Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 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.
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PMID:Evidence for the involvement of cerebral renin-angiotensin system (RAS) in stress analgesia. 354 Aug 14

Mean arterial pressure, heart rate, plasma catecholamines, renin activity, and vasopressin changes induced by a 30-degree head-up tilt were studied before and during epidural anesthesia with bupivacaine in eight elderly patients (ages 58-82 yr). The tilt performed before epidural anesthesia did not modify mean arterial pressure, heart rate, plasma catecholamines, renin activity, and vasopressin at 5 and 15 min. During epidural anesthesia, the superior level of analgesia ranged from T4 to T10. Epidural anesthesia induced significant (P less than 0.05) decreases from control values in mean arterial pressure and plasma norepinephrine (from 85 +/- 6 to 67 +/- 8 mmHg and from 600 +/- 108 to 307 +/- 77 pg/ml, respectively, mean +/- SEM) without significant changes in heart rate, plasma epinephrine, renin activity, and vasopressin. However 5 and 15 min after tilt, significant decreases from pretilt values were measured in mean arterial pressure (from 67 +/- 8 to 57 +/- 6 and 55 +/- 6 mmHg, respectively) and in heart rate (from 70 +/- 8 to 63 +/- 7 and 62 +/- 7 beats/min). Simultaneously, an increase in plasma vasopressin (from 14.8 +/- 5.5 to 36.2 +/- 10.3 and 40.0 +/- 10.5 pg/ml) was recorded, whereas plasma norepinephrine and epinephrine remained unchanged. Posttilt plasma renin activity values at 5 and 15 min were increased significantly when compared with the preepidural values (2,752 +/- 1,168, 2,410 +/- 1,214 and 713 +/- 190 pg X ml-1 X h-1, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of epidural anesthesia on catecholamines, renin activity, and vasopressin changes induced by tilt in elderly men. 388 49

Studies concerning the variations of the central renin-angiotensin system (RAS) during the immobilization stress in rats have shown a significant increase of the renin-like activity in the hypothalamus and the fronto-parietal cortex together with a manifest decrease in hypophysis and pineal gland. The resulted stress, analgesia, is blocked by the previous administration of naloxone and saralasin. The intracerebral administration of renin and angiotensin II increases the latency time to thermoalgesic stimuli which is reduced, as in the immobilisation stress, by naloxone and saralasin. The chemical hypophysectomy obtained by chronic treatment with dexamethasone, also inhibits the stress-induced analgesia. Epiphysectomy reduces all the same the analgesic effects of the immobilisation stress. The obtained experimental data argue in favour of the participation of the cerebral RAS in stress analgesia through the indirect mechanism of release of opioid peptides.
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PMID:Evidence of the involvement of cerebral renin-angiotensin in stress analgesia. 393 Nov 11

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

Glucose loading caused a significant increase in insulin response (IRI) in patients undergoing caesarean section both under general anaesthesia and under epidural analgesia. After a fast intravenous glucose loading given just before the administration of epidural bupivacaine, similar but more variable serum immunoreactive insulin levels were found as compared with those determined after a slower intravenous glucose infusion in patients under general anaesthesia. Plasma renin activity values did not change significantly in either group, but, differing from general anaesthesia, antidiuretic hormone levels (ADH) increased significantly in patients under epidural analgesia. The changes in IRI and ADH response may be caused by a higher psychic stress reaction of the conscious patients during caesarean section under epidural analgesia.
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PMID:Blood glucose, insulin, antidiuretic hormone and renin activity response during caesarean section performed under general anaesthesia or epidural analgesia. 704 9

This study was designed to evaluate effects of enalaprilat, an angiotensin-converting enzyme inhibitor, on hemodynamic and hormonal responses during surgery at endotracheal intubation, incision, and limb-tourniquet inflation. Thirty patients undergoing limb procedures with general anesthesia (N2O/narcotic technique) and a pneumatic tourniquet were randomized to receive either preoperative enalaprilat (1.25 mg intravenously [i.v.] 20 min prior to induction) or intraoperative enalaprilat (0.625 mg i.v. at the onset of tourniquet-associated hypertension), with appropriate placebo controls. Arterial blood pressure and heart rate increased significantly in response to intubation in the placebo group. Although there were no significant differences in catecholamine levels, plasma renin activity was significantly increased at postincision in the preoperative-enalaprilat group versus the placebo group. This suggests that activation of the renin-angiotensin system may play a key role in mediation of intraoperative hemodynamic responses to endotracheal intubation. With respect to tourniquet hypertension, preoperative or intraoperative treatment with enalaprilat reduced neither the pressor response to tourniquet inflation nor the amount of enflurane subsequently required to control arterial blood pressure. These findings suggest that this response is mediated by pain pathways, and may be treated more effectively with anesthesia/analgesia.
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PMID:Intraoperative hemodynamic, renin, and catecholamine responses after prophylactic and intraoperative administration of intravenous enalaprilat. 786 30

