Prolonged stimulation of atrial receptors alters renal hemodynamics and function primarily via myelinated vagal afferents and renal sympathetic efferents.
Renal nerve integrity mediates atrial receptor effects on kidney function in animals; leaves open translation to human cardiorenal syndromes.
To determine the precise contributory role of neural and humoral factors in the efferent mechanism of the atrial receptor-renal reflex, we have examined the effects of prolonged (45 min) stimulation of left atrial receptors on renal haemodynamics and function simultaneously in both kidneys (right kidney intact and left kidney denervated) of anaesthetized dogs. Aortic pressure in these dogs was held constant by means of an arterial reservoir connected to the aorta; heart rate changes were prevented by blocking beta 1-adrenoceptor activity with atenolol (2 mg kg-1 i.v.). Localized stimulation of atrial receptors in six dogs increased renal blood flow (6 +/- 2%), creatinine clearance (11 +/- 4%), urine flow (9 +/- 3%), sodium excretion (14 +/- 7%) and osmolal excretion (10 +/- 4%), and decreased free water clearance (14 +/- 7%) in intact kidneys, but led to no changes in denervated kidneys. In an additional four dogs, cooling the vagus nerves to 6-7 degrees C or cutting them in the neck abolished the renal responses to stimulation of atrial receptors in these stabilized preparations. These data clearly demonstrate that the renal responses to prolonged stimulation of atrial receptors are primarily mediated via myelinated vagal afferents and renal sympathetic efferents.
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Majid et al. (1995) studied this question.
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