Hyper-responsiveness to angiotensin II is related to cardiac structural adaptation in hypertensive subjects

Background Angiotensin II has been found to be a growth stimulating factor for myocardial cells. In humans, angiotensin II infusion causes vasoconstri ction in systemic and renal vasculature and leads to aldosterone secretion. Our hypothesis was that hyper-responsiveness to angiotensin II is related to left ventricular mass in human essential hypertension. Methods and results In 30 normotensive individuals and 30 subjects with mil d essential hypertension (white men, mean age 26 +/- 3 years), the responsi veness to angiotensin II was assessed by measuring changes in mean arterial pressure, renal blood flow, glomerular filtration rate and aldosterone sec retion in response to i.v. angiotensin II infusion (0.5 and 3.0 ng/kg per m in). The provoked changes to angiotensin II infusion were similar in the no rmotensive and hypertensive group with the exception of an exaggerated incr ease in mean arterial pressure in hypertensives (14 +/- 5 versus 10 +/- 5 m mHg, P < 0.001 at 3.0 ng/kg per min angiotensin II). The increase in mean a rterial pressure was correlated with left ventricular mass in hypertensive subjects (angiotensin II 0.5 ng/kg per min: r = 0.49, P < 0.005; angiotensi n II 3.0 ng/kg per min: r = 0.35, P < 0.05); no such correlation was found in the normotensive group. After taking into account baseline mean arterial pressure and body mass index, the increase in mean arterial pressure to an giotensin II 0.5 ng/kg per min was still correlated with left ventricular m ass (partial r = 0.50, P < 0.01). Similarly, the change of glomerular filtr ation rate but not of renal blood flow in response to angiotensin II 0.5 ng /kg per min was correlated with left ventricular mass, (r = 0.42, P < 0.02) in the hypertensive group but not in the normotensive one. This relationsh ip remained significant even after taking baseline glomerular filtration ra te, mean arterial pressure and body mass index into account (partial r = 0. 43, P < 0.05). Conclusion Hyper-responsiveness to angiotensin II is related to an increase d left ventricular mass in hypertensive subjects independent of blood press ure. J Hypertens 1999, 17:825-833 (C) Lippincott Williams & Wilkins.