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Clin Sci (Lond). 1991 Oct;81(4):491-7.
Effect of angiotensin-converting enzyme inhibitors on glomerular eicosanoid production in normotensive and spontaneously hypertensive rats.

Harding P, Stonier C, Aber GM.

Renal Research Laboratories, School of Postgraduate Medicine and Biological Sciences, University of Keele, Staffordshire, U.K.

1. This study was designed to examine the production of certain eicosanoids (prostaglandin E2), prostacyclin (as 6-keto-prostaglandin F1 alpha) and thromboxane A2 (as thromboxane B2) by glomeruli isolated from normotensive Wistar-Kyoto and spontaneously hypertensive rats both before and after the administration of one of three angiotensin-converting enzyme inhibitors, captopril, enalapril or fosinopril, for 10 days. 2. Measurements of glomerular eicosanoid production were made under basal conditions and in the presence of excess exogenous arachidonic acid. 3. The production of prostaglandin E2, 6-keto-prostaglandin F1 alpha and thromboxane B2 was greater by glomeruli from untreated spontaneous hypertensive rats (prostaglandin E2 2.24 +/- 0.41, 6-keto-prostaglandin F1 alpha 1.20 +/- 0.13 and thromboxane B2 2.75 +/- 0.43 ng 10 min-1 mg-1 of protein) than by those from Wistar-Kyoto rats (prostaglandin E2 1.41 +/- 0.28, 6-keto-prostaglandin F1 alpha 0.98 +/- 0.11 and thromboxane B2 1.29 +/- 0.24 ng 10 min-1 mg-1 of protein) under basal conditions. However, these differences only achieved statistical significance for thromboxane B2 (P less than 0.01). Similar strain-related differences were noted in the presence of arachidonic acid. 4. The ratio of glomerular (prostaglandin E2 + prostacyclin)/thromboxane A2 production was significantly lower in spontaneously hypertensive rats than in their normotensive counterparts under basal conditions with values of 1.3 +/- 0.18 and 2.2 +/- 0.20, respectively (P less than 0.01). 5. Angiotensin-converting enzyme inhibitors induced significant changes in the glomerular production of some eicosanoids, which differed both between strains and with the nature of the inhibitor.(ABSTRACT TRUNCATED AT 250 WORDS)

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Drugs Exp Clin Res. 1991;17(5):263-9.
The effect of enalapril on nephrotic proteinuria and determination of serum angiotensin-converting enzyme before and after treatment.

Bianchini G, Letizia C, Domenici A, Scavo D.

Division of Nephrology, University of Rome La Sapienza, Italy.

In order to evaluate the effect of an ACE-inhibitor (enalapril) on nephrotic proteinuria in patients with primitive nephropathies, to determine the SACE before and after treatment and to compare the variation of SACE levels with the variations of proteinuria, seventeen patients were studied (5 F, 12 M) aged between 10 and 68 years. All patients were evaluated in basal conditions for creatinine clearance, protidaemia, proteinuria, SACE and serum electrolytes. All but one patient had a renal biopsy. After basal evaluation nine patients received enalapril, 10 mg/die, for two weeks. After one week SACE levels were re-evaluated, while the proteinuria was re-evaluated several times during the two weeks of treatment. The results obtained suggest (1) SACE levels are significantly higher in patients with nephrotic syndrome than in normal patients (21.14 +/- 8.37 nmol/ml/min; N.V.:15.60 +/- 4.73; M +/- s.d.; p less than 0.01); (2) proteinuria is unresponsive to the ACE-inhibitor action (varied from 8.00 +/- 2.70 g/24 h to 7.74 +/- 3.19 g/24 h, p = NS); (3) no correlation exists between the reduction of SACE levels and variations of proteinuria.

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Am J Physiol. 1997 Sep;273(3 Pt 2):R942-6.
ANG II prolongs splanchnic nerve-mediated inhibition of duodenal mucosal alkaline secretion in the rat.

Johansson B, Holm M, Chen L, Pettersson A, Jonson C, Fandriks L.

Department of Physiology, Goteborg University, Sweden.

Hypovolemia inhibits duodenal mucosal alkaline (HCO-3) secretion by activation of sympathoadrenergic nerves. A possible involvement of the renin-angiotensin system was investigated. Experiments were performed on chloralose-anesthetized rats. The mucosal alkaline output by a duodenal segment was measured using in situ pH-stat titration equipment. A modest hypovolemia was induced by bleeding the animals approximately 10% of the total blood volume. This procedure decreased duodenal mucosal alkaline secretion to a sustained level of approximately 50% of baseline and reduced mean arterial pressure by approximately 20 mmHg. Intravenous pretreatment with the angiotensin-converting enzyme (ACE) inhibitor enalaprilate (0.7 mg/kg) or the angiotensin II-receptor antagonist losartan (10 mg/kg) altered the response to hypovolemia to a transient one, and alkaline secretion returned to the control level within 40-50 min. When exogenous angiotensin II was administered intravenously (0.25 and 0.75 microgram.kg-1.h-1), a hypovolemia-induced sustained depression of the secretion was observed even during ACE inhibition. Direct electrical stimulation (3 Hz, 5 V, 5 ms, bilaterally) of the peripheral splanchnic nerves decreased duodenal mucosal alkaline secretion to approximately 60% of the control level and increased mean arterial pressure by approximately 20 mmHg. However, in enalaprilate-pretreated animals, the inhibition of alkaline secretion due to splanchnic nerve stimulation was transient, a response that became sustained on angiotensin II substitution. These results suggest that the renin-angiotensin system prolongs the sympathoadrenergic inhibition of duodenal mucosal alkaline secretion and that angiotensin II, in this regard, acts mainly on the peripheral sympathetic efferents.

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