Prostaglandins inhibition

Sanders Did you ever look to see whether indomethacin (i.e. prostaglandin inhibition) decreases coupling between these Ca2+ waves and activation of BK channels Perhaps this is your time delay. Production of prostaglandin should activate protein kinase A because of cAMP production, and this will increase BK open probability. 

Young That s a good point. I have seen that indomethacin not only does prostaglandin inhibition but there also are other mechanisms, possibly as simple as intracellular binding of Ca2+ in terms of buffer. However, what you are saying is entirely possible. 

Taiwo YO, Levine JD. (1988). Prostaglandins inhibit endogenous pain control mechanisms by blocking transmission at spinal noradrenergic synapses. J Neurosci. 8(4) 1346-49. 

Prostaglandins inhibit the secretion of protons by the parietal cells in the stomach, which is normally increased in response to food and the hormone gastrin. Consequently, inhibition of prostaglandin synthesis by aspirin or other similar drugs results in increased secretion of protons by the stomach, which can result in considerable gastric discomfort and can, if chronic, lead to the development of a peptic ulcer. Consequently, there is some conflict between the use of such inhibitors to relieve chronic pain (see below), in diseases such as arthritis, and the risk of development of ulcers. 

FitzGerald GA. COX-2 and beyond approaches to prostaglandin inhibition in human disease. Nat Rev Drug Discov 2003 2 879-90. 

Prostaglandin inhibition. Ethanol (95%) extract of the dried fruit, at variable concentrations, was active . ... 

Diclofenac, a derivative of phenylacetic acid, is equipotent as an inhibitor of COX-1 and COX-2. In addition to prostaglandin inhibition a central analgesic action of diclofenac mediated by endogenous opioid peptides has been demonstrated. It can be administered orally, intramuscularly or intravenously, and is effective as a postoperative analgesic in a dose of 75-150 mg. The risks of adverse gastrointestinal effects is moderate and diclofenac does not appear to increase blood loss during or after surgery. 

Prostaglandin inhibition may result in reduced renal sodium excretion, impaired resistance to hypertensive stimuli, and reduced renal lithium excretion. Most NSAIDs inhibit platelet function may increase likelihood of bleeding due to other drugs that impair hemostasis. Most NSAIDs are highly bound to plasma proteins. 

N.A. Corylus avellana L. C. comuta Marsh. C. rostrata Marsh. C. americana Marsh. Tannins, essential oil, ferric oxide, beta-sitosterol.102 For coughs, colds, diuretic, prostaglandin inhibition, anti-inflammation. 

Prostaglandin inhibition of gastric acid secretion by blocking the formation of cyclic adenosine monophosphate... 

Combined oral contraceptives (COCs) are helpful, especially when prostaglandin inhibition fails. COCs are thought to relieve dysmenorrhoea by inducing endometrial thinning and inhibiting ovulation, resulting in low levels of uterine prostaglandins. 

ACE INHIBITORS, ANGIOTENSIN II RECEPTOR ANTAGONISTS ASPIRIN t risk of renal impairment. 1 efficacy of captopril and enalapril with high-dose (>100mg/day) aspirin Aspirin and NSAIDs can cause elevation of BP. Prostaglandin inhibition leads to sodium and water retention and poor renal function in those with impaired renal blood flow Monitor renal function every 3-6 months watch for poor response to ACE inhibitors when >100mg/day aspirin is given... 

Of adult asthmatics 2-20% have aspirin hypersensitivity (9). The mechanism is related to a deficiency in bronch-odilator prostaglandins prostaglandin inhibition may make arachidonic acid produce more leukotrienes with bronchoconstrictor activity. Oral challenge in asthmatic patients is an effective but potentially dangerous method for establishing the presence of aspirin hypersensitivity (63). 

Nielsen EH. Hyperkalaemic muscle paresis—side-effect of prostaglandin inhibition in a haemodialysis patient. Nephrol Dial Transplant 1999 14(2) 480-2. 

Tan SY, Shapiro R, Franco R et al. Indomethacin-induced prostaglandin inhibition with hyperkalemia. A reversible cause of hy-poreninemic hypoaldosteronism. Annals of Internal Medicine 1979 90 783-785. 

Alam S, Purdle DM, Johnson AG, Alam S, Purdie DM, Johnson AG. Evaluation ofthe potential interaction between NaCI and prostaglandin inhibition in elderly individuals with isolated systolic hypertension. Journal of Hypertension 1999 7 1195-1202. Brater DC, Anderson S, Baird Betal. Effects of ibuprofen, naproxen, and sulindacon prostaglandins in men. Kidney International 1985 27 66-73. 

About 5% of the filtered lithium may be actively reabsorbed in the thick ascending limb [19]. This active "reabsorption" can increase to about 15% after prostaglandin inhibition [9, 17]. These observations suggest that lithium clearance cannot be used as a precise marker of proximal fluid reabsorption. 

The search for specific inhibitors of cyclooxygenase has opened a new area of research in this field. This cnr.ynic occurs in two forms, cyclooxygenase I (COX-I) and cyclooxygenase 2 (COX-2). COX-1 is a constitutive cn/yme and plays a role in the production of essential prostaglandins. Inhibition of this cn/.yme by all the older, nonsclective NSAIDs is priinurily responsible for a number of their side effects. The COX-2 enzyme is induced in response to the release of several proinflammatory mediators, leading to the inflammatory response and pain. Thus, there was an active search for specific inhibitors of the COX-2 cn/.yme. This has been successful with the approval of three COX-2 inhibitors. discus.sud below. 

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