Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027960 (mole)
 21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was undertaken to investigate the influence of fasting (24 hours), epinephrine (four 0.25 mg/kg s.c. doses at hourly intervals), adrenocorticotropin (two 40 I.U. s.c. doses at 2-hour intervals) and immobilization stress (4 hours) on the response of rats to some coumarin or indanedione anticoagulants. The anticoagulants were always administered first and were followed immediately or within the next hour by the appropriate challenge. Fasting produced a significant enhancement of the antiprothrombin response to warfarin (0.5 mg/kg i.v. or 0.75-3.0 mg/kg s.c.), bishydroxycoumarin (7.5 mg/kg i.p. or 10 mg/kg s.c.) and phenindione (40 mg/kg p.o). Epinephrine and immobilization stress, but not adrenocorticotropin, similarly prolonged the prothrombin time after warfarin (0.75-3.0 mg/kg s.c.). When used in the absence of anticoagulants, all challenges had no effect on the prothrombin time. In addition, fasting did not affect the response of anticoagulated animals to vitamin K. Plasma free fatty acids were significantly increased by the various challenges. The binding constant of warfarin to undiluted plasma proteins were decreased from the control value by a factor of 1.7 and 2.0 as a result of immobilization stress and fasting, respectively. Fasting per se increased the amount of bound endogenous free fatty acids per mole of protein; the latter parameter was further increased in the presence of warfarin. The present data show that fasting and stress enhance the anticoagulant response to warfarin and suggest that this might be due to an interference of endogenous free fatty acids with binding of warfarin to plasma proteins.
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PMID:The influence of fasting and stress on the response of rats to warfarin. 5 16

(Des-Asp1)-angiotensin I, angiotensin II and III were evaluated for pressor activities in conscious nephrectomized rats and for steroidogenic actions in rat adrenal zona glomerulosa. The pressor effect of this angiotensin nonapeptide was similar to that found with mole-equivalent doses of angiotensin III (one-third as active as angiotensin II) and was significantly attenuated by pretreatment with the 0. jararaca nonapeptide converting enzyme inhibitor. Hence, (des-Asp1)-angiotensin I is a substrate for converting enzyme in vivo, and the rapid conversion indicates that an alternate pathway for the formation of angiotensin III could exist. (Des-Asp1)-angiotensin I possessed only 0.1% of the activity of angiotensin III as a steroidogenic agent in cell suspensions of rat adrenal zona glomerulosa. Angiotensin I was a weak steroidogenic agent in vitro (1%) and was not blocked by an inhibitor of converting enzyme. Adrenal cells dispersed from the outer zone of the cortex would appear to be devoid of significant converting enzyme activity.
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PMID:Role of converting enzyme in the cardiovascular and adrenal cortical responses to (des-Asp1)-angiotensin I. 18 74

1. The circulatory and metabolic effects of temperature reduction were studied in autoperfused canine subcutaneous adipose tissue in situ. 2. Cooling the adipose tissue sufficiently to reduce venous effluent temperature by 5--6 degrees C decreased blood flow from an average of 6.4--4.1 ml. min-1 . 100g-1. 3. Vasoconstrictor responses to sympathetic nerve stimulation (4 HZ) and injected noradrenaline (5 n-mole) were potentiated by cooling while vasodilator components of the vascular responses, such as autoregulatory escape and post-stimulatory hyperaemia, were virtually abolished by this treatment. 4. Oxygen uptake was reduced by cooling without signs of tissue hypoxia. This reduced oxygen demand may partly cause the decrease in adipose tissue blood flow. 5. Cooling inhibited glycerol mobilization from the adipose tissue during sympathetic nerve stimulation. Post-stimulatory lipolysis was, however, not inhibited. In vitro studies with 'perifused' rat fat cells suggest that this may be due to impaired inactivation of the lipolytic process, rather than to changes in transmitter removal, following stimulation at low temperature. 6. Cooling inhibited the mobilization of fatty acids more than that of glycerol, suggesting increased re-esterification of fatty acids within the tissue at low temperature. 7. It is concluded that cooling increases the sensitivity to vasoconstrictor stimuli and that inhibition of metabolic vasodilator mechanisms play a role for this effect. The stimultaneous inhibition of activating and inactivating mechanisms could explain the unchanged vascular and lipolytic responses to brief stimuli. Some possible implications of the present findings for the physiology of adipose tissue during cooling are discussed.
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PMID:Vascular and metabolic responses to adrenergic stimulation in isolated canine subcutaneous adipose tissue at normal and reduced temperature. 70 88

