Interaction between Angiotensin II and Mechanical Strain on Matrix Synthesis by Human Vascular Smooth Muscle Cells

Abstract

Infducfion: Multi-unit m i -'c d i e s quantifying muscle sympatWc nave activity (MSNA) in essdal aad 'bordsfine' hypatension havebeon inconSiracd Fathe first time smgle vamamhictor lmits (S-MSNA) wac studied in subject groups with a range of severity of essential hypertension compared to normotension. MelhodF: Seveaty four matched CaucaSiaa subjects (FM, 38:36; 22-75 years) fire from therapy, were grouped Bccording to their resting blood pnssurcs (BP) using the JNC-VI (1997) classification, into twHmd (NT), high n o d 0, Stage 1 (Em-I) and Stage 2 or 3 hypatcasion (EHT-2B). Continuous heart rate (HR), respiration, BP and synpalhdc activity were rccordtd in the resting state. N e d activity was quantified pcr 100 cardiac beats to allow for d i h c e s in HR.Results: Using ANOVA, d t s from the two methods of sympathdc assessment in the four groups of subjects are illustratcd below, s-MSNA (Fig. 1) and MSNA (Fig.2). wl EWT-M

Mechanical strain-induced human vascular matrix synthesis: The role of angiotensin II

“…In human VSM cells, both Angiotensin II (Ang II) and strain independently increase matrix synthesis. [8][9][10][11][12] Presently it is unclear whether mechanical strain and Ang II act synergistically to accelerate matrix synthesis by VSM cells. [13][14][15][16][17][18][19][20] Of particular importance, there have been no studies to date reporting the interaction between Ang II and mechanical strain in human VSM cells.…”