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[Expression and function of cardiovascular local renin-angiotensin system]
T Kudou1, H Kawaguchi, H Okamoto
1Cardiovascular medicine of Hokkaido University.
Nihon Rinsho. Japanese Journal of Clinical Medicine
|June 1, 1993
Summary
Systemic hypertension causes cardiac hypertrophy by increasing cardiac angiotensinogen messenger RNA (m-RNA) expression. Antihypertensive drugs effectively prevent this hypertrophy and reduce angiotensinogen m-RNA levels.
Area of Science:
- Cardiovascular physiology and pharmacology
- Molecular biology of the renin-angiotensin system
Context:
- The cardiovascular renin-angiotensin system regulates vascular tone, cardiac contractility, and growth.
- Systemic hypertension is known to induce cardiac hypertrophy, but the underlying mechanisms remain unclear.
- Antihypertensive drugs can prevent cardiac hypertrophy, but their specific molecular targets in this context are not fully understood.
Purpose:
- To investigate the role of cardiac angiotensinogen messenger RNA (m-RNA) expression in hypertension-induced left ventricular hypertrophy.
- To determine if antihypertensive drugs modulate cardiac angiotensinogen m-RNA expression in a genetic hypertension model.
Summary:
- In spontaneously hypertensive rats (SHR), left ventricular angiotensinogen m-RNA expression was twofold higher than in normotensive Wistar-Kyoto rats (WKY).
- All tested antihypertensive drugs prevented left ventricular hypertrophy in SHR.
- These drugs also significantly reduced the elevated left ventricular angiotensinogen m-RNA expression in SHR.
Impact:
- Suggests that increased cardiac angiotensinogen m-RNA expression is a key mechanism in hypertension-induced left ventricular hypertrophy.
- Demonstrates that antihypertensive drug treatments can modulate this cardiac renin-angiotensin system component.
- Provides a potential molecular target for preventing cardiac hypertrophy in hypertensive individuals.