Effect of Steroid Hormones and Diethylstilbestrol on Adrenomedullary Catecholamine Secretion

Wiechman, Beth E.; Borowitz, Joseph L.

doi:10.1159/000137252

Cited by 24 publications

(2 citation statements)

References 4 publications

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“…The adrenal medullary content of NA and adrenaline in female rats varies with the oestral cycle 47 , 48 and is less than that in male rats 10 . Similarly, oestradiol treatment has been shown to decrease adrenal medullary NA content in female rats 47 and also decrease the basal release 47 and stimulated release 49 of catecholamines from rat and bovine adrenal glands. These decreases in content and release do not appear to be related to decreases in catecholamine synthesis because oestrogen treatment has been shown to increase adrenal tyrosine hydroxylase activity in female rats 36 .…”

Section: Noradrenergic Neurotransmissionmentioning

confidence: 99%

Gender Differences in Sympathetic Nervous System Regulation

Hinojosa‐Laborde

Chapa

Lange

et al. 1999

Clin Exp Pharma Physio

211

137

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1. Females are protected against the development of hypertension. The purpose of the current review is to present the evidence for gender differences in the regulation of the sympatho-adrenal nervous system and to determine if these differences support the hypothesis that, in females, the regulation of the sympathetic nervous system (SNS) is altered such that sympatho-adrenal activation is attenuated or sympatho-adrenal inhibition is augmented. 2. The central control of sympatho-adrenal function is different in females and responses vary during the oestral and menstrual cycles. Pathways regulating the SNS appear to be less sensitive to excitatory stimuli and more sensitive to inhibitory stimuli in females compared with males. 3. Gender differences in arterial baroreflex sensitivity suggest that females may have a greater baroreflex sensitivity, such that alterations in blood pressure are more efficiently controlled than in males. Cardiopulmonary reflex inhibition of sympathetic nerve activity is greater in females, possibly resulting in a greater renal excretory function. 4. An attenuated sensitivity to adrenergic nerve stimulation, but not to noradrenaline (NA), suggests that gender differences in noradrenergic neurotransmission may protect females against sympathetic hyperactivity. Gender differences in the regulation of NA release via presynaptic alpha 2-adrenoceptors, the vasoconstrictor response to the cotransmitter neuropeptide Y and the clearance of catecholamines are consistent with this hypothesis. 5. Similarly, attenuated stress-induced increases in plasma catecholamines in women suggest that females are less sensitive and/or less responsive to adrenal medullary activation. This is supported by findings of gender differences in adrenal medullary catecholamine content, release and degradation. 6. We conclude that there is strong evidence that supports the hypothesis that, in females, the regulation of the SNS is altered such that sympatho-adrenal activation is attenuated or sympatho-adrenal inhibition is augmented.

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Section: Noradrenergic Neurotransmissionmentioning

confidence: 99%

Gender Differences in Sympathetic Nervous System Regulation

Hinojosa‐Laborde

Chapa

Lange

et al. 1999

Clin Exp Pharma Physio

211

137

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“…Probably this occurs as a consequence of a higher activity of the adrenal medulla (Zukowska-Grojec et al, 1991). This can be explained considering that elevated concentrations of estrogens in females increase adrenal release of catecholamines (Bengtsson and Marchall, 1983;Wiechman and Borowitz, 1979). Furthermore, estrogens reduce the enzymatic inactivation of catecholamines by inhibiting both the intraneuronal and, more potently, the extraneuronal NA uptake (Salt, 1972).…”

Section: Neuroendocrine System Mediates Myocardial Effects Of Noisementioning

confidence: 99%

Morphological alterations induced by loud noise in the myocardium: The role of benzodiazepine receptors

Gesi

Fornai

Lenzi

et al. 2002

Microscopy Res & Technique

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Noise represents an environmental stress factor affecting several organs and apparati, including the cardiovascular system. In experimental animals undergoing noise exposure, subcellular myocardial changes have been reported, especially at mitochondrial level; in particular, after 6 hours of exposure only the atrium exhibited significant mitochondrial alterations, whereas after 12 hours as well as subchronic exposure both atrium and ventricle were damaged. The first part of the present article overviews the experimental evidence on effects of noise on the myocardium. In the second part, the review analyzes the role of benzodiazepine receptors and the potential efficacy of benzodiazepine ligands in preventing the mitochondrial damage induced by noise exposure. Drugs acting at both central and peripheral benzodiazepine receptors significantly prevent this damage. Differences in the amount and the duration of the protective effect might depend on variability in the potency and pharmacokinetics of the specific drug. The effects of the combined treatment with selective and non-selective peripheral benzodiazepine ligands on noise stimulation are discussed at biochemical level reviewing studies on the effects of noise exposure on mitochondrial fractions.

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