The influence of Atriopeptins I and II on the relationship between glomerular filtration and natriuresis

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Abstract
The effects of two pure synthetic atrial natriuretic factors, Atriopeptin (AP) I and AP II, on the whole kidney glomerular filtration rate (GFR), sodium and potassium excretion (UNa V, UK V), urine flow rate (V) and arterial blood pressure (BP) were studied in adult male Sprague‐Dawley rats. The variables were measured during a control period and during 70 min of continuous intravenous infusion of AP I or AP II at a rate of 10 μg h‐1 kg‐1 body wt. A time control group was studied in parallel to see whether the variables under study changed with time. The AP I infusion did not affect GFR (change from 1.34 ± 0.10 to 1.24 ± 0.04 ml min‐1 g‐1 kidney wt), but was clearly natriuretic (UNa V changed from 0.071 ± 0.011 to 0.229 ± 0.038 μmol min‐1 g‐1 kidney wt, P < 0.01). The UK V increased from 0.504 ± 0.073 to 1.138 ± 0.121 μmol min‐1 g‐1 kidney wt, (P < 0.001) and V from 1.88 ± 0.10 to 2.94 ± 0.15 μl min‐1 g‐1 kidney wt, (P < 0.001). Urine osmolality (Uosm) and BP were unaffected. During AP II infusion GFR remained unchanged but was slightly below the pre‐infusion level during the last infusion period (1.05 ± 0.07 as against 1.37 ± 0.09 ml min‐1 g‐1 kidney wt, P < 0.05). Despite this fact, UNa± was significantly elevated throughout the infusion period. The UNa V increased from 0.100 ± 0.008 in the control period to 1.404 ± 0.432 μmol min‐1 g‐1 kidney wt (P < 0.01) after 50 min of infusion. During the period when GFR was slightly below the pre‐infusion level, UNa V was 1.364 ± 0.434 μmol min‐1 g‐1 kidney wt (P < 0.001). The UK V increased from 0.610 ± 0.175 in the control period to 1.266 ± 0.142 μmol min‐1 g‐1 kidney wt (P < 0.05). The urine flow rate increased from 1.95 ± 0.17 to 5.47 ± 0.88 μl min‐1 g‐1 kidney wt (P < 0.01), and Uosm decreased from 1922 ± 90 to 1644 ± 99 mosm kg‐1 H2O (P < 0.05), whilst BP fell from 114 ± 2 to a steady‐state level of 98 ± 3 mmHg (P < 0.001). It is concluded that Atriopeptin I and Atriopeptin II increase sodium excretion mainly by affecting tubular transport processes. Through its vascular effects, Atriopeptin II will also decrease the arterial blood pressure and, as previously shown, transiently increase medullary blood flow, and the latter increase may contribute to the natriuretic response.