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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A method is described to assay the adenosine content of human adipose tissue. Tissue pieces of 10-20 mg were frozen within 1 sec of excision by a conchotome. The pieces were pooled and ground in liquid nitrogen, divided into samples weighing 50-100 mg each and placed in perchloric acid. Neutralized defatted extracts were treated by Dowex AG-1 to remove nucleotides and lyophilized. The adenosine content was measured by RIA using antiserum raised against laevulinic acid (0(2'),3'-adenosine-acetal)-albumin conjugate. The adenosine content in human abdominal sc adipose tissue was 0.56 +/- 0.08 nmol/g of tissue (mean +/- SEM). This shows that adenosine is present in human adipose tissue at concentrations that have been shown to have regulatory effects on cAMP accumulation and lipolysis.
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PMID:Assay of adenosine in human adipose tissue. 407 80

The regulation of pepsin secretion was studied in the in vitro perfused mouse stomach. In contrast to acid secretion, basal pepsin release was not inhibited by 10(-4) M carbonyl cyanide m-chlorophenylhydrazine (CCCP) and by N2-induced hypoxia. Both secretions were not affected by 10(-3) M cimetidine, 10(-3) M atropine or cycloheximide (2 mg i.p. + 10(-5) M). Secretory responses to classical stimulants were similar to those obtained under in vivo conditions: carbamylcholine (CCH) and histamine stimulated acid and pepsin secretion in parallel, with a maximal pepsin/acid ration of 34 +/- 4 (mean +/- SEM) and 40 +/- 5, respectively. CCH-induced pepsin secretion was inhibited by atropine and pirenzepine. Dibutyrylic cyclic AMP(db-cAMP) strongly stimulated pepsin release. This stimulation was partially inhibited by trifluoperazine. Pentagastrin was a weak stimulant of pepsin secretion (pepsin/acid ratio: 10 +/- 3), whereas 10(-4) M bombesin and 10(-6) M salmon calcitonin had no effect. Omeprazole (H168/68) strongly inhibited basal acid secretion and stimulated pepsin release in a dose-and energy-dependent fashion. In contrast to acid, basal pepsin release probably represents an 'overflow secretion'. Although pepsin and acid are usually stimulated in parallel, dissociated responses are obtained under in vitro conditions, indicating that separate regulatory pathways exist.
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PMID:Pepsin secretion: neurohumoral regulation and drug effects. 610 Jun 25

A microradioimmunoassay for cAMP was developed in order to analyse the effects of alpha-adrenergic agonists on vasopressin (AVP)-induced cAMP cell accumulation in single pieces of microdissected medullary (MCT) and cortical (CCT) rat collecting tubules. Under the experimental conditions chosen (4 min of incubation in the presence of a phosphodiesterase inhibitor), no cAMP could be detected either in the bathing solution or in non-stimulating samples of tubule. In MCT, 10(-6) M AVP stimulated cAMP generation up to 128.3 +/- 9.0 (SEM) fmoles per mm of tubule per 4 min, N = 11. The response was dose-dependent with a KA value below 10(-10) M AVP. The addition of norepinephrine (NE) (10(-5) M in the presence of propranolol) suppressed the larger part of the response to AVP (from 92% with 2 X 10(-11) M AVP to 76% with 10(-6) M AVP); the addition of 10(-7) M NE still reduced by 59% the MCT response to 10(-10) M AVP (26.2 +/- 5.9 vs. 64.0 +/- 6.4 fmoles/mm, N = 3). In CCT, 10(-5) M NE reduced by 84% the cAMP generation induced by 10(-10) M AVP (8.8 +/- 2.0 vs. 54.2 +/- 3.5 fmoles/mm, N = 3). This inhibitory action of NE against the AVP effect in CCT was mimicked by 10(-7) M clonidine; in MCT it was suppressed by phentolamine and yohimbine, but not by prazosin, suggesting that alpha 2-adrenoreceptors are involved. On the other hand, the addition of the alpha-agonists to the incubation solution produced no inhibition of the cAMP cell accumulations induced by glucagon, calcitonin and isoproterenol in CCT, or glucagon in MCT, an observation demonstrating that alpha 2-adrenergic agonists selectively inhibit vasopressin-dependent cAMP generation by these nephron segments.
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PMID:Inhibition of alpha 2-adrenergic agonists on AVP-induced cAMP accumulation in isolated collecting tubule of the rat kidney. 614 67