This study evaluated, the influence of mode of delivery, obstetric analgesia and anaesthesia on the maternal plasma renin angiotension system (RAS) in the normotensive primigravidae (n-10) and those with Pregnancy Induced Hypertension (PIH) (n-18). A total of 56 plasma samples from these subjects were assayed for Plasma Renin Concentration (PRC) and Plasma Renin Activity (PRA), using the radio-immunoassay technique. The normotensive subjects had normal delivery, while their hypertensive counterparts were delivered vaginally under lumbar epidural analgesia (n = 10) and with Caesarean Section (n = 8). The blood sample for the study were taken pre-labour, and immediately after delivery. The mean pre-labour PRC and PRA levels for the normotensive subjects were 5.73 +/- 0.25, and 3.56 +/- 0.13 ngml.1hr-1; and the post-delivery PRC and PRA values were 4.43 +/- 0.18 and 2.1 +/- 0.05ngml-1hr-1 respectively. The mean pre-labour PRC and PRA levels for the hypertensive subjects, who were delivered under epidural analgesia were 6.38 +/- 0.52 and 3.64 +/- 0.09 ngml-1hr-1 and the post-delivery values for this group were 5.04 +/- 0.21 and 2.34 +/- 0.07 ngml-1hr-1 respectively. The mean pre-labour PRC and PRA levels for the hypertensive subjects who were delivered by Caesarean Section were 5.87 +/- 0.36 and 3.83 +/- 0.36 ngml-1hr-1 and their post-delivery PRC and PRA values were 4.55 +/- 0.30 and 2.30 +/- 0.09 respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Studies of the effect of mode of delivery: obstetric analgesia and anaesthesia on maternal Plasma Renin Concentration (PRC) and Plasma Renin Activity (PRA) in the normotensive and hypertensive primigravidae. 808 Aug 22

In order to find out whether epidural analgesia, significantly altered the maternal and cord venous Plasma Renin Concentration (PRC) and Plasma Renin Activity (PRA) in the primiparae, a radioimmunoassay measurement of these renin components was carried out on 40 maternal plasma and 18 cord venous plasma samples. The subjects were 20 primiparae who had uneventful antenatal course, 10 of whom were delivered under epidural analgesia, while others (control group) (n = 10) had routine narcotic analgesia in labour. Maternal venous blood samples were taken in the lateral recumbent position at induction of labour, and immediately after delivery, while the cord venous blood samples were obtained just before or immediately after expulsion of the placenta. The mean +/- SEN of maternal pre-induction PRC and PRA, in the control group were 5.56 +/- 0.32 and 3.81 +/- 0.17 nmgl-1hr-1; while the corresponding immediate post delivery values were 5.05 +/- 0.35 and 2.33 +/- 0.06 respectively. In the epidural analgesia group, the mean maternal pre-induction and immediate post-delivery PRC and PRA values were 5.68 +/- 0.22; 3.49 +/- 0.2; and 5.05 +/- 0.35 and 2.36 +/- 0.06 ngml-1hr-1 respectively. The mean cord venous plasma PRC and PRA in the control group were 3.22 +/- 0.17 and 1.18 +/- 0.03 respectively while the corresponding PRC and PRA values for the epidural analgesia group were 2.93 +/- 0.20, and 1.24 +/- 0.04 ngml-1hr-1 respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Studies of maternal plasma renin concentration (PRC) and plasma renin activity (PRA) and cord venous PRC and PRA in the primigravidae delivered under lumbar epidural analgesia. 819 60

Physiological stress is known to produce analgesia and memory disruption. Brain renin angiotensin system (RAS) has been reported to participate in stress response and plays a role in the processing of sensory information. Angiotensin receptors (AT), particularly AT1 subtypes have been reported to be distributed in brain areas that are intimately associated with stress response. The purpose of present study was to examine the modulation of AT1 receptor in the immobilization stress and angiotensin II (AngII)-induced analgesia and impaired retention, and to determine whether resultant behavioral changes involve common sensory signals. Result of present experiments showed that immobilization stress in mice and rats, and intracerebroventricular (ICV) administration of AngII (10 and 20 ng) in rats produced an increase in tail-flick latency. Similarly, post training administration of AngII or immobilization stress produced impairment of retention tested on plus-maze learning and on passive avoidance step-down task. Both these responses were sensitive to reversal by prior treatment with losartan (10 and 20 mg/kg), an AT1 AngII receptor antagonist. On the other hand, naloxone, an opiate antagonist preferentially attenuated the stress and AngII-induced analgesia and retention deficit induced by immobilization stress, but failed to reverse the AngII induced retention deficit. These results suggest immobilization stress-induced analgesia and impaired retention involves the participation of brain RAS. Further, failure of naloxone to reverse AngII-induced retention impairment shows. AngII-induced behavioral changes are under control of different sensory inputs.
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PMID:Brain renin angiotensin system (RAS) in stress-induced analgesia and impaired retention. 1044 91


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