Hypothalamus sympathetic actions

The mechanism of action of these drugs is caused by stimulation of o -adrenoreceptors in the inhibitory structure of the brain. It is believed that interaction of these drugs with adrenergic receptors is expressed in the suppression of vasomotor center neurons of the medulla, and reduction of hypothalamus activity, which leads to a decline in sympathetic impulses to the vessels and the heart. In summary, cardiac output and heart rate are moderately reduced, and consequently arterial pressure is reduced. 

The effects of the ergot alkaloids on the central nervous system are very diverse as sites of action are situated in the vasomotor center and the cardiac inhibitory center in the medulla oblongata as well as in the sympathetic structures of the diencephalon, particularly the hypothalamus. The inhibition of the vasomotor center and of tire baroceptive reflexes and the stimulation of the vagal nuclei are resppfisible for the vasodilator, hypotensive, and bradycardic effects, especially in the case of the peptide type of alkaloid. Some also have a stimulating effect on the vomiting center. 

Autonomic outputs. Hypoglycaemia and hypothermia both lead to snstained sympathetic responses. Subjects feel hungry and eat if possible, bnt they refine their other actions to suit the circumstances. Hypoglycaemia requires hepatic glycogenolysis and glnconeogenesis, while hypothermia requires increased heat prodnction and a redistribntion of blood flow. Sympathetic activity is controlled by the hypothalamns, which instrncts the adrenal medulla to secrete adrenalin. This is a rather blunt control, and so localised sympathetic responses (such as blood flow regulation) are mediated by individnal nerves. Parasympathetic activity can also respond to the hypothalamus, which controls the nnclens of the solitary tract. 

The sympathetic nervous system (SNS) plays a role in the "fight-or-flight response." Set in motion by activity in the limbic system and hypothalamus, the sympathetic system mobilizes the body to take action in response to dangerous situations. When the fight-or-flight response is activated, there is a sudden, massive increase in metabolic rate increased blood pressure and heart rate and the increased blood flow to the heart, brain, and muscles. Conversely, the parasympathetic system which is activated at times of relaxation and quiescence, acts to reduce heart rate and blood pressure in an overall attempt to conserve energy (see figure 3-1). 

It has been suggested that the vasodilation observed on stimulation of sympathetic fibers is a result of a sympathetic cholinergic innervation. In a recent study, Feigl stimulated the stellate ganglion and hypothalamus and found no evidence of cholinergic mediated coronary vasodilation. Information obtained by sympathetic stimulation of the coronary circulation has been recently criticized. The distribution of alpha and beta receptors within the coronary vasculature may vary with species and physiological state of the animal. Different experimental approaches may favor stimulation of either alpha or beta receptors. Other factors may be involved such as dose or time dependent actions of catecholamines on different receptors. 

Leptin acts on receptors in the arcuate nucleus of the hypothalamus, causing the release of anorexigenic peptides, including a-MSH, that act in the brain to inhibit eating. Leptin also stimulates sympathetic nervous system action on adipocytes, leading to uncoupling of mitochondrial oxidative phosphorylation, with consequent thermogenesis. 

A number of new MAO inhibitors were described in 1971 however, because of the limited clinical utility of these agents in the treatment of depression, they will not be reviewed in detail. Nonetheless, several of these substances are noteworthy. Sydnophene ( ) was Included in a series of sydnonimines examined for MAO-inhibitory activity. It demonstrated mild stimulant and antidepressive actions in extensive clinical studies in Russia. Another MAO-inhibitor, clorgiline (32. M B 9302) had antidepressive activity its clinical effects were similar to those of imipramine. Proportions of two forms of MAO (Type A, B) were found to vary in different areas of rat brain. The type A enzyme, predominant in sympathetic nerves, acted on both 5-HT and tyramlne and was Inhibited by 32. whereas type B-MAO was insensitive to and acted on tyramine, but not 5-HT. In humans, tranylcypromine and isocarboxazid Increased 5HT, NE and dopamine levels in various brain areas however, the effect of tranylcypromine was significantly greater than that of the other two on dopamine in the caudate nucleus and hypothalamus. In vitro. Lilly 516 1 ( ), like harmaline, preferentially blocked MAO oxidation of 5-HT, whereas tranylcypromine and pargyline selectively inhibited the oxidation of tyramine. ... 

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