The effect of captopril treatment on platelet angiotensin II levels was evaluated in 12 patients with essential hypertension. Captopril significantly lowered (p <0.01) mean arterial blood pressure in seven patients (Group 1) and was ineffective in five (Group 2). In Group 1, a marked decrease in plasma angiotensin II levels in both the supine (from 5.5 ± 0.5 to 2.8 ± 0.9 pg/ml) and the upright positions (from 17.5 ± 4.7 to 3.9 ± 1.6 pg/ml; p <0.0025) and a significant increase in platelet angiotensin II levels (from 10.5 ± 5.3 to 22.4 ± 17 pg/ml; p <0.05) after captopril treatment was observed. In Group 2, no variation was found in plasma angiotensin II levels, whereas platelet angiotensin II levels increased slightly (from 10.8 ± 3.1 pg/ml to 16.9 ± 5.2 pg/ml; NS). These findings suggest that the decrease in plasma angiotensin II levels can lead to an increase in platelet angiotensin II receptors or can lead to angiotensin II production in platelets through activation of a feedback mechanism. The second hypothesis suggest that platelets have alternative enzymatic pathways leading to angiotensin II production not inhibited by captopril. © 1988.

Effect of angiotensin converting enzyme inhibition on platelet angiotensin II content

Ferri C.;
1988-01-01

Abstract

The effect of captopril treatment on platelet angiotensin II levels was evaluated in 12 patients with essential hypertension. Captopril significantly lowered (p <0.01) mean arterial blood pressure in seven patients (Group 1) and was ineffective in five (Group 2). In Group 1, a marked decrease in plasma angiotensin II levels in both the supine (from 5.5 ± 0.5 to 2.8 ± 0.9 pg/ml) and the upright positions (from 17.5 ± 4.7 to 3.9 ± 1.6 pg/ml; p <0.0025) and a significant increase in platelet angiotensin II levels (from 10.5 ± 5.3 to 22.4 ± 17 pg/ml; p <0.05) after captopril treatment was observed. In Group 2, no variation was found in plasma angiotensin II levels, whereas platelet angiotensin II levels increased slightly (from 10.8 ± 3.1 pg/ml to 16.9 ± 5.2 pg/ml; NS). These findings suggest that the decrease in plasma angiotensin II levels can lead to an increase in platelet angiotensin II receptors or can lead to angiotensin II production in platelets through activation of a feedback mechanism. The second hypothesis suggest that platelets have alternative enzymatic pathways leading to angiotensin II production not inhibited by captopril. © 1988.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11697/214434
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