Transmembrane action potentials (APs) of electrically paced right-atrial tissue obtained from 38 patients of corrective open-heart surgery were analyzed. Two types of APs could be found. The APs of 20 patients (group I) were similar to those of other laboratory mammals. The average resting potential (RP) and the amplitude and maximum rate of rise of phase 0 of APs (Vmax) were -75 mV, 86 mV, and 152 V/sec, respectively, only the repolarization phase being more prolonged than that of other mammalian APs. Epinephrine (5.8 X 10(-6) mole/liter) increased the amplitude of APs and prolonged the plateau phase, producing odd-looking, humped APs. Prostacyclin-Na (6.7 X 10(-7) and 8.7 X 10(-6) mole/liter) increased Vmax. Celluline-A (a biological Ca-complex obtained from frog skin) increased both Vmax and the amplitude of APs and, similar to epinephrine, prolonged the plateau phase. In group I, postoperative arrhythmias occurred in only 1 of the 10 patients. APs obtained from another 18 preparations (group II) were characterized by low RP (-55 mV), small amplitude of AP (59 mV), slow rate of rise of AP (less than 10 V/sec), and very prolonged repolarization. This type of APs can be referred to as slow-response APs. Neither epinephrine, prostacylin-Na, nor celluline-A modified the characteristics of these slow-response APs. In group II, postoperative arrhythmias could be observed in 8 of the 10 patients.
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PMID:Physiological and pharmacological analysis of transmembrane action potentials of human atrial fibers. 388 30

Phosphorylation site stoichiometries were determined for skeletal muscle glycogen synthase purified from control, alloxan-diabetic, and epinephrine-treated rabbits. One method of analysis was direct determination of the total in vivo phosphate content of each site after reverse phase high performance liquid chromatography separation of a complete tryptic digest of the purified synthase. The second method of analysis, in vitro phosphorylation, was based on the premise that in vitro 32P incorporation into each site would be inversely related to the in vivo phosphate content of that site. Glycogen synthase from control rabbits had the following distribution of in vivo phosphate (mole of phosphate/mol of site): site 1a, 0.29 +/- 0.08; site 5, 0.62 +/- 0.07; site 3, 0.46 +/- 0.06; site 1b, 0.23 +/- 0.03; and site 2, 0.43 +/- 0.07. Synthase from diabetic rabbits had 2-fold elevations of in vivo phosphate contents of sites 2 and 3. Epinephrine resulted in increased phosphorylation in vivo of site 1b (2.0-fold), site 2 (2.0-fold), and site 3 (1.5-fold). The in vitro phosphorylation analysis showed decreased 32P incorporation in vitro (indicative of increased in vivo phosphorylation) as follows: epinephrine, site 1a, site 3, site 1b, site 2; diabetic, site 3, site 2. The effect of diabetes on the in vitro phosphorylation of sites 2 and 3 was reversed by insulin treatment. We conclude that the major effect of epinephrine, phosphorylation of sites 1a, 1b, and 2, is mediated by the activation of the cAMP-dependent kinase. The mechanisms accounting for the phosphorylation of site 3 in response to epinephrine and phosphorylation of sites 2 and 3 in the diabetic state are under investigation.
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PMID:Effects of epinephrine, diabetes, and insulin on rabbit skeletal muscle glycogen synthase. Phosphorylation site occupancies. 632 4

Adrenal proenkephalin contains the sequence -Asn-Ser-Ser- that is a typical site for the attachment of asparagine-linked carbohydrate. The 5300- and 18,200-Da bovine adrenal proteins derived from proenkephalin contain this recognition sequence and were therefore analyzed for the presence of both amino and neutral sugars. Les than 0.05 mol of amino sugar and less than 0.1 mol of neutral sugar were found per mole of each protein. No amino sugar was detected in other high-molecular-weight adrenal [Met]enkephalin-containing proteins. Together these findings indicate that bovine adrenal proenkephalin does not contain asparagine-linked carbohydrate.
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PMID:Is adrenal proenkephalin glycosylated? 687 Feb 64

A case of 37 years old woman with a classic form of Cogan-Reese iris naevus syndrome is presented. Closure angle glaucoma, being a part of syndrome, with glaucomatous disc damage was initially treated with drugs (betaxolol, trusopt) without effective IOP decrease. A surgery was performed (goniotrepanatio by Fronimopoulos modified by Palmberg, but without iridectomy), 5 fluorouracil subconjunctival injections were given to the patient postoperatively for 5 days. We received a good IOP control on the level of 12 mm Hg. The visual acuity was 1.0 after surgical procedure. We wanted to present this case because of its rarity and a typical surgical procedure (without applying iridectomy).
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PMID:[A case of Cogan-Reese syndrome (iris nevus syndrome)]. 957 20

