Lack of angiotensin I accumulation after converting enzyme blockade by enalapril or lisinopril in man. Antihypertensive and hormonal effects of lisinopril, a new angiotensin converting enzyme (ACE) inhibitor in patients with renovascular hypertension. Rx drugs

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The results of recent studies have demonstrated that angiotensin (Ang)-(1-7) contributes to the antihypertensive actions of either combined ACE/Ang II type 1 receptor blockade or ACE inhibition alone. The vasculature is a key site of action for either drug regimen, and evidence favors a local Ang system within these tissues. Because ACE may degrade Ang-(1-7), we determined whether ACE inhibition alters Ang-(1-7) release from the rat hindlimb perfused with Krebs-Ringer buffer containing Ficoll. Ang-(1-7) release averaged 36+/-13 fmol (period 1, 15-minute collection) and 44+/-11 fmol (period 2) in the control buffer. The addition of the ACE inhibitor lisinopril to the perfusion buffer augmented levels of Ang-(1-7) in periods 3 (144+/-39 fmol) and 4 (163+/-35 fmol; P<0.05 versus 1 or 2, n=8). HPLC and radioimmunoassay of effluent from control or lisinopril treatment demonstrated a single immunoreactive peak with a retention time identical to that of Ang-(1-7). The addition of the neprilysin inhibitor SCH 39370 reduced Ang-(1-7) release in the lisinopril buffer from 177+/-32 (period 1) and 173+/-39 (period 2) fmol to 112+/-24 (period 3) and 87+/-23 fmol (period 4; P<0.05 versus 1 or 2, n=6). Ang I metabolism in the collected perfusate revealed the formation of Ang-(1-7) that was sensitive only to thimet oligopeptidase inhibition; Ang II generation was not detected. The present study demonstrates the recovery of endogenous Ang-(1-7) from the perfused hindlimb. The release of Ang-(1-7) is significantly influenced by inhibition of ACE, which may reflect both increased substrate (Ang I) levels and reduced metabolism of the peptide. Neprilysin inhibition reduced but did not abolish Ang-(1-7) release, which suggests that other endopeptidases may contribute to the release of the peptide.

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Clin Sci (Lond). 1987 Mar;72(3):387-9.
Lack of angiotensin I accumulation after converting enzyme blockade by enalapril or lisinopril in man.

Nussberger J, Brunner DB, Waeber B, Biollaz J, Brunner HR.

In nine normal volunteers, a series of five venous blood samples was obtained before and up to 24 h after converting enzyme inhibition by a single oral dose of enalapril or lisinopril. Plasma renin activity and blood angiotensin I were measured. A close linear relationship was found between the increase in plasma renin activity and the increase in blood angiotensin I. The linear correlation between plasma renin activity and blood angiotensin I remained after converting enzyme inhibition. Thus, the rise in angiotensin I after inhibition of the conversion of angiotensin I to angiotensin II is due to an enhanced release of renin rather than to accumulation of angiotensin I.

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Acta Med Scand Suppl. 1986;714:33-42.
Antihypertensive and hormonal effects of lisinopril, a new angiotensin converting enzyme (ACE) inhibitor in patients with renovascular hypertension.

Karlberg BE, Rosenqvist U.

The antihypertensive and hormonal effects of a new ACE-inhibitor, lisinopril (MK-521), was studied in 11 patients with renal arterial stenosis (bilateral in 1). Oral doses exceeding 5 mg a day significantly reduced blood pressure (BP), the maximum fall occurring 6 h after taking the drug. At higher doses (20-80 mg/day) sustained antihypertensive effects persisted for 24 h. Lisinopril was equally effective in lowering supine and standing BP. When the drug was given stepwise in increasing doses, (5, 10, 20, 40, and in 5 cases 80 mg/day) the BP was successively normalized in 10 of 11 patients (supine BP less than 90 mmHg). 3 patients with low renin hypertension (LRH) responded less well to monotherapy on long-term treatment with lisinopril than the others. A significant increase in heart rate was observed, initially and after 1 month of treatment. After 5 days treatment with increasing doses the plasma concentrations of angiotensin II (AII) and aldosterone (Aldo) fell significantly to very low concentrations. However, on long term treatment (3 months) suppression of AII and Aldo did not always take place. A concomitant decrease in 24 h urinary aldosterone excretion occurred. No changes in renal function or other biochemical tests except for a slight increase in S-K were observed. There were no adverse side-effects. We conclude that lisinopril is an effective and safe medication for renovascular hypertension.

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