Why the study?
Does 6-OHDA administration into the ventral pons increase ACE activity in the amygdaloid complex in a neurogenic hypertensive model?
Does 6-OHDA administration into the ventral pons increase ACE activity in the amygdaloid complex in a neurogenic hypertensive model?
Increased specific ACE activity in the amygdaloid complex following norepinephrine depletion correlates with arterial blood pressure, suggesting a role in the development of neurogenic hypertension.
Increased amygdaloid ACE activity may contribute to neurogenic hypertension in this model; hypothesis-generating and leaves open any role for CNS ACE inhibition in humans.
The bilateral destruction of the ventral noradrenergic pathway induced by 6-hydroxydopamine (6-OHDA) administration into the ventral pons led to an increase in arterial blood pressure (ABP) and norepinephrine depletion in the amygdaloid complex, nucleus accumbens, septal area and olfactory bulb. Specific angiotensin converting enzyme (ACE) activity was significantly increased only in the amygdaloid complex (Control: 4.56 +/- 0.95; Vehicle: 4.08 +/- 1.07; 6-OHDA: 11.76 +/- 1.84). A significant correlation between arterial blood pressure and specific ACE activity levels in the amygdaloid complex was observed (r: 0.775; p less than 0.002). These results suggest that an increase in specific ACE activity of the amygdaloid complex after norepinephrine depletion could play a role in the development of hypertension in this model.
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Dabsys et al. (1988) studied this question.
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