Effect of indomethacin on the pharmacokinetics and pharmacodynamics of felodipine.

Hardy, BG; Bartle, W. R.; Myers, Mary Lee; Bailey, DG; Edgar, Boo

doi:10.1111/j.1365-2125.1988.tb05295.x

Cited by 20 publications

(11 citation statements)

References 17 publications

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“…However, in contrast to what was observed with other classes of antihypertensive drugs, the effects of calcium antagonists [24][25][26] and of pinacidil [27] seem to be unaf fected by NSAIDs.…”

Section: N S a Id S And Antihypertensive D Ru G Smentioning

confidence: 68%

Interaction of Antihypertensive Drugs with Anti-Inflammatory Drugs

Polónia¹

1997

Cardiology

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Nonsteroidal anti-inflammatory drugs (NSAIDs) can induce an increase in blood pressure (BP) and may potentially reduce the efficacy of several antihypertensive drugs. Probably the main mechanism of action is inhibition of prostaglandin (PG) synthesis since NSAIDs have higher propensity to increase BP as the regulation of BP (and renal function) is more PG-dependent and to interact with drugs (diuretics, β-blockers and ACE inhibitors) that may act through the increase of PG formation. In contrast, NSAIDs do not interact with calcium antagonists and central acting drugs which actions are apparently unrelated with renal/extrarenal production of PG. It has been claimed that inhibition of natriuretic PGs could explain the pressure effects of NSAIDs in treated hypertensive patients, but sodium retention may be not the single explanation for such an interaction. We found that despite indomethacin produced sodium retention after being added either to enalapril or nifedipine-GITS, it only attenuated (by 45%) the antihypertensive effects of enalapril. In alternative, since PG enhances vasodilatation and attenuates vasoconstrictor influences, some NSAIDs may counteract the PG-dependent vasodilatory tone in renal and extrarenal vascular beds that mediate the antihypertensive action of some drugs. Thus, since calcium antagonists are probably not affected by NSAIDs, they may be preferable to drugs like diuretics, β-blockers and ACE inhibitors for the treatment of high blood pressure control in hypertensive patients who are clinically suitable for NSAIDs therapy.

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Section: N S a Id S And Antihypertensive D Ru G Smentioning

confidence: 68%

Interaction of Antihypertensive Drugs with Anti-Inflammatory Drugs

Polónia¹

1997

Cardiology

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“…However, indometha cin did not always reduce resting diameters in this partic ular preparation [29], Nevertheless, some results suggest that prostaglandins can contribute directly or indirectly to the control of basal vascular tone in vivo. Inhibition of prostaglandin synthesis resulted in an elevation of blood pressure in awake dogs [30] and in healthy humans [31],…”

Section: Discussionmentioning

confidence: 99%

Mediator Role of Prostaglandins in Acetylcholine-lnduced Vasodilation and Control of Resting Vascular Diameter in the Hamster Cremaster Microcirculation in vivo

Wit

Bismarck

Pohl³

1993

J Vasc Res

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Acetylcholine (ACh) is widely used as a standard test substance for nitric oxide (NO)-mediated vasodilation. However, it also augments the release of prostaglandins, a group of other endothelium-derived smooth muscle relaxants. Using intravital microscopy in the cremaster muscle of anesthetized hamsters, we studied the relative roles of NO and prostaglandins in mediating ACh-induced dilation and in the control of basal vessel tone (253 arterioles in 31 experiments). N^ω-nitro-L-arginine (L·NNA), a competitive inhibitor of NO synthase, significantly reduced ACh-induced vasodilation (by 42-73%), irrespective of whether it was applied intravenously (30 mg/kg) or topically (30 µM). Additional indomethacin (3 µM, topical) nearly abolished the dilator response. In contrast, the vascular responses to the endothelium-independent dilator sodium nitroprusside were not affected. The resting diameters (range: 6–114 µm) were significantly (p < 0.05) reduced after L·NNA or indomethacin by 10.2 and 16.6% of control diameter, respectively. The constriction induced by L·NNA was stronger in larger (>50 µm) than in smaller (<50 µm) vessels, whereas indomethacin was equipotent in both groups. Thus, in addition to NO, dilating prostaglandins are important mediators of the ACh-induced dilation and contribute to the control of resting arteriolar diameter in the hamster cremaster microcirculation in vivo.

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“…However, using either of the definitions employed for this study NSAID usage significantly and independently predicted the presence of hypertension. Such a finding is supported by several randomized studies in younger subjects demonstrating an elevation of blood pressure with NSAID therapy (Chalmers et al, 1984;Gerber et al, 1990;Hardy et al, 1988;Wong et al, 1986). Since hypertension is a major risk factor for stroke and coronary heart disease amongst the elderly (Amery et al, 1981;Kannel et al, 1976), even a relatively small increase in the prevalence of hypertension with concomitant NSAID therapy is potentially important in social and economic terms, particularly in a community where the prevalence of usage of these drugs is very high.…”

Section: Discussionmentioning

confidence: 88%

Non‐steroidal anti‐inflammatory drugs and hypertension in the elderly: a community‐based cross‐sectional study.

Simons

et al. 1993

Brit J Clinical Pharma

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1 Whether non-steroidal anti-inflammatory drug (NSAID) usage in the elderly elevates blood pressure or antagonises the blood pressure-lowering effect of antihypertensive medication is presently unknown. The primary aims of this study were to estimate the prevalence of NSAID usage, to evaluate the prescription of NSAIDs for arthritis and to determine whether NSAID usage was an independent predictor of hypertension in a large elderly community. 2 All non-institutionalised elderly (> 60 years) residents of Dubbo, NSW who attended for a baseline assessment were enrolled (1237 males, 1568 females). A questionnaire was administered and blood pressure was measured according to the Prineas protocol. The frequency of NSAID usage was determined, with stratification by age, sex, blood pressure group and history of arthritis. 3 NSAID usage was 26% overall (females 28%, males 23%), increased with age and was higher in females than males for every age group studied. Amongst patients with a past history of 'arthritis', 45% were using NSAIDs. Twelve percent were taking NSAIDs and antihypertensive medication concurrently, constituting the population at risk of an adverse drug-drug interaction. Employing a multiple logistic regression model which adjusted for several confounders in the cross-sectional analysis, NSAID usage significantly predicted the presence of hypertension (odds ratio: 1.4, 95% confidence interval: 1.1-1.7) with an attributable risk of 29%. 4 Amongst non-institutionalised elderly persons, NSAID usage may be an independent risk factor for hypertension. Considering the substantial consumption of NSAIDs by elderly patients, physicians should review their NSAID prescribing patterns for this community group.

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Effect of indomethacin on the pharmacokinetics and pharmacodynamics of felodipine.

Cited by 20 publications

References 17 publications

Interaction of Antihypertensive Drugs with Anti-Inflammatory Drugs

Interaction of Antihypertensive Drugs with Anti-Inflammatory Drugs

Mediator Role of Prostaglandins in Acetylcholine-lnduced Vasodilation and Control of Resting Vascular Diameter in the Hamster Cremaster Microcirculation in vivo

Non‐steroidal anti‐inflammatory drugs and hypertension in the elderly: a community‐based cross‐sectional study.

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