Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fourteen patients with invasive bladder cancer were treated by bilateral internal iliac artery infusion of cisplatin, with or without other anticancer agents, and concurrent radiotherapy. Angiotensin II was simultaneously infused in 10 cases. Of the 14 patients, complete response and partial response were achieved in 9 (64%) and 3, respectively. Hematuria was controlled in all 8 patients, and pain was relieved in 3 of 4 patients. Side effects were observed in 8 patients: appetite loss in 8, nausea and/or vomiting in 7, and leukocytopenia in 6 patients, in 3 of whom radiotherapy had to be intermittent because of severe leukocytopenia (less than 2000/mm3). However, restoration of leukocytopenia occurred one week later. Thus, intra-arterial anticancer agents including cisplatin together with concurrent radiation may be one of the most effective therapies for invasive bladder cancer.
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PMID:[Combined treatment of invasive bladder cancer by intra-arterial infusion chemotherapy of cisplatin with or without other anticancer agents and concurrent radiotherapy--initial response and side effects]. 164 10

The clinical efficacy and indications for Angiotensin II (AT II)-induced hypertension chemotherapy were evaluated as a drug delivery system in 101 patients with advanced carcinoma. The sites of primary tumor studied included stomach (44), pancreas (18), colon (16), esophagus (6), bile duct (4), liver (3), breast (7) and 3 other single organs. Seventy four cases had distant metastases (lymph node (25), liver (29), peritoneum (16), and lung (4)). Additionally, the protocol was used 12 cases as postoperative adjuvant chemotherapy and 15 cases following exploratory laparotomy. The blood pressure was elevated to a level 1.5 times base-line. The regimens used consisted of MMC + ADR (55), FAM (38) and CDDP (8). The dosages administered were MMC 7 mg/m2, ADR 14 mg/m2 and 5-FU 350 mg/m2. The cancer chemotherapy protocol with AT II was repeated for an average of 2.6 cycles with a 2-3 week interval. The drug concentration in tumor tissues was increased 1.7 fold by AT II treatment. The response rate was 15.8% (CR 7 and PR 9), and in those patients with lymph node, liver and peritoneal metastases was 48.0, 6.9 and 6.3%, respectively. The serum levels of tumor markers decreased in 9 patients. Subjective symptoms, such as hoarseness, edema and pain, were improved. The mean survival in patients with distant metastasis who responded was 343 days, and in nonresponders was only 168 days (p less than 0.05). The side effects of this therapy were slight, typically being grade 1 and 2. Thus, the chemotherapeutic agents studied in conjunction with AT II were effective in patients with lymph node metastasis. Additionally, this regimen could be performed safely with minimal side effects.
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PMID:Clinical evaluation of chemotherapy under angiotensin II-induced hypertension in patients with advanced cancer. 213 Jul 94

Neuroendocrine activation in acute myocardial infarction (AMI) may have important physiological consequences for myocardial perfusion and function. We measured plasma angiotensin II in 60 patients with AMI within 6 hours of pain and on days 1-3 and day 10. On admission, AII was normal at 9.9 + 1.3 pmol/l (normal range 2-12 pmol/l). At day 3, AII rose markedly to 77.5 + 25.0 in those with heart failure (group 1, n = 13); but AII also rose in uncomplicated patients (group 2, n = 47) to 27.8 + 4.0 (p less than 0.001). At day 10, levels of AII remained high, especially in group 1 (50.5 + 22.2 vs 6.1 + 1.5, p less than 0.005). Thus neuroendocrine activation, present early in AMI, is seen in both uncomplicated infarcts and in those developing heart failure. Angiotensin II mediated vasoconstriction perhaps enhanced by catecholamines could have deleterious effects on myocardial function and perfusion, and indicates the potential for angiotensin-converting enzyme inhibitors in early AMI.
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PMID:Neuroendocrine activation in acute myocardial infarction. 244 Nov 95

Ten patients with advanced bladder cancer were treated with intra-arterial infusion therapy. The patients consisted of nine males and one female between 55 and 82 years old (median: 70 years). In all patients, cisplatinum (CDDP) (2 mg/kg), aclacinomycin (ACR) (0.5 mg/kg) and Angiotensin II (25 mg) were infused via the internal iliac artery for a period of about 30 minutes. Seven patients also received X-ray therapy with a linac. The efficacy of this therapy was assessed by computed tomographic scanning, sonography and cystoscopy. As a result of this assessment, 2 patients were rated complete response "(CR)", 6 partial response (PR) (showing 50% or more reduction in the lesion) and 2 no change "(NC)". To compare the efficacy of this therapy for two histopathologically defined groups of patients (patients with grades 2 and 3 cancer), one patient was rated "CR", four "PR" and two "NC" in the grade 3 group (total 7 patients), while one was rated "CR" and two "PR", in the grade 2 group (total 3 patients). In effective cases, pollakiuria and miction pain disappeared shortly following intra-arterial infusion therapy. As for side effects of the therapy, mild nausea or vomiting was observed in all patients, while leukopenia was noted in one patient.
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PMID:[Treatment of advanced bladder cancer with intra-arterial infusion of cisplatinum (CDDP) and aclacinomycin (ACR), combined with angiotensin II]. 342 16

