Central opiate system modulation of the area postrema pressor pathway

Area of Science:

• Neuroscience
• Cardiovascular Physiology

Background:

• Angiotensin II administered via vertebral arteries influences central sympathetic vasomotor activity at the area postrema.
• The precise mechanism remains unclear, but emerging evidence suggests a role for the opiate system.

Purpose of the Study:

• To investigate the interaction between the endogenous opiate system and angiotensin II's central pressor effects.
• To determine if opiate receptor blockade or activation modifies the pressor response to angiotensin II.

Main Methods:

• Experiments were conducted on dogs anesthetized with chloralose.
• Naloxone (an opiate antagonist) and morphine (an opiate agonist) were administered.
• Pressor responses to vertebrally administered and intravenously infused angiotensin II were measured.
• Responses to norepinephrine were also assessed for comparison.

Main Results:

• Naloxone significantly blunted the pressor response to vertebral angiotensin II by 50%.
• Morphine administration doubled the pressor response to vertebral angiotensin II.
• Neither naloxone nor morphine affected pressor responses to intravenous angiotensin II or vertebral/intravenous norepinephrine.

Conclusions:

• The findings indicate a significant interaction between the endogenous opiate system in the medulla and the pressor effects of angiotensin II at the area postrema.
• This suggests a previously unrecognized role for central opiates in mediating angiotensin II-induced hypertension.