiac Hypertrophy Induced by Chronic Isoproterenol Infusion.

Ozaki

Kawashima

Yamashita

et al. 2002

Circ J

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“…These compensatory mechanisms are beneficial during stress and acute changes in the circulatory system [24,29,30,45]. However, these compensatory mechanisms are deleterious over the long term, particularly in the pathogenesis of human heart failure and experimentally induced animal heart failure [22,26]. Elevated sympathetic activity has been demonstrated in human heart failure and experimental models of heart failure [1,9,32,36,38,39].…”

Section: Discussionmentioning

confidence: 99%

“…Elevated plasma noradrenaline (NA) has been shown to contribute to the pathological chronotropic response, which leads to progression of CHF [9,32,36,38,39,44]. Chronic adrenergic stimulation has been shown to have a direct cardiotoxic effect [22,26], and elevated NA levels are associated with a poorer prognosis and increased mortality [9,11,31].The purpose of this study was to measure the plasma concentrations of the catecholamines NA and adrenaline (AD) in dogs with naturally acquired heart disease, mitral regurgitation (MR), tricuspid regurgitation (TR), and dilated cardiomyopathy and right ventricle heart failure due to Dirofilalia imitis infection. We also evaluated in changes in the plasma concentrations of NA and AD during rest, light stress, running, and recovery from running in iatrogenic mitral regurgitation dogs.…”

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confidence: 99%

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Heart Rate Modulation by Sympathetic Nerves in Dogs with Heart Failure.

Uechi

Shimizu

Mizuno

2002

The Journal of Veterinary Medical Science

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ABSTRACT. To clarify heart rate modulation by the sympathetic nervous system, dogs with naturally acquired and experimentally induced heart failure were examined. Heart rate and plasma catecholamine concentrations were measured in clinically healthy dogs (contr ol dogs) and dogs with mitral regurgitation (MR) during a resting period, a standing period, a period of standing in a medical examination room (to which the dogs were unaccustomed), a running period, and a period of recovery after running. The heart rate and plasma cate cholamine concentration increased in control dogs during the standing period and the medical examination room period, relative to the resting period. However, dogs with MR did not exhibit any clear increase in heart rate or catecholamine concentration under these light stress conditions. Running stress increased plasma catecholamine levels in control dogs; however, dogs with MR did not exhibit any significant changes. Thirty-two dogs with naturally acquired heart disease were classified as grades I to III on the ISACHC scale. The degree of increase in heart rate and plasma catecholamine levels in dogs with naturally acquired heart failure depended on their degree of heart failure. In conclusion, an increased heart rate and an activated sympathetic nervous system were observed, even in mild heart failure. This chronically activated sympathetic activity is expected to increase myocardial oxygen consumption, myocardial hypertrophy, and fibrosis, and to portend a poorer prognosis in heart failure. KEY WORDS: catecholamine, exercise, mitral regurgitation, stress.J. Vet. Med. Sci. 64(11): 1023-1029, 2002 Congestive heart failure (CHF) is characterized by increased peripheral vascular resistance and tachycardia. The reduced cardiac output in cardiac disease leads to failure of the peripheral blood circulation because of decreased parasympathetic tone and increased sympathetic tone [1,9,32,36,38,39]. Neurohumoral activation of the sympathetic nervous system and the renin-angiotensin-aldosterone axis, etc. increases circulating blood volume and arterial pressure by causing vasoconstriction and sodium and fluid retention [16]. Elevated plasma noradrenaline (NA) has been shown to contribute to the pathological chronotropic response, which leads to progression of CHF [9,32,36,38,39,44]. Chronic adrenergic stimulation has been shown to have a direct cardiotoxic effect [22,26], and elevated NA levels are associated with a poorer prognosis and increased mortality [9,11,31].The purpose of this study was to measure the plasma concentrations of the catecholamines NA and adrenaline (AD) in dogs with naturally acquired heart disease, mitral regurgitation (MR), tricuspid regurgitation (TR), and dilated cardiomyopathy and right ventricle heart failure due to Dirofilalia imitis infection. We also evaluated in changes in the plasma concentrations of NA and AD during rest, light stress, running, and recovery from running in iatrogenic mitral regurgitation dogs. MATERIALS AND METHODSThe methods used in this study ...

