Treatment With Lisinopril Normalizes Serum Concentrations of Procollagen Type III Amino-Terminal Peptide in Patients With Essential Hypertension

Abstract

Procollagen type III amino-terminal peptide (PIIIP) is cleaved off procollagen type III during the biosynthesis of type III collagen. Thus, to assess the synthesis of collagen type III in essential hypertension, we determined the serum concentrations of PIIIP in 24 patients with never-treated essential hypertension and in 30 normotensive controls. In addition, serum concentrations of PIIIP were measured in 15 patients after receiving lisinopril during 6 months. Serum PIIIP was higher in hypertensives than controls (11.20 +/- 0.76 v 8.47 +/- 0.77 ng/mL, mean +/- SEM, P < .01). A direct correlation was found between serum PIIIP and plasma renin activity (r = 0.54, P < .01) in the group of hypertensives. In addition, serum PIIIP was correlated inversely with maximal early transmitral flow velocity measured during diastole by Doppler echocardiography (r = -0.74, P < .001) in the group of hypertensive patients. The serum PIIIP levels decreased significantly in patients treated with lisinopril (11.76 +/- 0.84 v 8.47 +/- 0.66 ng/mL, P < .01). A significant increase of plasma renin activity and a significant decrease of plasma aldosterone was observed in these patients after treatment with lisinopril. These results suggest that increased collagen type III synthesis is present in patients with essential hypertension. Abnormal synthesis of collagen type III in essential hypertension may be related to the activity of circulating renin-angiotensin-aldosterone system. Whether an excessive synthesis of myocardial collagen type III is responsible for increased serum PIIIP present in essential hypertension deserves further investigation.