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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies concerning variations of the central renin-angiotensin system (RAS) during immobilization stress in rats have shown a significant increase in renin-like activity in the hypothalamus and fronto-parietal cortex, together with a definite decrease in the hypophysis and pineal gland. The resultant stress analgesia is blocked by the previous administration of naloxone and saralasin (angiotensin II antagonist). The intracerebral administration of renin and angiotensin II produces an increase in latencies to thermoalgesic stimuli; this is reduced, as is immobilization stress, by naloxone and saralasin. Both chemical hypophysectomy obtained by dexamethasone pretreatment as well as surgical epiphysectomy block the stress-induced analgesia. The experimental data obtained argue in favour of the participation of the cerebral RAS in stress analgesia through the indirect mechanism of release of opioid peptides.
Pain 1986 Nov
PMID:Evidence for the involvement of cerebral renin-angiotensin system (RAS) in stress analgesia. 354 Aug 14

Except for infections (pyelonephritis, abscess of the kidney), which cause symptoms such as pyuria, pain and fever, most diseases of the renal parenchyma were unknown in Greek and Roman antiquity. Even in the Renaissance they were not yet properly identified. Edema was generally thought to be related to liver disease. Proteinuria was discovered at the end of the 18th century. In 1827 Bright provided the first, almost complete clinical description of the various forms of acute and chronic glomerulonephritis and showed that they were accompanied by macroscopic changes in the kidneys. Between 1850 and 1885, Frerichs, Klebs and Langhans described the primary glomerular lesions. The amount of new knowledge acquired during the 20th century has been tremendous, and covers the mechanism of urine formation, the role of sodium retention in edematous states, the physiology and physiopathology of the renin-angiotensin-aldosterone system, the glomerular origin of the nephrotic syndrome, new methods of investigation, progress in histology and immunology, the discovery of many tubular syndromes, the introduction of antibiotics and antihypertensive drugs, and the development of dialysis and transplantation.
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PMID:[On the history of kidney disease]. 355 Oct 58

Parathyroid hormone, thyrocalciotonin, testosterone, estradiol, aldosterone and renin activity of the blood plasma were radioimmunoassayed in 142 patients with neurological manifestations of lumbar osteochondritis. The blood levels of parathyroid hormone and, to a lesser degree, those of thyrocalciotonin were elevated. The levels depended on the severity and duration of the pain syndrome while thyrocalciotonin excretion depended on the degree of the degenerative dystrophic process in the spinal column. Prolonged pain syndrome was associated with an inhibited function of the gonads and the mineralocorticoid layer of the adrenals. A hypothesis is advanced, which explains the participation of the endocrine glands in the etiopathogenesis of lumbar osteochondritis and its neurological manifestations.
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PMID:[Role of various endocrine glands in the pathogenesis of the neurologic symptoms of lumbar osteochondrosis]. 389 Apr 27

Polypeptides are endogenous agents, involved in the regulation of many physiologic functions and the pathogenesis of several diseases. Polypeptide antagonists form a group of new chemical entities which may provide valid therapeutic agents. Some polypeptides (angiotensin, kinins) are released through the action of proteolytic enzymes (renin, kallikreins) and act as hormones or autacoids; others (substance P, neurotensin) are synthetized by nervous cells to serve as neurotransmitters or neuromodulators. The main homeostatic role of the renin-angiotensin system is to uphold high systemic arterial blood pressure. Overproduction of renin and insufficient checking of renin secretion are among the most common causes of arterial hypertension. Several forms of arterial hypertension (neurovascular, idiopathic) benefit from a reduction in renin-angiotensin system activity. This is achieved either through decreasing renin secretion, by inhibiting conversion of angiotensin I into angiotensin II, or through blocking the peripheral actions (at the receptor sites) of angiotensin II. Renin secretion is very significantly reduced by beta-blocking agents (propranolol); conversion of angiotensin I into angiotensin II is inhibited by teprotide, captopril and their derivatives; peripheral actions of angiotensin II are blocked by saralasin. Bradykinin and related agents produce vasodilation, increase vascular permeability and stimulate pain fibers. Kinins thus reproduce the cardinal features of inflammation and are held to be mediators of the inflammatory reaction. The substance P neuropeptide is found in the brain and bowel; it may act as a transmitter of the sensation of pain at the spinal cord and central nervous system sites. Among other effects outside of the brain, substance P is a potent vasodilator and inhibits renin secretion. Neurotensin is a neuropeptide which produces hypothermia, muscular relaxation and analgesia. Outside of the brain, this peptide is involved in the regulation of gastric secretion, intestinal motility and insulin and glucagon secretion. The vasoactive intestinal peptide, found in certain cholinergic nerve endings, is a large peptide which inhibits gastric secretion, intestinal motility and vascular tone.
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PMID:[Polypeptides and antagonists]. 620 6

A new case of analbuminemia in a fifty-four-year-old French woman is described. The patient was admitted to a hospital cardiology department for thoracic pain. Consanguinity between the patient's parents was established. Proteins were studied both during the acute phase and the subsequent remission. Total serum protein concentrations were stable, around 5.3 g. Hypoalbuminemia was compensated initially by alpha-2-globulins and subsequently by beta globulins. Increases in serum cholesterol and serum beta lipoproteins were recorded. Hydroelectrolytic balance was normal. Orthostatic renin and aldosterone release was significantly increased, denoting response to lowered hydrostatic pressure. A minor increase in serum thyroxin was recorded, probably because of the increase in thyroxin binding globulin.
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PMID:[Biological study of a case of analbuminemia]. 630 Oct 31