Pigmented nodular cortical hyperplasia. a rare cause of Cushing's syndrome, is characterized by resistance to inhibition with dexamethasone and normal sized adrenal glands with multiple, small, pigmented nodules. The disorder may be a component of a syndrome inherited as an autosomal dominant pattern that includes intra- and extracardiac myxomas, lentiginous lesions, blue nevi, other functional endocrire tumors, and perppheral nerve tumors (Carney's complex). We report a patient in whom bilateral myelolipomas were found, in addition to the usual features of this complex. A 29-yr old man was admitted to the hospital for Cushing's syndrome of probably more than 15 yr duration. Physical examination showed diffuse facial hyperchromatic macules. 02-05 cm, predominantly around the lips and on the palmar surfaces of the fingers. Results with dexamethasone suppression nocturnal testing (1 and 8 mg) were compatible with an adrenal adenoma. The computed tomography (CT) of the sella turcica was normal. Adrenal CT showed a tumor in the left gland with a double component one solid and another suggestive of fat, consistent with an angiomyelolipoma. Following 5 wk treatment with ketoconazole, 800 mg per day po, serum cortisol decreased to 5.9 Ag/dL. morning and evening, respectively. Bilateral adrenalectomy was performed. Pathologic examination revealed pigmented nodular cortical hyperplasia and a dominant myelolipoma in the left adrenal. A microscopic myelolipoma was identified in the right adrenal. An echocardiogram showed a mass on the posterior wall of the left ventricle which was a myxoma. Study of the patient's family disclosed two sisters with facial lentigines. Echocardiograms were performed on all available first degree relatives: all were normal. Nocturnal inhibition with dexamethasone revealed that one of the patient's sisters with lentigines also had hypercortisolism. Myelolipoma has been reported in association to Cushing syndrome in humans and experimentally after pituitary extracts in animals. The relationship between this finding and the Carney's complex remain elusive.
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PMID:Myelolipoma: A New Adrenal Finding in Carney's Complex? 1211 6

Iridocorneal endothelial (ICE) syndrome is a group of ocular conditions characterized by corneal proliferative endotheliopathy in which secondary corneal edema, peripheral anterior synechiae, and abnormalities of the iris stroma are the common features. The etiology remains unclear, but may be related to viral infection with Herpes simplex or Epstein-Barr virus. The pathogenesis of the ICE syndrome is believed to result from an abnormality of the corneal endothelial cells (causing corneal edema), with secondary spreading of the cells over the trabecular meshwork region (causing anterior synechiae and elevated intraocular pressure [IOP]) and across the surface of the iris (responsible for the formation of iris holes, pupillary distortion, and iris noduli). The disease complex, which includes essential iris atrophy, Chandler's syndrome, and iris nevus (Cogan-Reese) syndrome, is almost always unilateral, nonfamilial, and typically occurs in females during young adulthood. ICE syndrome is commonly progressive and frequently complicated by secondary glaucoma and corneal decompensation. In Chandler's syndrome, iris changes are less pronounced and corneal edema more frequent than in essential iris atrophy or Cogan-Reese syndrome. Glaucoma associated with ICE syndrome is often difficult to manage and is usually treated with medications and/or filtering surgery. Glaucoma filtering surgery is usually successful when done early, but may fail due to endothelialization of the fistula by the abnormal corneal endothelium.
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PMID:[Iridocorneal endothelial syndrome and glaucoma]. 1731 7

Cytochrome P4502E1 levels in microsomal and lysosomal liver fractions was studied in Wistar rats treated with epinephrine (5.5 x 10(-6) mole/g, i.p., 1 h before test) on the background of isoniazid administration (daily dose 250 mg/kg, i.p., for 3 days). Epinephrine administration resulted in increased cytochrome P4502E1 level in the vacuole/lysosome apparatus of rat liver. On the background of isoniazid administration, cytochrome P4502E1 level and p-nitrophenol-hydroxylase activity in both low- and high-density lysosomes were decreased. Epinephrine administration under these conditions increased the cytochrome P-4502E1 level in lysosomes due to autophagy.
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PMID:[Effect of adrenaline on the cytochrome P4502E1 content in microsomes and lysosomal fractions induced by isoniazid in rats]. 1865 56


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