Evidence supporting a physiological role for proANP-(1-30) in the regulation of renal excretion.
The experiments, performed in pentobarbital sodium-anesthetized rats, consisted of a 1-h equilibration period followed by two 30-min control periods. Subsequently, synthetic rat pro atrial natriuretic peptide (ANP) [proANP-(1-30)] (n = 8) was given as a bolus of 10 microg in 1 ml of 0.9% saline followed by an infusion at 30 ng/min (20 microl/min) for six additional periods. Control rats (n = 6) received only 0.45% saline in the appropriate volumes. Mean arterial pressure, renal blood flow, and glomerular filtration rate did not change significantly in either group during the proANP-(1-30) infusion. Urine flow and potassium excretion increased approximately 50% in the proANP-(1-30)-infused group only (P < 0.05). Sodium excretion and fractional excretion of sodium, expressed as the change from their own baselines, were significantly increased by the proANP-(1-30) infusion (P < 0.05), whereas cGMP excretion was similar in both groups. These results suggest that the rat sequence of proANP-(1-30) produces a natriuresis in the rat independent of changes in hemodynamics and renal cGMP production. In a second study, rats (n = 8) were prepared as above and pretreated with 0.4 ml iv of rabbit serum containing an antibody directed against proANP-(1-30) (anti-proANP group). The rats were volume expanded with 3 ml of 6% albumin in Krebs and observed for 3 h to determine if the anti-proANP would attenuate the responses to volume expansion. Control rats (n = 7) received 0.4 ml of normal rabbit serum. The elevation in potassium excretion in response to volume expansion was significantly attenuated in the anti-proANP group (P < 0.05). Sodium excretion and urine flow responses also tended to be reduced but not significantly. These results suggest that in the rat, proANP-(1-30) plays a physiological role in regulating renal excretion.
Dietz
J R
JR
Department of Physiology and Biophysics and the University of South Florida, Cardiac Hormone Center, Tampa, Florida 33612, USA. jdietz@hsc.usf.edu
Scott
D Y
DY
Landon
C S
CS
Nazian
S J
SJ
D000818:Animals; D000906:Antibodies / Q000494:pharmacology; D009320:Atrial Natriuretic Factor / Q000008:administration & dosage / Q000494:pharmacology* / Q000502:physiology*; D004231:Diuresis / Q000187:drug effects*; D005919:Glomerular Filtration Rate / Q000187:drug effects; D007262:Infusions, Intravenous; D007275:Injections, Intravenous; D007444:Inulin / Q000493:pharmacokinetics; D007668:Kidney / Q000098:blood supply / Q000187:drug effects / Q000502:physiology*; D008297:Male; D009318:Natriuresis / Q000187:drug effects; D010446:Peptide Fragments / Q000008:administration & dosage / Q000494:pharmacology* / Q000502:physiology*; D011188:Potassium / Q000652:urine; D011498:Protein Precursors / Q000008:administration & dosage / Q000494:pharmacology* / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow / Q000187:drug effects; D013997:Time Factors; D014563:Urodynamics / Q000187:drug effects* / Q000502:physiology
D000906:Antibodies; D010446:Peptide Fragments; D011498:Protein Precursors; C054547:atrial natriuretic factor prohormone (1-30), human; D009320:Atrial Natriuretic Factor; D007444:Inulin; D011188:Potassium