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“…19 In WT mice, 5 days of perfusion produced a marked increase in the ratio of cardiac mass to tibia length (CMTL) (59Ϯ17%, ISO versus WT) ( Figure 1A). The ISO perfusion induced an important tachycardia (62Ϯ4% in WT-ISO versus WT) ( Figure 1B).…”

Section: Role Of 5-ht 2b Rs In Iso-mediated Cardiac Hypertrophy In Vivomentioning

confidence: 99%

Involvement of the Serotonin 5-HT _2B Receptor in Cardiac Hypertrophy Linked to Sympathetic Stimulation

et al. 2004

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Background-The serotonergic 5-HT 2B receptor regulates cardiomyocyte development and growth. A putative contribution of this receptor to fibroblast-dependent cardiac function has not been identified. Methods and Results-By mimicking sympathetic stimulation with chronic isoproterenol perfusion in vivo, we found that mice developed a cardiac hypertrophy, which was prevented by exposure to the 5-HT 2B receptor antagonists SB206553 or SB215505 or in 5-HT 2B receptor-knockout mice. The isoproterenol-induced hypertrophy was associated with an increase in the plasma levels of interleukin-1␤ and tumor necrosis factor-␣ but not interleukin-6. In contrast, the plasma isoproterenol-induced cytokine increase was not observed in either 5-HT 2B receptor-mutant or wild-type mice perfused with isoproterenolϩSB206553. We demonstrated that stimulation of wild-type cardiac fibroblasts by isoproterenol markedly increased the production of the interleukin-6, interleukin-1␤, and tumor necrosis factor-␣ cytokines. Strikingly, we found that this isoproterenol-induced cytokine production was abolished by SB206553 or in 5-HT 2B receptor-knockout fibroblasts. Serotonin also stimulated production of the 3 cytokines in wild-type fibroblasts, which was effectively reduced in 5-HT 2B receptor-knockout fibroblasts. Conclusions-Our results demonstrate for the first time that 5-HT 2B receptors are essential for isoproterenol-induced cardiac hypertrophy, which involves the regulation of interleukin-6, interleukin-1␤, and tumor necrosis factor-␣ cytokine production by cardiac fibroblasts.

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Effects of Chronicβ-Adrenergic Receptor Stimulation in Mice

Cited by 104 publications

References 0 publications

Overexpression of Endothelial Nitric Oxide Synthase Attenuates Cardiac Hypertrophy Induced by Chronic Isoproterenol Infusion.

Overexpression of Endothelial Nitric Oxide Synthase Attenuates Cardiac Hypertrophy Induced by Chronic Isoproterenol Infusion.

Heart Rate Modulation by Sympathetic Nerves in Dogs with Heart Failure.

Involvement of the Serotonin 5-HT _2B Receptor in Cardiac Hypertrophy Linked to Sympathetic Stimulation

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Effects of Chronicβ-Adrenergic Receptor Stimulation in Mice

Cited by 104 publications

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Overexpression of Endothelial Nitric Oxide Synthase Attenuates Cardiac Hypertrophy Induced by Chronic Isoproterenol Infusion.

Overexpression of Endothelial Nitric Oxide Synthase Attenuates Cardiac Hypertrophy Induced by Chronic Isoproterenol Infusion.

Heart Rate Modulation by Sympathetic Nerves in Dogs with Heart Failure.

Involvement of the Serotonin 5-HT 2B Receptor in Cardiac Hypertrophy Linked to Sympathetic Stimulation

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Involvement of the Serotonin 5-HT _2B Receptor in Cardiac Hypertrophy Linked to Sympathetic Stimulation