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Adrenal one

The chemistry of most of the drugs in this family is quite simple, accounting in part for the very large number of analogues which have been made. The foundation for the chemistry in this series was laid long ago by Stolz in his classic synthesis of the ophthalmic agent adrenal one (3) in which he reacted catechol with chloroacetyl chloride and then displaced the reactive chlorine atom with methylamine to complete the synthesis. Borohydride reduction would have given epinephrine (adrenaline). [Pg.38]

In the anterior pituitary gland (see Hormones, anteriorpituitaryhormones), both adrenocorticotropic hormones (ACTH) and the endogenous opiate hormone, P-endorphin, are synthesized from a common prohormone (2) (see Opioids,endogenous). In the adrenal medulla, five to seven copies of another opiate hormone, methionine—enkephalin (Met-enkephalin), and one copy of leucine—enkephalin (Leu-enkephalin) are synthesized from each precursor molecule (3). [Pg.171]

The adrenal cortex produces steroidal hormones that are associated with carbohydrate, fat, and protein metabolism, electrolyte balance, and gonadal functions (58). One of these, cortisone [53-06-5] ( ) demonstrated a remarkable ability to relieve the symptoms of inflammatory conditions... [Pg.387]

It was known for some time that even after the corticoids had been separated from crude extracts of the adrenal cortex, the remaining material, the so-called "amorphous fraction" still possessed considerable mineralocorticoid activity. Aldosterone (250), one of the last steroids to be isolated from this fraction, proved to be the active principle. This compound proved to be an extremely potent agent for the retention of salt, and thus water, in body fluids. An antagonist would be expected to act as a diuretic in those edematous states caused by excess sodium retention. Although aldosterone has been prepared by both total and partial synthesis, the complexity of the molecule discouraged attempts to prepare antagonists based directly on the parent compound. [Pg.206]

Myosin-I molecules have several IQ sequences on or near the head and have light chains associated with them (Cheney and Mooseker, 1992 Cheney et al., 1993). Frequently, the light chains appear to be calmodulin molecules and some myosin-I molecules can bind three to four molecules of calmodulin at one time. Brush-border and adrenal myosin-I also bind calmodulin. Acanthamoeba myosin-I has a light chain that can be removed, in vitro, without adversely affecting the ATPase activity or the heavy chain phosphorylation (Korn and Hammer, 1988). The role of these calmodulin molecules in regulating myosin-I is complex and poorly understood. One possibility is that the calmodulin molecules dissociate from the heavy chains when calcium binds to the calmodulin, thereby imparting greater flexibility to the head of the myosin-I molecules. [Pg.70]

As might be expected, mRNA for the 5-HT transporter is found in high concentrations in the Raphe nuclei but it is also found in other brain regions. Whether this means that non-5-HT neurons can synthesise this protein is unknown but there is some evidence that it is synthesised in astrocytes, at least. One complication is that there are multiple forms of mRNA for the 5-HT transporter, but there is, as yet, no evidence for transporter subtypes in the CNS. However, it must also be remembered that 5-HT transporters are found in the peripheral tissues, notably platelets, mast cells, the placental brush-border and adrenal chromaffin cells and it is possible that these are not all identical. [Pg.195]

Eight rats had at least one of the tumors tabulated here. In addition, the following miscellaneous tumors were noted 1 rat had cortical adenoma of adrenal gland, 1 had follicular adenoma of thyroid gland, and 1 had pulmonary adenoma. [Pg.312]

The testes and adrenal glands produce 90% and 10%, respectively, of circulating testosterone. Testosterone enters prostate cells, where predominantly type II 5a-reductase activates testosterone to dihydrotestosterone, which combines with a cytoplasmic receptor. The complex enters the nucleus and induces changes in protein synthesis which promote glandular tissue growth of the prostate. Thus, 5a-reductase inhibitors (e.g., finasteride and dutas-teride) directly interfere with one of the major etiologic factors of BPH. [Pg.792]

Adrenalectomy Surgical removal of one or both adrenal glands. [Pg.1559]

The endogenous release of the potent vasoconstrictor neuropeptide Y (NPY) is increased during sepsis and the highest levels are detected in patients with shock (A8). NPY is a 36-amino-acid peptide belonging to the pancreatic polypeptide family of neuroendocrine peptides (T2). It is one of the most abundant peptides present in the brain and is widely expressed by neurons in the central and peripheral nervous systems as well as the adrenal medulla (A3). NPY coexists with norepinephrine in peripheral sympathetic nerves and is released together with norepinephrine (LI9, W14). NPY causes direct vasoconstriction of cerebral, coronary, and mesenteric arteries and also potentiates norepinephrine-induced vasoconstriction in these arterial beds (T8). It appears that vasoconstriction caused by NPY does not counterbalance the vasodilatator effects of substance P in patients with sepsis. The properties of vasodilatation and smooth muscle contraction of substance P are well known (14), but because of the morphological distribution and the neuroendocrine effects a possible stress hormone function for substance P was also advocated (J7). Substance P, which is a potent vasodilatator agent and has an innervation pathway similar to that of NPY, shows a low plasma concentration in septic patients with and without shock (A8). [Pg.95]

Compared to a,-receptors, a2-receptors have only moderate distribution on the effector tissues however, they have important presynaptic effects. Alpha-one receptors are found on effector tissue cells at the neuroeffector junction the a2-receptors are found on the varicosities of the postganglionic neuron. Norepinephrine released from this neuron not only binds to the a.j-receptors on the effector tissue to cause some physiological effect but also binds to the a2-receptors on the neuron. Alpha-two receptor stimulation results in presynaptic inhibition" or in a decrease in the release of norepinephrine. In this way, norepinephrine inhibits its own release from the sympathetic postganglionic neuron and controls its own activity. Both ar and a2-receptors have equal affinity for norepinephrine released directly from sympathetic neurons as well as circulating epinephrine released from the adrenal medulla. [Pg.102]


See other pages where Adrenal one is mentioned: [Pg.261]    [Pg.118]    [Pg.199]    [Pg.129]    [Pg.524]    [Pg.261]    [Pg.118]    [Pg.199]    [Pg.129]    [Pg.524]    [Pg.8]    [Pg.224]    [Pg.544]    [Pg.446]    [Pg.10]    [Pg.6]    [Pg.354]    [Pg.88]    [Pg.118]    [Pg.202]    [Pg.573]    [Pg.430]    [Pg.442]    [Pg.153]    [Pg.6]    [Pg.89]    [Pg.146]    [Pg.172]    [Pg.437]    [Pg.441]    [Pg.442]    [Pg.237]    [Pg.42]    [Pg.128]    [Pg.608]    [Pg.760]    [Pg.35]    [Pg.203]    [Pg.77]    [Pg.48]    [Pg.56]    [Pg.176]    [Pg.320]    [Pg.127]   
See also in sourсe #XX -- [ Pg.7 , Pg.38 ]




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