Long-term hypotensive and renal effects of atrial natriuretic peptide

J. P. Granger, T. J. Opgenorth, J. Salazar, J. C. Romero, John C Jr. Burnett

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Abstract

The present study was designed to examine the short-term and long-term effects of increased plasma levels of atrial natriuretic peptide on the glomerular filtration rate, sodium excretion, and arterial pressure. Intravenous infusion of synthetic atrial natriuretic peptide (2 μg/kg/bolus, 50 ng/kg/min continuous infusion) for 45 minutes in six conscious dogs increased plasma levels of immunoreactive atrial natriuretic peptide from 69 ± 10 to 233 ± 14 pg/ml. Short-term increases in plasma levels of atrial natriuretic peptide increased the glomerular filtration rate from 53 ± 15 to 82 ± 16 ml/min and increased sodium excretion from 74.4 ± 32.6 to 146.9 ± 38.1 μEq/min. Mean arterial pressure decreased slightly, from 88 ± 3 to 83 ± 3 mm Hg, whereas no changes occurred in plasma renin activity (2.0 ± 0.6 to 1.6 ± 0.8 ng of angiotensin I per milliliter per hour) or plasma aldosterone concentration (6.9 ± 2.3 to 8.1 ± 3.9 ng/dl). To determine whether the short-term effects of atrial natriuretic peptide on the glomerular filtration rate and sodium excretion lead to a sustained reduction in mean arterial pressure, atrial natriuretic peptide (50 ng/kg/min) was infused intravenously for 5 days in six conscious dogs. Long-term infusion increased plasma levels of immunoreactive atrial natriuretic peptide from 27 ± 5 to 292 ± 31 pg/ml. The infusion caused only a transient increase in sodium excretion and had no significant long-term effect on the glomerular filtration rate. Mean arterial pressure decreased from 90 ± 3 to 74 ± 3 and 75 ± 4 mm Hg by Days 4 and 5 of the infusion. Plasma renin activity and aldosterone were unchanged during the infusion, despite the large decrease in arterial pressure. These results demonstrate that short-term increases in plasma levels of atrial natriuretic peptide result in marked increases in the glomerular filtration rate and sodium excretion but only a slight decrease in mean arterial pressure. Long-term elevation of plasma atrial natriuretic peptide, however, results in a greater reduction in arterial pressure without having significant effects on the glomerular filtration rate of sodium excretion.

Original languageEnglish (US)
JournalHypertension
Volume8
Issue number6 II MONOGR. 122
StatePublished - 1986

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Atrial Natriuretic Factor
Glomerular Filtration Rate
Kidney
Arterial Pressure
Sodium
Aldosterone
Renin
Dogs
Angiotensin I
Intravenous Infusions

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Granger, J. P., Opgenorth, T. J., Salazar, J., Romero, J. C., & Burnett, J. C. J. (1986). Long-term hypotensive and renal effects of atrial natriuretic peptide. Hypertension, 8(6 II MONOGR. 122).

Long-term hypotensive and renal effects of atrial natriuretic peptide. / Granger, J. P.; Opgenorth, T. J.; Salazar, J.; Romero, J. C.; Burnett, John C Jr.

In: Hypertension, Vol. 8, No. 6 II MONOGR. 122, 1986.

Research output: Contribution to journalArticle

Granger, JP, Opgenorth, TJ, Salazar, J, Romero, JC & Burnett, JCJ 1986, 'Long-term hypotensive and renal effects of atrial natriuretic peptide', Hypertension, vol. 8, no. 6 II MONOGR. 122.
Granger JP, Opgenorth TJ, Salazar J, Romero JC, Burnett JCJ. Long-term hypotensive and renal effects of atrial natriuretic peptide. Hypertension. 1986;8(6 II MONOGR. 122).
Granger, J. P. ; Opgenorth, T. J. ; Salazar, J. ; Romero, J. C. ; Burnett, John C Jr. / Long-term hypotensive and renal effects of atrial natriuretic peptide. In: Hypertension. 1986 ; Vol. 8, No. 6 II MONOGR. 122.
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AB - The present study was designed to examine the short-term and long-term effects of increased plasma levels of atrial natriuretic peptide on the glomerular filtration rate, sodium excretion, and arterial pressure. Intravenous infusion of synthetic atrial natriuretic peptide (2 μg/kg/bolus, 50 ng/kg/min continuous infusion) for 45 minutes in six conscious dogs increased plasma levels of immunoreactive atrial natriuretic peptide from 69 ± 10 to 233 ± 14 pg/ml. Short-term increases in plasma levels of atrial natriuretic peptide increased the glomerular filtration rate from 53 ± 15 to 82 ± 16 ml/min and increased sodium excretion from 74.4 ± 32.6 to 146.9 ± 38.1 μEq/min. Mean arterial pressure decreased slightly, from 88 ± 3 to 83 ± 3 mm Hg, whereas no changes occurred in plasma renin activity (2.0 ± 0.6 to 1.6 ± 0.8 ng of angiotensin I per milliliter per hour) or plasma aldosterone concentration (6.9 ± 2.3 to 8.1 ± 3.9 ng/dl). To determine whether the short-term effects of atrial natriuretic peptide on the glomerular filtration rate and sodium excretion lead to a sustained reduction in mean arterial pressure, atrial natriuretic peptide (50 ng/kg/min) was infused intravenously for 5 days in six conscious dogs. Long-term infusion increased plasma levels of immunoreactive atrial natriuretic peptide from 27 ± 5 to 292 ± 31 pg/ml. The infusion caused only a transient increase in sodium excretion and had no significant long-term effect on the glomerular filtration rate. Mean arterial pressure decreased from 90 ± 3 to 74 ± 3 and 75 ± 4 mm Hg by Days 4 and 5 of the infusion. Plasma renin activity and aldosterone were unchanged during the infusion, despite the large decrease in arterial pressure. These results demonstrate that short-term increases in plasma levels of atrial natriuretic peptide result in marked increases in the glomerular filtration rate and sodium excretion but only a slight decrease in mean arterial pressure. Long-term elevation of plasma atrial natriuretic peptide, however, results in a greater reduction in arterial pressure without having significant effects on the glomerular filtration rate of sodium excretion.

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