Renovascular resistance and noradrenaline

Area of Science:

• Nephrology
• Cardiovascular Physiology
• Neuroendocrinology

Background:

• Renal nerve stimulation can induce cortical vasoconstriction via direct smooth muscle activation or the renin-angiotensin system.
• Noradrenaline (NA), a renal neurotransmitter, is known to affect renal hemodynamics.

Purpose of the Study:

• To investigate the mechanisms underlying noradrenaline (NA)-induced cortical vasoconstriction in the baboon kidney.
• To determine the roles of the renin-angiotensin system and alpha-adrenergic receptors in this response.

Main Methods:

• Infusion of high-dose noradrenaline (NA) into the baboon renal artery.
• Administration of converting enzyme inhibitor (SQ20881) and angiotensin II antagonist (saralasin).
• Use of alpha-adrenergic blocking agent (phenoxybenzamine) to block specific receptors.

Main Results:

• High-dose NA infusion caused significant cortical vasoconstriction.
• This vasoconstriction was markedly reduced by SQ20881 and saralasin, indicating renin-angiotensin system involvement.
• Complete abolition of vasoconstriction occurred with the addition of phenoxybenzamine, suggesting alpha-adrenergic mediation.

Conclusions:

• Noradrenaline-induced cortical vasoconstriction in the baboon kidney is mediated by a dual mechanism.
• Activation of both the renin-angiotensin system and alpha-adrenergic receptors is crucial for this vasoconstrictive effect.