The neuroendocrinology of congestive heart failure. (1/17)

The syndrome of heart failure is still imperfectly understood. It is defined as effort intolerance caused by heart disease, often with a neuroendocrine response that leads to fluid retention and promotes an adverse vicious circle. The cause of this response is generally thought to be a low blood pressure, leading to adrenergic and rennin-angiotensin activation. The result is increased peripheral vasoconstriction, which maintains the blood pressure while punishing the already failing myocardium by demanding more work against the increased afterload. The evolution of heart failure is traced out from an initial pressure or volume overload that initiates a series of growth signals to cause myocardial growth. Why the apparently well-compensated LV should degenerate into failure is not clear, but impaired coronary flow reserve and excess angiotensin II activity with fibrosis and apoptosis all probably play a role. The collagen matrix normally limits cardiac chamber expansion so that matrix remodeling under the influence of matrix metalloproteinases is required for the LV to enlarge in volume. Regarding the neuroendocrine responses, excess adrenergic activity promotes failure by myocardial membrane damage and calcium overload, and by increasing the myocardial oxygen demand and the afterload. Beta2- adrenergic stimulation may (unexpectedly) be anti-apoptotic and cardioprotective. Activation of the rennin-angiotensin system (RAS) is clearly very harmful, as shown by numerous studies in which inhibiting agents have reduced human mortality. Specific adverse consequences of RAS activation include (1) excessive peripheral vasoconstriction; (2) aldosterone-mediated sodium retention and myocardial fibrosis; (3) increased endothelial damage; and (4) excessive angiotensin II effects at intracellular sites. Other neuroendocrine changes are increased levels of endothelin and of cytokines such as tumour necrosis factor-alpha. Ergoreflexes from the ailing skeletal muscle may further promote adrenergic and RAS activation. Conversely, increased release of natriuretic peptides from the left heart is cardioprotective by limiting fluid retention and promoting vasodilation. Current therapies of heart failure are largely based on inhibition of the neuroendocrine response.  (+info)

The influence of gonadal hormones on neuronal excitability, seizures, and epilepsy in the female. (2/17)

It is clear from both clinical observations of women, and research in laboratory animals, that gonadal hormones exert a profound influence on neuronal excitability, seizures, and epilepsy. These studies have led to a focus on two of the primary ovarian steroid hormones, estrogen and progesterone, to clarify how gonadal hormones influence seizures in women with epilepsy. The prevailing view is that estrogen is proconvulsant, whereas progesterone is anticonvulsant. However, estrogen and progesterone may not be the only reproductive hormones to consider in evaluating excitability, seizures, or epilepsy in the female. It seems unlikely that estrogen and progesterone would exert single, uniform actions given our current understanding of their complex pharmacological and physiological relationships. Their modulatory effects are likely to depend on endocrine state, relative concentration, metabolism, and many other factors. Despite the challenges these issues raise to future research, some recent advances have helped clarify past confusion in the literature. In addition, testable hypotheses have developed for complex clinical problems such as "catamenial epilepsy." Clinical and animal research, designed with the relevant endocrinological and neurobiological issues in mind, will help advance this field in the future.  (+info)

Minireview: The neuroendocrinology of the suprachiasmatic nucleus as a conductor of body time in mammals. (3/17)

Circadian rhythms in physiology and behavior are regulated by a master clock resident in the suprachiasmatic nucleus (SCN) of the hypothalamus, and dysfunctions in the circadian system can lead to serious health effects. This paper reviews the organization of the SCN as the brain clock, how it regulates gonadal hormone secretion, and how androgens modulate aspects of circadian behavior known to be regulated by the SCN. We show that androgen receptors are restricted to a core SCN region that receives photic input as well as afferents from arousal systems in the brain. We suggest that androgens modulate circadian behavior directly via actions on the SCN and that both androgens and estrogens modulate circadian rhythms through an indirect route, by affecting overall activity and arousal levels. Thus, this system has multiple levels of regulation; the SCN regulates circadian rhythms in gonadal hormone secretion, and hormones feed back to influence SCN functions.  (+info)

Paracrinicity: the story of 30 years of cellular pituitary crosstalk. (4/17)

Living organisms represent, in essence, dynamic interactions of high complexity between membrane-separated compartments that cannot exist on their own, but reach behaviour in co-ordination. In multicellular organisms, there must be communication and co-ordination between individual cells and cell groups to achieve appropriate behaviour of the system. Depending on the mode of signal transportation and the target, intercellular communication is neuronal, hormonal, paracrine or juxtacrine. Cell signalling can also be self-targeting or autocrine. Although the notion of paracrine and autocrine signalling was already suggested more than 100 years ago, it is only during the last 30 years that these mechanisms have been characterised. In the anterior pituitary, paracrine communication and autocrine loops that operate during fetal and postnatal development in mammals and lower vertebrates have been shown in all hormonal cell types and in folliculo-stellate cells. More than 100 compounds have been identified that have, or may have, paracrine or autocrine actions. They include the neurotransmitters acetylcholine and gamma-aminobutyric acid, peptides such as vasoactive intestinal peptide, galanin, endothelins, calcitonin, neuromedin B and melanocortins, growth factors of the epidermal growth factor, fibroblast growth factor, nerve growth factor and transforming growth factor-beta families, cytokines, tissue factors such as annexin-1 and follistatin, hormones, nitric oxide, purines, retinoids and fatty acid derivatives. In addition, connective tissue cells, endothelial cells and vascular pericytes may influence paracrinicity by delivering growth factors, cytokines, heparan sulphate proteoglycans and proteases. Basement membranes may influence paracrine signalling through the binding of signalling molecules to heparan sulphate proteoglycans. Paracrine/autocrine actions are highly context-dependent. They are turned on/off when hormonal outputs need to be adapted to changing demands of the organism, such as during reproduction, stress, inflammation, starvation and circadian rhythms. Specificity and selectivity in autocrine/paracrine interactions may rely on microanatomical specialisations, functional compartmentalisation in receptor-ligand distribution and the non-equilibrium dynamics of the receptor-ligand interactions in the loops.  (+info)

Epigenetics and its implications for behavioral neuroendocrinology. (5/17)

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Governor Pio Pico, the monster of California...no more: lessons in neuroendocrinology. (6/17)

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Roles of oestrogen receptors alpha and beta in behavioural neuroendocrinology: beyond Yin/Yang. (7/17)

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Neuroendocrinology and sexual differentiation in eusocial mammals. (8/17)

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