Angiotensin II infusion at 1 pmol/min significantly augmented sympathetically induced venoconstriction caused by a deep breath compared to control veins (P<0.01).
Does low-dose angiotensin II infusion augment sympathetically induced venoconstriction in normal volunteers?
Low-dose angiotensin II augments sympathetically induced venous tone via a presynaptic mechanism, providing a physiological basis for the venodilating properties of ACE inhibitors.
p-value: p=<0.01
The constriction produced by a single deep breath was measured simultaneously in two adjacent hand veins in normal volunteers. One vein was infused with angiotensin II (ANG II) while the other acted as a control. 2. At a dose lower than that required to produce direct venous constriction (1 pmol/min), ANG II significantly augmented the constriction caused by a deep breath in eight subjects (P less than 0.01). The same dose had no effect on the venoconstriction caused by infused noradrenaline (NA) in a further six subjects. 3. It is concluded that ANG II at low doses may cause venoconstriction indirectly by augmenting sympathetically induced venous tone via a presynaptic mechanism. This observation may help to explain the apparent venodilating property of angiotensin-converting enzyme inhibitors in clinical situations where the renin-angiotensin system is stimulated.
Benjamin et al. (Sat,) conducted a other in Normal volunteers (n=14). Angiotensin II (ANG II) vs. Control (adjacent hand vein) was evaluated on Constriction caused by a single deep breath (p=<0.01). Angiotensin II infusion at 1 pmol/min significantly augmented sympathetically induced venoconstriction caused by a deep breath compared to control veins (P<0.01).