Effect of age on cardiac norepinephrine release in the female rat

Snyder, David; Johnson, Mark D.; Eskin, Bernard A.; Wang, W.; Roberts, Jay

doi:10.1007/bf03324337

Cited by 6 publications

(5 citation statements)

References 27 publications

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“…Our findings are relevant to the results of a number of studies that have linked NE to cardiomyopathies (25)(26)(27). They are also consistent with studies that have linked excessive NE stimulation in the heart to arrhythmias and other potentially damaging effects due to increased oxygen demand and free radical formation (18,(28)(29)(30)(31)(32)(33).…”

Section: Discussionsupporting

confidence: 90%

“…Previously, we have demonstrated that in contrast to male rats, female rats do not show an age-related reduction in depolarization-elicited NE release from cardiac synaptosomes (25). Indeed, female rats exhibit a (nonsignificant) tendency for an age-dependent increase in NE release (25).…”

mentioning

confidence: 78%

“…Depolarization-induced release of eH]-NE from cardiac synaptosomes was performed as previously described (22)(23)(24)(25). Briefly, synaptosomes were prepared by digesting minced heart tissue with collagenase (class II; Worthington Biochemical, Lakewood, NJ) followed by homogenization in 0.32 M sucrose.…”

Section: Methodsmentioning

confidence: 99%

“…The amount of eH]-NE in each 5-min fraction was determined by scintillation counting. As previously described (25), the fraction of the total eH]-NE released into each fraction was calculated. Furthermore, net fractional release of eH]-NE due to depolarization was calculated as the fractional release induced by the high K+ buffer minus the basal fractional release.…”

Section: Methodsmentioning

confidence: 99%

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Cardiac Norepinephrine Release: Modulation by Ovariectomy and Estrogen

Eskin

Snyder

Roberts

et al. 2003

Exp Biol Med (Maywood)

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Previously, we have demonstrated that in contrast to male rats, female rats do not show an age-related reduction of depolarization-elicited norepinephrine (NE) release from cardiac synaptosomes (resealed nerve terminals). These results suggest that sex hormones such as estrogen may modulate NE release from cardiac synaptosomes prepared from female rats. The present study was designed to test the hypotheses that long-term estrogen depletion, resulting from ovariectomy, and estrogen replacement alters depolarization-elicited NE release from cardiac synaptosomes. Female F344 rats were divided into two groups, one of which underwent bilateral ovariectomy, whereas the other underwent a sham operation. Three ovariectomized subgroups received daily injections of conjugated equine estrogens, delta8,9-dehydroestrone or 17 alpha-dihydroequilenin. Another ovariectomized control subgroup and the sham-operated animals received daily injections of vehicle. After 90 or 270 days of treatment, the animals were sacrificed. Cardiac synaptosomes were prepared from each heart, incubated with [(3)H]-NE, and used to evaluate NE release capacity by exposure to 50 mM K(+). The effectiveness of the ovariectomy and the estrogenic actions of the test compounds was confirmed by evaluating vaginal smears, determining uterine weights, and measuring serum luteinizing hormone (LH) concentrations. Ovariectomy (after both 90 and 270 days) significantly increased depolarization-induced NE release compared with sham-operated rats. Treatment with all three estrogenic preparations reduced NE release in ovariectomized rats to values similar to those observed in sham-operated animals. Interestingly, NE release rates from rats treated with conjugated estrogens for 270 but not 90 days were significantly below that observed in age-matched sham animals. These results demonstrate that estrogen modulates depolarization-elicited NE release from cardiac nerve terminals. Such modulation may represent a protective action by estrogen at the cardiac synapse.

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Section: Discussionsupporting

confidence: 90%

mentioning

confidence: 78%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Cardiac Norepinephrine Release: Modulation by Ovariectomy and Estrogen

Eskin

Snyder

Roberts

et al. 2003

Exp Biol Med (Maywood)

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“…On the other hand, it was indicated that female rats did not show an age-related reduction in depolarization-elicited NE release from cardiac synaptosomes and rather exhibited a tendency for an age-dependent increase in NE release. 22 Moreover, Moldovanova et al 23 have suggested that sex hormones alter the hemodynamic response to NET inhibition in women. Taken together, it seems likely that sex hormones may modulate NE release after I/R, but the underlying mechanism remains to be determined.…”

Section: Introductionmentioning

confidence: 99%

Sex Differences in Postischemic Cardiac Dysfunction and Norepinephrine Overflow in Rat Heart

Fukumoto

Yamashita

Tawa

et al. 2012

Journal of Cardiovascular Pharmacology

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The purpose of this study is to elucidate the relationship between sex difference and norepinephrine (NE) release in the pathogenesis of myocardial ischemia/reperfusion (I/R) injury. Isolated male and female rat hearts were subjected to 40-minute global ischemia followed by 30-minute reperfusion. Compared with male hearts, I/R-induced cardiac dysfunction, such as decreased left ventricular developed pressure and dP/dtmax and increased left ventricular end diastolic pressure, was significantly attenuated in female hearts. An excessive NE overflow in the coronary effluent from the postischemic heart in females was much less than that in males. These sex differences were abolished by ovariectomy, but in vivo treatment with 17β-estradiol recovered it. This ameliorating effect of 17β-estradiol was not observed in the presence of nitric oxide (NO) synthase inhibitor N-nitro-L-arginine. When NOx (NO2/NO3) levels in the coronary effluent after onset of reperfusion were measured, reversed correlated relationships between NOx production and I/R-induced cardiac dysfunction, and NE overflow, were observed. These findings suggest that sex differences in the postischemic cardiac dysfunction are closely related to the NE overflow from the postischemic heart and that estrogen plays a key role in the cardioprotective effect against I/R injury in female rats, by suppressing NE release via the enhancement of NO production.

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