Tyramine‐induced endogenous noradrenaline efflux from <i>in situ</i> cardiac sympathetic nerve ending in cats

Takauchi, Yuji; Yamazaki, Toji; Akiyama, Tsuyoshi

doi:10.1046/j.1365-201x.2000.00664.x

Cited by 12 publications

(7 citation statements)

References 25 publications

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“…Total incorporation of 3 H-NE into ovarian tissue increased moderately during the neonatal-infantile period (d [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] and then abruptly during the second half of juvenile development (d 26 -30), remaining elevated at puberty (d [31][32][33][34][35], and after the first ovulation (d 40) (Fig. 1A).…”

Section: Incorporation Of 3 H-ne During Postnatal Ovarian Developmentmentioning

confidence: 97%

“…After a 3 min collection period in the presence of tyramine, the tissues were challenged again with K ϩ . The dose of tyramine we used has been shown to fully displace endogenous NE from synaptic vesicles (20).…”

Section: Ne Releasementioning

confidence: 99%

“…To biochemically characterize NE outflow, we challenged the ovaries using two manipulations routinely used to study basic properties of functional noradrenergic synapses: 1) dependence to extracellular calcium and 2) displacement of NE stored in vesicles by tyramine, a false neurotransmitter (20).…”

Section: Ne Releasementioning

confidence: 99%

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Functional Development of the Ovarian Noradrenergic Innervation

et al. 2007

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A substantial fraction of the noradrenergic innervation targeting the mammalian ovary is provided by neurons of the celiac ganglion. Although studies in the rat have shown that noradrenergic nerves reach the ovary near the time of birth, it is unknown how the functional capacity of this innervation unfolds during postnatal ovarian development. To address this issue, we assessed the ability of the developing ovary to incorporate and release (3)H-norepinephrine. Incorporation of (3)H-norepinephrine was low during the first 3 wk of postnatal life, but pharmacological inhibition of norepinephrine (NE) neuronal uptake with cocaine showed that an intact transport mechanism for NE into nerve terminals is already in place by the first week after birth. Consistent with this functional assessment, the mRNA encoding the NE transporter was also expressed in the celiac ganglion at this time. During neonatal-infantile development [postnatal (PN) d 5-20], the spontaneous, vesicle-independent outflow of recently taken up NE was high, but the NE output in response to K(+)-induced depolarization was low. After PN d 20, spontaneous outflow decreased and the response to K(+) increased markedly, reaching maximal values by the time of puberty. Tyramine-mediated displacement of NE stored in vesicles, which displace vesicular NE, showed that vesicle-dependent NE storage becomes functional by PN d 12 and that vesicular release increases during the juvenile-peripubertal phases of sexual development. These results indicate that vesicular release of NE from ovarian noradrenergic nerves begins to operate by the third week of postnatal life, becoming fully functional near the time of puberty.

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Section: Incorporation Of 3 H-ne During Postnatal Ovarian Developmentmentioning

confidence: 97%

Section: Ne Releasementioning

confidence: 99%

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Functional Development of the Ovarian Noradrenergic Innervation

et al. 2007

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“…Additionally, sympathetic nervous control of the peripheral vasculature was assessed by measuring the degree of arterial constriction after application of tyramine (10 −6 to 10 −2 mol/L). Tyramine releases norepinephrine from perivascular sympathetic nerve endings without affecting presynaptic reuptake (Takauchi et al 2000). Because the contractile response to tyramine reflects the total norepinephrine content of the perivascular sympathetic nerve endings, this is a pharmacological method for assessing sympathetic nerve function in vivo.…”

Section: Peripheral Arterial Controlmentioning

confidence: 99%

Hypoxia Disturbs Fetal Hemodynamics and Growth

2007

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Low-birth-weight babies have an increased risk of cardiovascular disease (CVD) in later life. The authors hypothesize that fetal hypoxia alters the structure and function of the developing cardiovascular system resulting in CVD. They investigated the effects of chronic hypoxia on cardiac performance, hemodynamic control, and growth during the second half of embryonic chick development. Three stages of hemodynamic adaptations were identified in hypoxic chick embryos. At embryonic day 13 (E13), heart rate and blood pressure were higher in hypoxic embryos. At E17, this was followed by sympathetic hyperinnervation of peripheral arteries, resulting in increased vasoconstriction during a chemoreflex. This was accompanied by dilatation of the left ventricle and a 50% reduction in cardiac contractility. E19 hypoxic embryos had a 33% higher baseline vascular tone, but failed to maintain blood pressure during acute stress, indicating cardiac failure. Reduced body, heart, and liver weights followed the hemodynamic changes. Chronic hypoxia induces dilated cardiomyopathy and sympathetic hyperinnervation of the peripheral vasculature leading to aberrant fetal hemodynamics and fetal growth restriction. This study identifies that alterations in fetal hemodynamic regulation are in the causal pathway between disturbances in fetal environment, restricted fetal growth and CVD, and establishes fetal hypoxia as a novel risk factor for cardiovascular disease.

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“…Tyramine releases norepinephrine from perivascular sympathetic nerve endings without affecting presynaptic reuptake. Because the contractile response to tyramine reflects the total norepinephrine content of the perivascular sympathetic nerve endings, 10 this is a sophisticated method for assessing sympathetic nerve function in vivo.…”

Section: Peripheral Arterial Controlmentioning

confidence: 99%

Hypoxia Induces Aortic Hypertrophic Growth, Left Ventricular Dysfunction, and Sympathetic Hyperinnervation of Peripheral Arteries in the Chick Embryo

et al. 2002

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Background-Low birth weight is associated with an increased incidence of cardiovascular diseases, including hypertension, later in life. This suggests that antenatal insults program for fetal adaptations of the circulatory system. In the present study, we evaluated the effects of mild hypoxia on cardiac function, blood pressure control, and arterial structure and function in near-term chick embryos. Methods and Results-Chick embryos were incubated under normoxic (21% O 2 ) or hypoxic (15% O 2 ) conditions and evaluated at incubation day 19 by use of histological techniques, isolated heart preparations, and in vivo measurements of sympathetic arterial tone and systemic hemodynamics. Chronic hypoxia caused a 33% increase in mortality and an 11% reduction in body weight in surviving embryos. The lumen of the ascending aorta in hypoxic embryos was 23% smaller. Left ventricular systolic pressure was 22% lower, and heart weight/body weight ratio was 14% higher. In resistance arteries of hypoxic embryos, in vivo baseline tone was 23% higher, norepinephrine sensitivity was similar, and norepinephrine release from sympathetic nerves increased 2-fold, indicating sympathetic hyperinnervation. Mean arterial pressure and heart rate were similar under resting conditions, but chronically hypoxic embryos failed to maintain blood pressure during acute stress. Conclusions-This study indicates that mild hypoxia during embryonic development induces alterations in cardiac and vascular function and structure and affects hemodynamic regulation. These findings reveal that antenatal insults have profound effects on the control and design of the circulatory system that are already established at birth and may program for hypertension and heart failure at a later age.

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Tyramine‐induced endogenous noradrenaline efflux from in situ cardiac sympathetic nerve ending in cats

Cited by 12 publications

References 25 publications

Functional Development of the Ovarian Noradrenergic Innervation

Functional Development of the Ovarian Noradrenergic Innervation

Hypoxia Disturbs Fetal Hemodynamics and Growth

Hypoxia Induces Aortic Hypertrophic Growth, Left Ventricular Dysfunction, and Sympathetic Hyperinnervation of Peripheral Arteries in the Chick Embryo

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