Target organ . | Biological effects . |
---|---|
Kidney | Increased GFR by inducing vasodilatation of afferent arterioles and vasoconstriction of efferent arterioles |
Induction of natriuresis by inhibiting Na+, H+ exchanger in the proximal tubule, Na+, Cl− co-transporter in the distal tubule and Na+ channels in the collecting duct | |
Induction of diuresis due to inhibition of AVP-induced acquaporin-2 incorporation into collecting ducts' apical membrane | |
Cardiac | Reduction in preload leading to fall in cardiac output |
Inhibition of cardiac remodelling | |
Haemodynamic | Vasorelaxation |
Elevating capillary hydraulic conductivity | |
Decreased cardiac preload and afterload | |
Endocrine | Suppression of the following: |
- Renin–Ang–aldosterone axis | |
- Sympathetic outflow | |
- AVP | |
- Endothelin | |
Mitogenesis | Inhibition of mitogenesis in VSMC |
Inhibition of growth factor-mediated hypertrophy in fibroblasts |
Target organ . | Biological effects . |
---|---|
Kidney | Increased GFR by inducing vasodilatation of afferent arterioles and vasoconstriction of efferent arterioles |
Induction of natriuresis by inhibiting Na+, H+ exchanger in the proximal tubule, Na+, Cl− co-transporter in the distal tubule and Na+ channels in the collecting duct | |
Induction of diuresis due to inhibition of AVP-induced acquaporin-2 incorporation into collecting ducts' apical membrane | |
Cardiac | Reduction in preload leading to fall in cardiac output |
Inhibition of cardiac remodelling | |
Haemodynamic | Vasorelaxation |
Elevating capillary hydraulic conductivity | |
Decreased cardiac preload and afterload | |
Endocrine | Suppression of the following: |
- Renin–Ang–aldosterone axis | |
- Sympathetic outflow | |
- AVP | |
- Endothelin | |
Mitogenesis | Inhibition of mitogenesis in VSMC |
Inhibition of growth factor-mediated hypertrophy in fibroblasts |