Stimulatory effect of enprostil, an anti-ulcer prostaglandin, on gastric mucus secretion

Waterbury, L. David; Mahoney, Janette M.; Peak, Tina M.; Cohn, Ronald G.; Garay, Gabriel L.

doi:10.1016/s0002-9343(86)80007-9

Cited by 9 publications

(1 citation statement)

References 14 publications

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“…Protaglandins inhibit the secretion of gastric acid, stimulate the secretion of mucus and bicarbonate and provide cytoprotection for the gastric mucosa (Robert et al 1979;Deakin et al 1986;Highland and Upson 1986;Russell 1986;Thomas et al 1986;Waterbury et al 1986;Monk and Clissold 1987;Seidler et al 1989). In 5 fasting, normal mature horses, oral administration of a single dose (5 pgkg bwt) of misoprostol, a synthetic methyl ester analogue of PGE, resulted in a maximum mean gastric pH 5 at 4 h and remained above basal for the 8 h test period (Sangiah et al 1989).…”

Section: Synthetic Prostaglandinmentioning

confidence: 99%

A review of medical treatment for peptic ulcer disease

MacAllister

1999

Equine Veterinary Journal

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Section: Synthetic Prostaglandinmentioning

confidence: 99%

A review of medical treatment for peptic ulcer disease

MacAllister

1999

Equine Veterinary Journal

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Angiotensin-Converting Enzyme Inhibition and Renal Protection

Hollenberg

Raij²

1993

Arch Intern Med

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The role of hypertension in the pathogenesis of renal damage is a subject of both historical interest and current investigation. Because of the difficulty associated with studying the pathophysiologic role of glomerular injury in systemic hypertension, experimental models have provided much of the data in this field. The mechanisms leading to glomerular injury are complex and not fully elucidated. Mesangial and endothelial cell injury are thought to be important pathophysiologic mechanisms in the renal injury associated with hypertension. One hypothesis suggests that glomerular hypertension (ie, a hemodynamic event) is the primary pathogenetic mechanism, but another supports the notion that glomerular hypertrophy (ie, abnormal growth-related events) contributes to injury. The intrarenal renin-angiotensin system may play an important pathogenetic role in end-stage renal disease. Angiotensin-converting enzyme (ACE) inhibition has been shown to arrest the progression of renal injury in animal models. Although the clinical database is incomplete, the findings of anecdotal reports and short-term studies suggest that ACE inhibition may preserve renal function in patients with scleroderma renal crisis, reduce proteinuria in patients with diabetic nephropathy, and normalize renal hemodynamics in patients with a variety of renal diseases. The beneficial effects of ACE inhibition may be due to both hemodynamic (eg, reduction in glomerular capillary and intraglomerular pressures) and nonhemodynamic (eg, potassium-sparing and reduction in mesangial proliferation) mechanisms. The precise role of ACE inhibitors in the prevention of renal damage awaits the results of ongoing long-term, double-blind clinical studies. Nevertheless, ACE inhibition may be an appropriate therapeutic alternative in the hypertensive patient whose renal injury is progressing despite aggressive antihypertensive therapy.

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