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

J Hypertens. 1999 Jun;17(6):825-33. doi: 10.1097/00004872-199917060-00015.

Abstract

Background: Angiotensin II has been found to be a growth stimulating factor for myocardial cells. In humans, angiotensin II infusion causes vasoconstriction 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 mild essential hypertension (white men, mean age 26+/-3 years), the responsiveness to angiotensin II was assessed by measuring changes in mean arterial pressure, renal blood flow, glomerular filtration rate and aldosterone secretion in response to i.v. angiotensin II infusion (0.5 and 3.0 ng/kg per min). The provoked changes to angiotensin II infusion were similar in the normotensive and hypertensive group with the exception of an exaggerated increase in mean arterial pressure in hypertensives (14+/-5 versus 10+/-5 mm Hg, P<0.001 at 3.0 ng/kg per min angiotensin II). The increase in mean arterial pressure was correlated with left ventricular mass in hypertensive subjects (angiotensin II 0.5 ng/kg per min: r = 0.49, P<0.005; angiotensin 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 angiotensin II 0.5 ng/kg per min was still correlated with left ventricular mass (partial r = 0.50, P<0.01). Similarly, the change of glomerular filtration 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 relationship remained significant even after taking baseline glomerular filtration rate, 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 increased left ventricular mass in hypertensive subjects independent of blood pressure.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aldosterone / blood
  • Angiotensin II / administration & dosage*
  • Angiotensin II / pharmacokinetics
  • Blood Pressure / drug effects
  • Blood Pressure Monitoring, Ambulatory
  • Drug Hypersensitivity / blood
  • Drug Hypersensitivity / diagnostic imaging
  • Drug Hypersensitivity / physiopathology*
  • Echocardiography
  • Follow-Up Studies
  • Glomerular Filtration Rate / drug effects
  • Heart Ventricles / diagnostic imaging
  • Heart Ventricles / drug effects*
  • Heart Ventricles / physiopathology
  • Humans
  • Hypertension / blood
  • Hypertension / physiopathology*
  • Injections, Intravenous
  • Male
  • Predictive Value of Tests
  • Radioimmunoassay
  • Renal Circulation / drug effects
  • Vasoconstrictor Agents / administration & dosage*
  • Vasoconstrictor Agents / pharmacokinetics

Substances

  • Vasoconstrictor Agents
  • Angiotensin II
  • Aldosterone