Activation of the AT1 angiotensin receptor is a clinically important maladaptive response during cardiac hypertrophy. Autocrine and paracrine effects of locally generated angiotensin II, are believed to be the main mediators of these responses. However, a recent report has suggested that mechanical stress can activate AT1 receptors independently of angiotensin II generation. This finding, as well as recent studies on intracrine effects and the pharmacological consequences of receptor hetero- oligomerization, suggest that unexpected mechanisms could contribute to the role of the renin-angiotensin system during cardiac hypertrophy.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism