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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred ten patients of both sexes with mild to moderate essential hypertension were studied in this double-blind, multicenter study. In the double-blind portion of this study, which covered weeks 11 to 14, 71 patients were evaluated to determine the effect of Clinoril (sulindac, MSD), piroxicam, and placebo on the hypotensive effect of propranolol. All 110 patients were considered for safety evaluation. Patients treated with propranolol alone were distributed randomly into three groups (Clinoril, piroxicam and placebo) and compared in a 15-week study with four periods (I through IV). Having fulfilled the criteria for hypertension (I) and having been successfully controlled with propranolol alone (II), patients were entered into a double-blind period (III) comparing the three drug treatments during four weeks followed by one week of propranolol alone (IV). During period III, patients treated with piroxicam had significantly greater (p less than 0.05) increases in supine and standing diastolic blood pressure than patients treated with Clinoril. No clinical difference was shown between patients treated with Clinoril and placebo. At the end of period IV patients treated with piroxicam maintained the increase in their diastolic blood pressure, in contrast to Clinoril and placebo where no clinical difference was noted. Significantly more patients treated with piroxicam than Clinoril had a 10 mmHg or greater increase of their supine diastolic blood pressure. These results show that Clinoril does not blunt the antihypertensive effect of propranolol in patients with mild to moderate hypertension in contrast to piroxicam. This is an extension of a report previously published in Advances in Therapy, Vol. 2, No. 4, July/August 1985.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of Clinoril (sulindac, MSD), piroxicam and placebo on the hypotensive effect of propranolol in patients with mild to moderate essential hypertension. 354 Nov 68

Prostaglandins are ubiquitous biologically active compounds that are involved in inflammatory reactions, hemostasis, and, under certain circumstances, the maintenance of renal function. NSAIDs, which inhibit PG synthesis, are used therapeutically most often as antiinflammatory agents in conditions of inflammation and pain, mostly of a nonurologic nature. However, since NSAIDs inhibit systemic PG synthesis, administration of NSAIDs can lead to adverse side effects. For example, the gastrointestinal irritation caused by NSAIDs probably reflects removal of a cytoprotective effect of gastrointestinal PGs. Similarly, the kidney may be especially susceptible to adverse effects of NSAIDs. In diseases such as peptic ulcers, diabetes, hypertension, congestive heart failure, liver disease with ascites, and renal insufficiency, PGs seem to play a protective role in the kidney. This protective role, which results from increased synthesis of vasodilator PGs in the face of elevated vasoconstrictors, is diminished in the presence of NSAIDs. Other side effects include the antagonism by NSAIDs of the action of diuretics, such that the dose of the diuretic must be adjusted accordingly. The diuretic triamterene should not be used in conjunction with indomethacin due to several reported cases of toxicity. Another drug interaction involves the salicylates, which have been shown to diminish the uricosuric effects of probenecid and sulfinpyrazone. Likewise, since corticosteroids increase the renal clearance of salicylates, it is important to monitor the patient carefully following termination of steroid treatment in patients receiving large doses of salicylates, since this change in elimination can precipitate toxicity. In addition, the NSAIDs bind to plasma proteins and, as such, can displace or be displaced by other drugs that bind in the same manner and can result in either decreased efficacy or toxicity. Despite the fact that the kidney may not be the target of NSAID therapy, renal function may be adversely affected by NSAID treatment. It has therefore been proposed that a renal-sparing NSAID would be a very useful therapeutic agent. Sulindac (Clinoril) has been suggested to be such an agent, eg, able to inhibit systemic PG synthesis (usually monitored by measuring serum thromboxane synthesis) without an apparent effect on renal PG synthesis (monitored by measurement of urinary PGs). However, recent data have suggested that Sulindac does inhibit renal PG synthesis and does not exhibit selectivity. The reasons for the discrepancy are not clear, but may relate to the doses or time intervals examined.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Indications and contraindications for the use of nonsteroidal antiinflammatory drugs in urology. 393 61