Activation of the ovine fetal adrenal gland after pulse ACTH (P-ACTH) administration is associated with an increase in plasma cortisol levels. We have investigated whether cortisol may play a role in this adrenal activation process. The ability of fetal adrenal cells to accumulate cAMP in response to ACTH in vitro was compared in fetuses (day 132 of gestation) that had received infusions (100 h) in utero of 1) saline or saline + tartrate (0.5 ml for 15 min/2 h) (n = 4); 2) P-ACTH (66.6 ng/min for 15 min/2 h) (n = 4); 3) P-ACTH + metopirone (31.3 mg/h) (n = 4), to inhibit 11 beta-hydroxylase activity. Control fetuses showed no significant increase in plasma cortisol levels throughout the infusion and there was no significant accumulation of cAMP by fetal adrenal cells in vitro in response to ACTH. There was a significant (P less than 0.05) increase in plasma cortisol concentrations from 2.21 +/- 0.47 (mean +/- SEM) ng/ml at 0 h to 35.7 +/- 11.6 ng/ml at 96 h in fetuses receiving P-ACTH in vivo. In these fetuses there was a significant (P less than 0.05) accumulation of cAMP after addition of ACTH by fetal adrenal cells in vitro (mean increment delta = 48 pmol). This rise in plasma cortisol was prevented in fetuses receiving P-ACTH + metopirone. Further, metopirone treatment prevented the increase in fetal adrenal weight and accumulation of cAMP after in vitro ACTH that normally followed ACTH treatment in vivo. This effect was not overcome by further addition of guanylylimido-diphosphate. These experiments raise the possibility that cortisol might mediate the increase in cAMP accumulation resultant upon in vivo P-ACTH treatment.
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PMID:In vivo adrenocorticotropin (1-24)-induced accumulation of cyclic adenosine monophosphate by ovine fetal adrenal cells is inhibited by concomitant infusion of metopirone. 620 13

Plasma cAMP was determined using the method of Tovey et al. in normal pregnant women with a mean concentration of 18.9 +/- 0.8 pmol/ml (x- +/- SEM). Between weeks 9-12 and 33-36 of gestation, there were two peaks, with a mean cAMP of 22.5 +/- 2.4 which were significantly increased in comparison to the other weeks of pregnancy. Significantly decreased values were found in patients with threatened abortion (weeks 12-28) which terminated in abortion (11.6 +/- 2.4; p < 0.01). In premature labor no differences were found. During therapy with fenoterol there were highly significantly increased plasma cAMP levels (48.2 +/- 2.8; p < 0.0005). During thyroid hormone therapy in euthyroid goiter, cAMP was significantly decreased (14.0 +/- 1.4; p < 0.05). 1 week after cessation of therapy a highly significant increase of cAMP was observed (38.2 +/- 6.9; p < 0.0005). There was a negative linear regression between T3 and cAMP (2p < 0.01). In pregnancy with hypertension cAMP was significantly elevated (30.5 +/- 3.8 p < 0.0005), but nearly normal under antihypertensive therapy. In pregnancy with edema only, no difference was found. Induction of labor with PGE2 alpha was followed by a decrease of plasma cAMP.
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PMID:Plasma cAMP in normal and abnormal human pregnancy. 625 65

Male Wistar rats were fed a fluoride deficient diet (less than 0.5 parts/10(6) F), and either distilled water or fluoridated water (1.0 parts/10(6)). By week 3, the control group had urinary excretions of 106 +/- 5 nmol cAMP/day (mean +/- SEM) whereas the experimental group excreted 129 +/- 6 nmol cAMP/day. After 111 days, the control group excreted 270 +/- 26 nmol cAMP/day compared to 600 +/- 78 nmol cAMP/day for the experimental group. Body weight, food and water consumption, urine volume, and urinary creatinine and phosphate levels were not significantly different between the two groups. Tissue cAMP levels were determined after 4, 6 and 16 weeks. By week 4, the rats receiving the fluoridated water had significantly higher levels of cAMP in the liver (113 per cent) tibia (130 per cent), femur (89 per cent) and heart (35 per cent). At week 6, the liver (119 per cent), tibia (296 per cent), heart (168 per cent), kidney (73 per cent) and submandibular gland (27 per cent) had significantly higher levels of cAMP. By week 16, the liver, femur, kidney and submandibular gland continued to have elevated levels of cAMP. Liver glycolytic metabolites were determined after 6 weeks, and the results suggested a decrease in pyruvate kinase activity.
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PMID:The effects of fluoridated water on rat urine and tissue cAMP levels. 628 41

The adrenergic system may have an influence on the severity and activity of bronchial asthma. It has been suggested that there might be a relationship between the allergic process and the adrenergic system. Therefore this system was studied before and after an allergen challenge. Two parameters were measured: in vivo: propranolol threshold measurement to assess adrenergic involvement; in vitro: the beta-adrenergic response of peripheral lymphocytes as parameter for beta-receptor function. Seven allergic asthmatics who were not treated with beta-stimulants or corticosteroids and seven normals inhaled house dust mite extract. On the days before and after the challenge, propranolol threshold measurements were performed. Six patients had a dual reaction after a house dust mite inhalation; one patient had an early response. The propranolol threshold changed from 1.32% (SEM 0.16) on the day before challenge to 0.86% (SEM 0.19) on the day after (0.02 less than P less than 0.025). In the same patients the maximal cAMP response of lymphocytes in the presence of 10(-6) mM isoproterenol changed from 339% (SEM 18.9) above basal level before the allergen challenge to 194% (SEM 24.6) after the challenge (0.001 less than P less than 0.005). The pre-challenge beta-response of lymphocytes of the asthmatic patients was comparable with that of normal lymphocytes (298% SEM 59.8). The results suggest that an allergen-induced asthmatic attack may lead to an impaired beta-adrenergic function.
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PMID:The role of the adrenergic system in allergy and bronchial hyperreactivity. 629 Feb 51