Decapeptide ceruletide (CRL), chemically related to cholecystokinin and gastrin, proved to have remarkable analgesic properties when administered to a group of 22 burned patients, 15 patients with acute myocardial infarction, and 8 patients suffering from pain caused by malignant tumours with metastases. Its effect was such, that many of the patients required no other analgesics (opiates) even after a prolonged administration (up to 10 days) of CRL. In some of the patients a marked euphoria developed. There were no substantial changes in EEG records during CRL administration in 15 controls, among them 4 epileptics. It is probable that CRL helps to activate the internal analgesic system. In the burned patients cortisol, testosterone, renin, prolactin and tri-iodothyronine (T3) levels in serum (plasma) were measured (radio-immunoassays). CRL did not block the stress response (no drop of increased cortisol levels, no increase in low T3 levels), but it modified (influenced) it (drop of the high renin levels, and a tendency to increase the very low testosterone levels). CRL appears to act as an endorphin releaser, as evidenced by the plasma levels of beta-endorphins (quotations). CRL and similar drugs may represent a new, more physiological and probably safer approach to the management of pain.
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PMID:Endorphin releasers: a new possible approach to the treatment of pain after burns--a preliminary report. 631 91

Using the tail-flick method in 45 rats with a chronic cannula stereotaxically implanted in the third ventricle, a rapid onset, dose related and short lasting analgesia was obtained after intracerebroventricular injection of Ang II 10-15 ng/kg or renin 0.03-0.1 U. Analgesic effects of the endogenous and exogenous Ang II are prevented by naloxone--1 mg/kg i.p. The inhibition of serotonin synthesis with PCPA--400 mg/kg/day i.p. for five days as well as the serotonin-receptor block with ketanserin 0.1 mg/kg i.p. partially prevent analgesic effects of Ang II and renin intracerebral administration. The increase of the pain perception threshold after infusing into the brain Ang II or renin points out a new functional consequence of the possible opioid participation in the central effects of renin-angiotensin system.
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PMID:Possible opioid participation in the analgesic effects of the renin-angiotensin system. 641 96

Plasma renin activity (PRA) was measured in 23 patients (pts.) affected by myocardial infarction (AMI), and in a control group of 4 normal subjects, during bed rest. A blood sample was drawn every 12 hours to determine PRA pattern curve during 5 days in Coronary Care Unit. The initial PRA was in the normal range in all pts., but it rose subsequently. The highest level was reached on the 4th day. The mean value of PRA at this time was significantly higher than the initial one (p less than 0.01). Such increasing PRA was not correlated with age, sex, infarction site, infarction dimension, pain, blood pressure, arrhythmias, bed rest. At variance with the experience of others, we were not able to show a significant correlation between PRA and plasma K+ levels. Diuretic and/or beta-blocker agents too, did not influence this increase of PRA in AMI. Our results are compared with those previously reported in the literature and the possible pathophysiological mechanisms are discussed.
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PMID:[Behavior of plasma renin activity in acute myocardial infarct]. 675 84

The classic triad of hematuria, pain and presence of a palpable flank mass is found only in few patients with renal carcinoma. Hematuria, the main symptom, occurs in nearly the half of patients. Blood levels of erythropoetin and renin are often elevated and may be of value as biochemical tumor markers. Chemotherapeutic agents do not alter the course of metastatic renal carcinoma significantly. Vinblastine is the most effective available drug currently. Progestins or androgens cause tumor regression very seldom. If antioestrogens or immuntherapeutic regimens may improve therapeutic results, is not to be decided at present.
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PMID:[Clinical aspects and chemotherapy of adenocarcinoma of the kidney]. 722 39

Non-steroidal anti-inflammatory drugs (NSAID) are now commonly used in the treatment of postoperative pain. In normovolaemic conditions, prostaglandins do not seem to play a substantial role in maintaining renal function. However, numerous studies have shown that during activation of vasoconstrictor systems the synthesis of renal prostaglandins counteracts the vasoconstrictor effects and thereby maintains renal function. In animals, renal blood flow and GFR are markedly decreased when an NSAID is administered in the presence of renal hypoperfusion. Major surgery decreases renal function secondary to stimulation of the adrenosympathetic system and the renin-angiotensin system, and it has previously been demonstrated that maintenance of renal blood flow during laparotomy in dogs depends on an intact prostaglandin synthesis. Perioperative effects of NSAIDs are only sparsely investigated in humans, and studies on the effect on renal haemodynamics have not been presented. As in unanaesthetized volunteers, NSAID have been found to decrease the postoperative excretion of water, sodium and potassium. It therefore still remains unclarified whether general anaesthesia and surgery increase the risk of renal side effects of NSAIDs. Because of the potential risk of peri- and postoperative complications that may further deteriorate renal function, NSAIDs should not be used preoperatively, and not in patients in unstable haemodynamic states.
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PMID:[Renal side-effects of intraoperative and postoperative pain treatment with non-steroidal anti-inflammatory drugs]. 777 Sep 68


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