In this review, the emerging functional roles of the brain angiotensin system have been considered. The major effects of Ang II can be classified into three groups, which imply three possible functions: The first, and largest, group is actions associated with the regulation of body fluid volume in response to hypovolemia. These include thirst, blood pressure increase, vasopressin release, sodium appetite and excretion, and ACTH and aldosterone release. This function alone has important implications for the control of blood pressure and the disease of hypertension. Another possible function is a role for angiotensin in the activity of gonadotropic hormone releasing hormones and pituitary hormones during the reproductive cycle and pregnancy. A third group of functions is the synaptic, neurotransmitter interactions of Ang II with catecholamines, serotonin, prostaglandins, and other peptides, not all of which could be reviewed here due to space limitations. This interaction is significant for all functions mentioned and leads to alterations in motivation (thirst, pain), memory (and possibly learning), and motor control. The amount of data available, however, is so limited that to claim angiotensin plays any major role in the latter functions would be premature. Throughout this review, we compared the central and peripheral effects of Ang II. We suggest that normally, a blood-CVO barrier prevents diffusion of peripheral Ang II to brain receptors inside the BBB. Because of this mechanism, the responses to the two routes of administration are distinctly different. When systemic peptide levels are low, Ang II activates only receptors in the CVOs; however, when these levels are high, the peptide diffuses to receptors that are normally activated only by brain Ang II.
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PMID:Functions of angiotensin in the central nervous system. 355 9

The central effect of angiotensin II on the analgesic action of morphine in mice was investigated using the tail-pinch and hot plate tests. Angiotensin II (0.1-10 pmol), given intracerebroventricularly (i.c.v.), had no effect on the nociceptive sensitivity but did produce a dose-dependent attenuation of the morphine-induced analgesia. A specific angiotensin II antagonist, Saralasin (1 pmol), which in itself had no analgesic effect, significantly potentiated the morphine-induced analgesia. These results suggest that angiotensin II probably plays the physiological role of an anti-opioid substance in pain-modulating systems in the brain.
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PMID:Intracerebroventricular administration of angiotensin II attenuates morphine-induced analgesia in mice. 408 Jan 8

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

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

The effect of iontophoretically applied noradrenaline, angiotensin II and vasopressin on blood flow and sensitivity to heat was investigated in the capsaicin-treated forearms of 52 healthy volunteers. Non-specific effects of a 4-min saline iontophoresis were investigated in another 19 subjects. Pretreatment with phentolamine inhibited vasoconstriction and thermal hyperalgesia to noradrenaline, indicating that alpha-adrenoceptors mediated these responses. The intensity of thermal hyperalgesia differed significantly across the following treatments: saline (heat pain threshold 1.1 degrees C lower than at control sites), angiotensin II (3.4 degrees C), noradrenaline (6.4 degrees C) and vasopressin (9.0 degrees C). Decreases in skin blood flow were significantly greater after the iontophoresis of noradrenaline (65% reduction from baseline) and vasopressin (68%) than after the iontophoresis of angiotensin II (45%). In contrast to the other two drugs, angiotensin II induced thermal hyperalgesia in proportion to the intensity of vasoconstriction. The findings suggest that iontophoretic currents induce minor non-specific thermal hyperalgesia. Angiotensin II appears to increase sensitivity to heat by an ischaemic mechanism, whereas an additional non-vascular influence contributes to thermal hyperalgesia induced by noradrenaline and vasopressin. These mechanisms could contribute to hyperalgesia in chronic inflammatory or neuropathic pain syndromes.
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PMID:The effect of noradrenaline, angiotensin II and vasopressin on blood flow and sensitivity to heat in capsaicin-treated skin. 961 98

The aim of this paper is to study the synergistic anti-analgesic effect of angiotensin II (Ang II) plus cholecystokinin octapeptide (CCK-8). Our previous studies have shown that both CCK-8 and Ang II are potent anti-opioid substances. Intracerebroventricular (i.c.v.) injection of CCK-8 or Ang II dose-dependently antagonizes morphine-induced analgesia (MIA). In the present study, we observed the combined effect of CCK-8 and Ang II in antagonizing MIA. CCK-8 and Ang II were injected intracerebroventricularly to rats in various proportions and doses. The results were analyzed with isobolographic analysis. Combined injection of CCK-8 and Ang II in a ratio of 1 ng: 2.5 microg or 1 ng: 5 microg produced significantly greater effect in antagonizing MIA. The ED(50) of the two ratios are only 18.5% and 27.5%, respectively, of the theoretical dose of simple addition. We conclude that CCK-8 and Ang II used in such dose ratios may antagonize MIA synergistically.
Pain 2000 Apr
PMID:Synergistic effect of cholecystokinin octapeptide and angiotensin II in reversal of morphine induced analgesia in rats. 1078 20


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