We investigated the effects of uraemia and haemodialysis on the basal activity of adenylate cyclase and the cyclic-AMP content of human platelets in patients with end-stage renal insufficiency, patients receiving maintenance haemodialysis, and as controls healthy voluntary subjects. Basal adenylate cyclase activity in terminal renal disease (creatinine clearance less than 15 ml/min/1.73 m2) was 824 +/- SEM 57, in comparison to the healthy subjects with 453 +/-SEM 28 (P less than 0.001). We also found significant elevation (P less than 0 . 001) of platelet cAMP levels as compared to the controls. Basal adenylate cyclase activity and platelet cAMP levels were approximately normal in the dialysed patients. These results show that uraemic toxins adversely affect the platelet AC-cAMP system, possibly causing impaired platelet aggregation and the bleeding diathesis of uraemia.
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PMID:Adenylate cyclase activity and cAMP content of human platelets in uraemia. 629 33

To elucidate the changes in mineral metabolism and blood concentrations of calciotropic hormones which accompany GH therapy, we studied 12 GH-deficient children for 5 days before and for 1 week after high dose (5 IU/day) GH therapy, and again at 1 month, 3 months, and 1 yr of replacement therapy (0.1 IU/kg to a maximum dose of 2 IU three times weekly). All responded with acceleration of height velocity, and bone ages advanced appropriately. Fasting serum ionized calcium levels did not change: 4.11 +/- 0.06 (SEM) mg/dl before, 4.19 +/- 0.05 for the week of high dose therapy, and 4.20 +/- 0.14 during replacement therapy. Likewise, fasting serum parthormone did not vary: 38.9 +/- 2.6 muleq/ml before to 44.1 +/- 9.2 at 1 yr. Twenty four-hour nephrogenous cyclic AMP (NcAMP) did not vary over the first week (1.2 +/- 0.7 nmol/dl glomerular filtrate before, 1.3 +/- 0.4 after 1 week), but increased to 5.3 +/- 1.9 after 1 yr (alpha less than 0.001). The response of ionized calcium and parathormone to a standardized disodium EDTA infusion of 50 mg/kg also did not change. The mean fasting serum calcitonin level was not different before therapy (29.4 +/- 2.8 pg/ml), after 1 week (21.5 +/- 1.8), or after 1 yr (42.4 +/- 11.0). However, the mean serum 1,25-dihydroxyvitamin D concentration rose from 33.1 +/- 3.3 pg/ml before therapy to 68.3 +/- 12.3 on the seventh day of high dose therapy (alpha less than 0.01), returning to pretherapy values by 1 month. We conclude that high dose GH therapy in GH-deficient children raises 1,25-dihydroxyvitamin D concentration acutely, but that long term, physiological replacement therapy does not cause such an effect. Because NcAMP excretion rose in the absence of an increase in serum parathormone concentration, we conclude that GH sensitizes the kidney to a cAMP-mediated effect of parathormone.
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PMID:Effects of growth hormone replacement therapy on 1,25-dihydroxyvitamin D and calcium metabolism. 630 26

beta-Adrenergic receptors on human mononuclear leukocytes were assessed using [125I]iodohydroxybenzylpindolol binding. Subjects were studied supine and after being ambulatory, a maneuver that increases plasma catecholamines approximately two-fold. beta-Receptor affinity for agonists, measured by the competition of [125I]iodohydroxybenzylpindolol binding by (-)isoproterenol was significantly reduced with ambulation and this reduction was associated with a reduction in the proportion of beta-receptors binding agonist with a high affinity from a mean (+/- SEM) of 42 +/- 5 to 24 +/- 2% (P less than 0.01). In a parallel series, beta-adrenergic-stimulated adenylate cyclase activity was also reduced with postural change from 4.6 +/- 1.1 to 2.4 +/- 0.6 pmol [32P]cAMP/min per mg protein (P less than 0.05) after ambulation. Similar reductions in the proportion of receptors binding agonist with a high affinity were seen after infusion of norepinephrine. We conclude that the maneuver of ambulation reduces leukocyte beta-receptor responsiveness and affinity for agonists, probably by the effect of increased plasma catecholamines mediating an uncoupling of the beta-receptor-adenylate cyclase complex.
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PMID:Dynamic regulation of leukocyte beta adrenergic receptor-agonist interactions by physiological changes in circulating catecholamines. 630 44


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