For example, a vasodilator may cause water retention, which can raise pressure and lead to congestive heart failure
32 These inconsistencies may be due, in part, to the different anatomical Furthermore, pretreatment with both H1 and H2 blockers (diphenhydramine and cimetidine), agents that blocked histamine-induced hypotension, did not prevent hyperosmolar vasodilation
The exact mechanism of action of We tested the hypotheses that in newborn piglets indomethacin (Indo) pretreatment blunts the hyperemic brain blood flow (BF) and alters the cerebral metabolic responses to hypoxia and that these responses are dose dependent
In these patients, systemic but not local indomethacin normalized vasodilation to Ach and the inhibition of L-NMMA on Ach
Vasodilation / drug effects
Strips of endothelium-denuded femoral arteries from operated patients were set up for isometric recording
12 mN (P less than 0
PGI 2 and PGE 2 inhibit gastric acid secretion and have vasodilator effects on the vessels of the gastric mucosa
Our results demonstrated that stimulation of AT(2) receptors caused a significant vasodilation through local production of BK in resistant arteries of rat mesentery in a flow-dependent manner
Therefore, hyperosmolar vasodilation is not caused by the systemic release of histamine or by the effects of prostaglandins
18K06704/The Ministry of Education, Culture, Sports, Science, and Technology of Japan
, flow-mediated vasodilation) went in parallel with a reduced GFR in two studies on patients with moderate-to-severe renal insufficiency 112, 113 and was also fairly well associated with inflammation in the second of these studies 113, 114
How it works
L-NMMA caused greater inhibition of the bradykinin-induced relaxation in coronary resistance arteries from ET pigs relative to arteries from SED pigs and eliminated the training-induced enhancement Impaired acetylcholine-mediated vasodilation in patients with congestive heart failure
However, there were not significantly affected the vasodilation effects pretreated with cyclooxygenase inhibition by indomethacin (Indo) or β-noradrenergic inhibition by propranolol (Prop)
Mouse brain endothelial cells (MBEC) converted 20-HETE to 20-OH-PGE(2), which was as potent as PGE(2) in dilating the Treatment of K+ channel inhibitor (TEA, 10 mM) or sGC inhibitor (ODQ, 10 μM) or COX-2 inhibitor (indomethacin, 10 μM) did not affect the vanillin-induced vasodilation either
To test the role of prostaglandins as regulators of cerebral vascular function, we examined cerebral vasodilator responses to CO(2) (cerebrovascular reactivity) in young (26 ± 5 yr; 6 males/6 females) and older (65 ± 6 yr, 5 males/5 females) healthy humans before and There were significant differences between shear stress-induced and PGI 2-induced vasodilation in dilatory ratios against high concentrations of indomethacin in B10 (Fig
These results are not compatible with the hypothesis that intrarenal prostaglandins mediate or amplify the renal vasodilator response to BK
Indomethacin alone did not alter However, the vasodilator response of the upstream femoral artery of ≤5 minutes of lower limb occlusion led to an almost entirely NOS-dependent vasodilation of the femoral artery ≤60 sec after cuff release
A study by Akerman, using a rodent TAC model has shown that indomethacin reduces firing in the trigeminal cervical complex elicited by superior salivatory nucleus- and also dural-evoked stimulations
In rat mesenteric arteries, in the presence of L-NAME, ODQ, and indomethacin, ACh-induced vasodilation was significantly attenuated and blocked by respective 0
The analgesic, antipyretic and anti-inflammatory effects of indomethacin as well as adverse reactions associated with the drug occur as a result of decreased prostaglandin synthesis
Indomethacin is FDA-approved to manage acute pain, rheumatoid arthritis, ankylosing spondylitis, osteoarthritis, bursitis
Indomethacin (10 microM; 20 min) significantly increased Ach-induced vasodilation (EC(50) decreased from 8
Inhibition of both eNOS with L-NAME and cyclooxygenase with indomethacin significantly reduced acetylcholine-mediated vasodilation in microvessels obtained from ET subjects before WL
In conclusion, we suggest that indomethacin increases Ach-induced vasodilation causing an increase of reactive oxygen species and in particular of ONOO
Indomethacin is widely used as a tool to study contributions a hole 2 cm in diameter was made in the skull over the parietal of prostanoids to cerebral vascular control
The hydroalcoholic extract of onion peel relaxed vasoconstriction induced by K + /PHE which was not attenuated by endothelial removal, L-NAME (100
Purpose: To evaluate whether prostaglandins are mediators of the hypercapnia-associated vasodilation of the optic nerve head vessels
Further we describe a differentiating effect of indomethacin inhibiting
The effects of indomethacin, a cyclooxygenase inhibitor, on vasodilator responses to bradykinin and nitroglycerin were investigated in the peripheral vascular bed of the anesthetized cat
Stimulated release of vasodilator prostaglandins and nitric oxide by angiotensin II may counteract the vasoconstrictor effects of this octapeptide
By 2 h, small but Also indomethacin (a cyclooxygenase pathway inhibitor of prostaglandin synthesis) did not affect hyperosmolar vasodilation or the fall in systemic vascular resistance
Responses of pial arterioles to topically applied arachidonic acid, conversion of exogenous arachidonic acid to prostanoids, and pial arteriolar dilation to hypercapnia were examined before and at progressive times after treatment with indomethacin (5 mg/kg i
For mesenteric arteries, ACh-mediated vasodilation was significantly blunted with the potassium channel antagonist tetraethylammonium chloride (TEA, 10 mM); whereas responses were only moderately impaired with endothelial disruption or inhibition of prostaglandins (indomethacin, 10 μM)
Inhibition of NO-synthase by NG-nitro-L-arginine methyl ester (L-NAME) and guanylyl cyclase by 1H-[1,2,3] oxadiazolo [4,4-a]quinoxalin-1-one (ODQ) reduces the vasodilator effect Hemodynamic endothelial dysfunction (i
Dose-response curves to heparin and enoxaparin were generated
Indomethacin works by blocking the effects of the enzymes cyclooxygenase (COX)-1 and COX-2
5 On histology, telangiectasia without prominent inflammation can be seen, but there are no pathognomonic findings
Treatment with indomethacin is able to inhibit prostaglandin production, and one case report describes the normalization of both CGRP and VIP levels following administration of indomethacin (09)