Nonsteroidal Anti-Inflammatory Drugs and Antihypertensives

Sahloul, Mhd Zaher; al-Kiek, Radwan; Ivanovich, Peter; Mujais, Salim

doi:10.1159/000186173

Cited by 25 publications

(6 citation statements)

References 33 publications

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“…Several potential mechanisms of the effects of ns-NSAIDs on renal pathophysiology have been proposed. These mechanisms include: (1) inhibition of COX, which reduces systemic and renal PG synthesis (Meade et al 1993;Wen 1997); (2) inhibition of PGs by NSAIDs counteracting the hypotensive effects of ACE-I, which blocks ACE and successively increases bradykinin levels, allowing increased renal release of vasodilatory and natriuretic PGs (Blumberg et al 1977;Linz et al 1995); (3) alterations in systemic vascular resistance and cardiac output (de Leeuw 1996); and (4) alterations in the renin-angiotensin-aldosterone system (Houston 1991;Lopez-Ovejero et al 1978;Sahloul et al 1990;Wen 1997). It should be noted that aldosterone can promote endothelial dysfunction independent of blood pressure through COX-2-derived PGI 2 vasoconstriction in both normotensive and hypertensive conditions in rats (Blanco-Rivero et al 2005).…”

Section: Pathophysiologic Role Of Cyclooxygenases In the Kidneymentioning

confidence: 99%

Pathophysiology of Cyclooxygenase Inhibition in Animal Models

Radi

2009

Toxicol Pathol

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Cyclooxygenase (COX) catalyzes the conversion of arachidonic acid into prostaglandins (PGs), which play a significant role in health and disease in the gastrointestinal tract (GI) and in the renal, skeletal, and ocular systems. COX-1 is constitutively expressed and found in most normal tissues, whereas COX-2 can be expressed at low levels in normal tissues and is highly induced by pro-inflammatory mediators. Inhibitors of COX activity include: (1) conventional nonselective, nonsteroidal anti-inflammatory drugs (ns-NSAIDs) and (2) COX-2 selective nonsteroidal antiinflammatory drugs (COX-2 s-NSAIDs). Inhibition of COX-1 often elicits GI toxicity in animals and humans. Therefore, COX-2 s-NSAIDs were developed to provide a selective COX-2 agent, while minimizing the attendant COX-1-mediated GI toxicities. Rats and dogs overpredict COX inhibition for renal effects such as renal handling of electrolytes in humans. COX inhibitors are shown to have both beneficial and detrimental effects, such as on healing of ligament or tendon tears, on the skeletal system in animal models. Certain ophthalmic conditions such as glaucoma and keratitis are associated with increased COX-2 expression, suggesting a potential role in their pathophysiology.

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Section: Pathophysiologic Role Of Cyclooxygenases In the Kidneymentioning

confidence: 99%

Pathophysiology of Cyclooxygenase Inhibition in Animal Models

Radi

2009

Toxicol Pathol

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“…Paracetamol must be considered as a safe alternative to NSAIDs for the relief of mildto-moderate pain in elderly patients, in patients with kidney disease (144), hypertension (56,93,104,110,166,184,185,225), congestive heart failure (81,85,98,139,157). In such patients, NSAIDs, for their mechanism of action, may worsen the renal and cardiovascular function, besides causing gastrointestinal damage (23,85,227,228,229).…”

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confidence: 99%

Paracetamol: New Vistas of an Old Drug

et al. 2006

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Paracetamol (acetaminophen) is one of the most popular and widely used drugs for the treatment of pain and fever. It occupies a unique position among analgesic drugs. Unlike NSAIDs it is almost unanimously considered to have no antiinflammatory activity and does not produce gastrointestinal damage or untoward cardiorenal effects. Unlike opiates it is almost ineffective in intense pain and has no depressant effect on respiration. Although paracetamol has been used clinically for more than a century, its mode of action has been a mystery until about one year ago, when two independent groups (Zygmunt and colleagues and Bertolini and colleagues) produced experimental data unequivocally demonstrating that the analgesic effect of paracetamol is due to the indirect activation of cannabinoid CB 1 receptors. In brain and spinal cord, paracetamol, following deacetylation to its primary amine (p-aminophenol), is conjugated with arachidonic acid to form N-arachidonoylphenolamine, a compound already known (AM404) as an endogenous cannabinoid. The involved enzyme is fatty acid amide hydrolase. N-arachidonoylphenolamine is an agonist at TRPV1 receptors and an inhibitor of cellular anandamide uptake, which leads to increased levels of endogenous cannabinoids; moreover, it inhibits cyclooxygenases in the brain, albeit at concentrations that are probably not attainable with analgesic doses of paracetamol. CB 1 receptor antagonist, at a dose level that completely prevents the analgesic activity of a selective CB 1 receptor agonist, completely prevents the analgesic ac- 250CNS Drug Reviews Vol. 12, No. 3-4, pp. 250-275 © 2006 tivity of paracetamol. Thus, paracetamol acts as a pro-drug, the active one being a cannabinoid. These findings finally explain the mechanism of action of paracetamol and the peculiarity of its effects, including the behavioral ones. Curiously, just when the first CB 1 agonists are being introduced for pain treatment, it comes out that an indirect cannabinomimetic had been extensively used (and sometimes overused) for more than a century.

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“…Наиболее часто применяемыми группами препаратов для лечения АГ, по данным проведенного нами анализа, являются ингибиторы ангиотензинпревращающего фермента (иАПФ) и бета-адреноблокаторы (БАБ) -71,1% и 40% пациентов, соответственно. Антагонисты кальция на амбулаторном этапе получали только 18,2% больных РА, в то время как они не теряют эффективность (по имеющимся данным) при сочетании с НПВП в отличие от БАБ и иАПФ [11][12][13][14]. По данным литературы, препараты из группы блокаторов ан-…”

Section: результаты и обсуждениеunclassified

Arterial Hypertension in Patients With Rheumatoid Arthritis

Никитина

Ребров

2009

Racionalʹnaâ farmakoterapiâ v kardiologii

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Цель. Изучить частоту встречаемости и особенности артериальной гипертонии (АГ) у больных ревматоидным артритом (РА). Материал и методы. В исследование включены 584 пациента, находившиеся на лечении в ревматологическом отделении Саратовской областной клинической больницы. Результаты. АГ выявлена у 58,6% больных РА, что существенно выше распространенности АГ в популяции. Отмечено нарастание числа случаев АГ с увеличением продолжительности РА и при высокой активности заболевания. Заключение. Высокая частота встречаемости АГ у больных РА, быстрый рост заболеваемости АГ в первые годы развития РА требуют контроля уровня артериального давления у больных РА для наиболее ранней диагностики и своевременного лечения АГ. В связи с частым и регулярным применением нестероидных противовоспалительных препаратов предпочтение следует отдавать антагонистам кальция и блокаторам ангиотензиновых рецепторов II типа, что в реальной клинической практике не всегда выполняется.

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Nonsteroidal Anti-Inflammatory Drugs and Antihypertensives

Cited by 25 publications

References 33 publications

Pathophysiology of Cyclooxygenase Inhibition in Animal Models

Pathophysiology of Cyclooxygenase Inhibition in Animal Models

Paracetamol: New Vistas of an Old Drug

Arterial Hypertension in Patients With Rheumatoid Arthritis

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