Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Drug
Enzyme
Compound
Query: UNIPROT:P01350 (
gastrin
)
9,683
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
There is an increasing use and variety of beta-adrenoceptor blocking agents (beta-blockers) available for the treatment of hyperthyroidism. Recent comparative studies suggest that atenolol (200mg daily), metoprolol (200mg daily); acebutolol (400mg daily), oxprenolol ( 160mg daily), nadolol ( 80mg daily) and timolol (20mg daily) produce a beneficial clinical response equal to that seen with propranolol ( 160mg daily). Most beta-blockers reduce resting heart rate by approximately 25 to 30 beats/min, although a lesser reduction is seen with those possessing intrinsic
sympathomimetic
activity such as oxprenolol and pindolol. While earlier studies employing large doses of intravenous propranolol concluded that beta-blockade reduced myocardial contractility, more recent non-invasive studies suggest that the predominant cardiac effect is on heart rate. In patients with cardiac failure, beta-blockers may, however, produce a profound fall in cardiac output. Nevertheless, in combination with digoxin they may be useful in controlling the atrial fibrillation of thyrocardiac disease. beta-Blockers improve nervousness and tremor (although to a lesser extent with cardioselective agents) and severe myopathy, and they also reduce the frequency of paralysis in patients with thyrotoxic periodic paralysis. There is often subjective improvement in sweating but usually no major effect on eye signs. Recent studies show a 10% reduction in oxygen consumption/basal metabolic rate with long term oral use of selective or nonselective beta-blockers. In addition, many agents (propranolol, metoprolol, nadolol and sotalol but not acebutolol, atenolol or oxprenolol) reduce circulating tri-iodothyronine (T3) concentration by between 10 and 40%, although the clinical significance of this effect (if any) is not established. beta-Blockers may also have endocrinological effects on
gastrin
, cyclic AMP, catecholamines and other hormone levels. Given in adequate dosage, propranolol has been shown to control thyrotoxic hypercalcaemia. Minor side effects (nausea, headaches, tiredness, etc.) are quite common but overall beta-blockers are well tolerated by the thyrotoxic patient. The major use of these drugs is in symptomatic control while awaiting definitive diagnosis or treatment. As an adjunct to antithyroid drugs or radioactive iodine, beta-blockers will produce a satisfactory clinical response in the weeks to months before these forms of therapy produce a euthyroid state. beta-Blockers are more convenient than antithyroid drugs in the control of patients receiving therapeutic radioiodine, in that continuous therapy and assessment of biochemical response is possible.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:Use of beta-adrenoceptor blocking drugs in hyperthyroidism. 614 1
The effect of 6-hydroxydopamine, propranolol, phentolamine, alpha-methyl-tyrosine and alpha-methyl-tyrosine plus propranolol on serotonin-stimulated
gastrin
secretion in rats has been examined.
Gastrin
secretion in response to administration of serotonin alone (10 mg/kg i.p.) was significantly reduced in rats pretreated with 6-hydroxydopamine or with propranolol. These results suggest that the effect of exogenous serotonin on
gastrin
secretion can be described as
sympathomimetic
and indirect. The serotonin-stimulated
gastrin
secretion was significantly enhanced by previous administration of phentolamine. Pretreatment with alpha-methyl-tyrosine also elevated serotonin-stimulated
gastrin
secretion, indicating that in the presence of diminished concentrations of the catecholamines, the influence of exogenous serotonin on secretion by G cells is increased. This enhancement in the serum
gastrin
levels was also reduced to a significant extent by simultaneous administration of propranolol, which suggested the activation of G-cell beta-adrenergic receptors after serotonin administration.
...
PMID:Possible mechanism of stimulation of gastrin secretion by exogenous serotonin in rats. 625 18
To ascertain whether any of the well-known effects of intravenous ethanol on pancreatic and gastric secretion could be due to its metabolite--acetaldehyde, a strong cytotoxic and
sympathomimetic
agent--acetaldehyde was given intravenously for 1 h (50, 100, and 200 mg/kg/h) in seven dogs. Acetaldehyde did not modify pancreatic secretion stimulated with secretin and caerulein, but under basal conditions 200 mg/kg/h slightly increased the volume and protein content of pancreatic juice. Acetaldehyde increased gastric secretion up to 4.03 meq/15 min in a dose-dependent manner, while serum
gastrin
remained unchanged. The increase of acidity persisted after propranolol and was inhibited but not abolished by ganglionic blockade. It can be concluded that physiological concentrations of acetaldehyde do not interfere with pancreatic secretion and that it is possible that the stimulatory effect of ethanol on gastric secretion is mediated at least partly through acetaldehyde.
...
PMID:The effect of acetaldehyde on pancreatic and gastric secretion. 720 90