Dopaminergic modulation of physiological and pathological neurohumoral activation in man.
Close relations exist between the peripheral dopaminergic system, and the sympathetic nervous and renin-angiotensin-aldosterone system: D1 dopamine receptor stimulation-induced vasodilation may activate the sympathetic nervous and renin-angiotensin system in vivo, presynaptic D2 dopamine receptor stimulation is known to inhibit stimulated norepinephrine release from sympathetic nerve terminals, in experimental conditions both in vitro and in vivo. Endogenous dopamine has a tonic inhibitory effect on aldosterone release. Conversely, basal sympathetic activity has been found to be required for the natriuretic effect of dopamine in proximal renal tubules. Other relations include the conversion of dopamine to other catecholamines, and co-release. This review considers the reflection of some of these relations and their clinical significance in man in physiological and pathophysiological conditions, especially congestive heart failure. An inhibitory effect of the nonselective dopamine agonist ibopamine on plasma norepinephrine levels was found in normal man during exercise but not at rest, and in patients with several degrees of congestive heart failure, both at rest and during exercise. Infusions of dopamine 1 microgram/kg/min, but not 3 micrograms/kg/min were found to lower plasma norepinephrine levels during sympathetic stimulation by exercise or by a cold pressor test in normal man. Dopamine antagonists enhance the rise in plasma norepinephrine levels during exercise, indicating that endogenous dopamine also inhibits norepinephrine release. Both phentolamine and prazosin abolish the natriuretic effects of dopamine in man, even when the renal hemodynamic effect of dopamine is unaffected. In conclusion, it is important to be aware of clinically significant interactions between the peripheral dopaminergic and sympathetic nervous system at different levels.
Department of Medicine, University Hospital Groningen, The Netherlands.
A J
AJ
Smit
A G
AG
Lieverse
D
D
van Veldhuisen
A R
AR
Girbes
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D001711:Biotransformation / Q000502:physiology; D004298:Dopamine / Q000502:physiology*; D018491:Dopamine Agonists / Q000494:pharmacology; D006333:Heart Failure / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D007668:Kidney / Q000187:drug effects; D008297:Male; D018377:Neurotransmitter Agents / Q000502:physiology*; D017447:Receptors, Dopamine D1 / Q000819:agonists; D012084:Renin-Angiotensin System / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology / Q000503:physiopathology
D000317:Adrenergic alpha-Antagonists; D018491:Dopamine Agonists; D018377:Neurotransmitter Agents; D017447:Receptors, Dopamine D1; D004298:Dopamine