ABSTRACT
Recent studies have demonstrated the presence of angiotensin II (Ang II) in human platelets. The aim of the present study was to determine whether in vitro platelet aggregation induces Ang II release. We studied 20 healthy volunteers, and found that some aggregant stimuli can cause the platelet to release this peptide. Release of Ang II was greater with thrombin (40.7%) than with ADP (29%), while N-ethylmaleimide was almost ineffective. The release of Ang II following in vitro aggregant stimuli suggests that this may be one of the mechanisms through which platelets can locally modulate vascular tone and perhaps promote atherogenesis.
Subject(s)
Angiotensin II/metabolism , Blood Platelets/metabolism , Platelet Aggregation , Adenosine Diphosphate , Adult , Blood Platelets/drug effects , Endothelium, Vascular/drug effects , Ethylmaleimide , Humans , In Vitro Techniques , Platelet Aggregation/drug effects , ThrombinABSTRACT
We evaluated the effect of nicardipine treatment on platelet angiotensin II content in 18 essential hypertensive patients. Nicardipine induced a decrease in platelet angiotensin II content in all patients (-14%), but particularly in 10 (P less than 0.05; -20.5%). No other differences were found between these patients and the others. Further investigations are required to determine whether platelet angiotensin II content reduction contributes to the prophylactic and therapeutic effects of calcium antagonists on atherosclerosis.
Subject(s)
Angiotensin II/analysis , Blood Platelets/analysis , Hypertension/blood , Nicardipine/pharmacology , Aged , Clinical Trials as Topic , Female , Humans , Male , Middle Aged , Time FactorsSubject(s)
Angiotensin II/analysis , Blood Platelets/chemistry , Hypertension/blood , Adult , Angiotensin II/blood , Humans , Middle AgedABSTRACT
The effect of captopril treatment on platelet angiotensin II levels was evaluated in 12 patients with essential hypertension. Captopril significantly lowered (p less than 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 less than 0.0025) and a significant increase in platelet angiotensin II levels (from 10.5 +/- 5.3 to 22.4 +/- 17 pg/ml; p less than 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 suggests that platelets have alternative enzymatic pathways leading to angiotensin II production not inhibited by captopril.
