Adrenergic sodium handling and the natriuretic action of calcium antagonists.
Stimulation and denervation experiments have provided evidence that adrenergic mechanisms can enhance sodium and water reabsorption from the renal tubule, and that this influence is probably exerted on the entire tubular extent. Reflexes originating from cardiopulmonary and renal receptors can control adrenergic renal sodium handling, and evidence has recently been presented that a reno-renal reflex tonically inhibits the contralateral sympathetic control of tubular reabsorption of sodium and water. Other investigations indicate that adrenergic renal sodium handling is mediated through alpha-rather than beta-receptors, and that the alpha-receptors are of the alpha 1-subtype. The question of whether the natriuretic action of calcium antagonists is, at least in part, mediated by interference with adrenergic control of tubular reabsorption cannot yet be definitely answered. Although available data are only preliminary, they do not support an important action of calcium antagonists on adrenergic renal sodium handling, but a separate contribution of impaired adrenergic control and of a direct tubular effect of calcium antagonists cannot be excluded.
Zanchetti
A
A
Stella
A
A
Golin
R
R
D000320:Adrenergic Fibers / Q000502:physiology*; D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D002415:Cats; D007668:Kidney / Q000187:drug effects* / Q000294:innervation / Q000502:physiology; D007684:Kidney Tubules / Q000502:physiology; D009318:Natriuresis / Q000187:drug effects*; D011941:Receptors, Adrenergic / Q000502:physiology; D012018:Reflex / Q000502:physiology; D014630:Vagus Nerve / Q000502:physiology
D002121:Calcium Channel Blockers; D011941:Receptors, Adrenergic