Differing hemodynamic responses to atrial natriuretic factor in two models of hypertension

M. Volpe, R. E. Sosa, F. B. Muller, M. J. Camargo, N. Glorioso, J. H. Laragh, T. Maack, S. A. Atlas

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Abstract

Hemodynamic responses to synthetic atrial natriuretic factor (ANF), were studied in renin-dependent two-kidney, one-clip (2K,1C) and deoxycorticosterone (DOC) salt-treated hypertensive rats as well as normotensive controls. ANF infusion (800 pmol/kg prime, 120 pmol·kg-1·min-1 for 60 min) decreased blood pressure (BP) more in conscious 2K,1C (-24 ± 4%) than in DOC salt-treated (-12 ± 4%, P <0.05) or control rats. Hemodynamic parameters were also evaluated during graded infusion of three doses, each for 30 min. At 24 and 120 pmol·kg-1·min-1, ANF lowered BP in 2K,1C rats, both conscious (from 156 ± 6 to 144 ± 7, P <0.05 and 135 ± 5 mmHg, P <0.05) and anesthetized (from 148 ± 7 to 138 ± 7, P <0.05 and 128 ± 7, P <0.05). In anesthetized 2K,1C, BP changes were associated with reduction in total peripheral resistance (TPR) that became significant at 120 pmol·kg-1·min-1 (-10 ± 2%), whereas cardiac output (CO) and stroke volume (SV) were unchanged. In DOC-salt-treated rats these doses did not lower BP despite progressive falls in CO (-7 ± 3% and -24 ± 5%, P <0.05) and SV (-8 ± 2% and -23 ± 5%, P <0.05), which were balanced by a simultaneous rise in TPR (+12 ± 4% and +26 ± 10%, P <0.05). At 600 pmol·kg-1·min-1, ANF reduced BP in both conscious and anesthetized 2K,1C (-19 ± 2% and -17 ± 2%), DOC-salt-treated rats (-10 ± 2%, -16 ± 2%), and control rats (-9 ± 3%, -14 ± 3%). At this dose, ANF lowered CO in anesthetized 2K,1C (-17 ± 2%) as well as DOC-salt-treated rats (-33 ± 6%), but SV fell significantly only in DOC-salt-treated rats (-29 ± 5%) as TPR rose further (+31 ± 10%). In conclusion, hemodynamic responses to ANF vary according to both the dose and the mechanisms sustaining hypertension. Lower doses of ANF appear to preferentially reduce BP by antagonizing the action of vasoconstrictors such as angiotensin II.

Original languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume250
Issue number5
Publication statusPublished - 1986

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Atrial Natriuretic Factor
Desoxycorticosterone
Hemodynamics
Hypertension
Salts
Blood Pressure
Cardiac Output
Vascular Resistance
Stroke Volume
Cardiac Volume
Vasoconstrictor Agents
Renin
Surgical Instruments
Angiotensin II
Kidney

ASJC Scopus subject areas

  • Physiology

Cite this

Volpe, M., Sosa, R. E., Muller, F. B., Camargo, M. J., Glorioso, N., Laragh, J. H., ... Atlas, S. A. (1986). Differing hemodynamic responses to atrial natriuretic factor in two models of hypertension. American Journal of Physiology - Heart and Circulatory Physiology, 250(5).

Differing hemodynamic responses to atrial natriuretic factor in two models of hypertension. / Volpe, M.; Sosa, R. E.; Muller, F. B.; Camargo, M. J.; Glorioso, N.; Laragh, J. H.; Maack, T.; Atlas, S. A.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 250, No. 5, 1986.

Research output: Contribution to journalArticle

Volpe, M, Sosa, RE, Muller, FB, Camargo, MJ, Glorioso, N, Laragh, JH, Maack, T & Atlas, SA 1986, 'Differing hemodynamic responses to atrial natriuretic factor in two models of hypertension', American Journal of Physiology - Heart and Circulatory Physiology, vol. 250, no. 5.
Volpe, M. ; Sosa, R. E. ; Muller, F. B. ; Camargo, M. J. ; Glorioso, N. ; Laragh, J. H. ; Maack, T. ; Atlas, S. A. / Differing hemodynamic responses to atrial natriuretic factor in two models of hypertension. In: American Journal of Physiology - Heart and Circulatory Physiology. 1986 ; Vol. 250, No. 5.
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title = "Differing hemodynamic responses to atrial natriuretic factor in two models of hypertension",
abstract = "Hemodynamic responses to synthetic atrial natriuretic factor (ANF), were studied in renin-dependent two-kidney, one-clip (2K,1C) and deoxycorticosterone (DOC) salt-treated hypertensive rats as well as normotensive controls. ANF infusion (800 pmol/kg prime, 120 pmol·kg-1·min-1 for 60 min) decreased blood pressure (BP) more in conscious 2K,1C (-24 ± 4{\%}) than in DOC salt-treated (-12 ± 4{\%}, P <0.05) or control rats. Hemodynamic parameters were also evaluated during graded infusion of three doses, each for 30 min. At 24 and 120 pmol·kg-1·min-1, ANF lowered BP in 2K,1C rats, both conscious (from 156 ± 6 to 144 ± 7, P <0.05 and 135 ± 5 mmHg, P <0.05) and anesthetized (from 148 ± 7 to 138 ± 7, P <0.05 and 128 ± 7, P <0.05). In anesthetized 2K,1C, BP changes were associated with reduction in total peripheral resistance (TPR) that became significant at 120 pmol·kg-1·min-1 (-10 ± 2{\%}), whereas cardiac output (CO) and stroke volume (SV) were unchanged. In DOC-salt-treated rats these doses did not lower BP despite progressive falls in CO (-7 ± 3{\%} and -24 ± 5{\%}, P <0.05) and SV (-8 ± 2{\%} and -23 ± 5{\%}, P <0.05), which were balanced by a simultaneous rise in TPR (+12 ± 4{\%} and +26 ± 10{\%}, P <0.05). At 600 pmol·kg-1·min-1, ANF reduced BP in both conscious and anesthetized 2K,1C (-19 ± 2{\%} and -17 ± 2{\%}), DOC-salt-treated rats (-10 ± 2{\%}, -16 ± 2{\%}), and control rats (-9 ± 3{\%}, -14 ± 3{\%}). At this dose, ANF lowered CO in anesthetized 2K,1C (-17 ± 2{\%}) as well as DOC-salt-treated rats (-33 ± 6{\%}), but SV fell significantly only in DOC-salt-treated rats (-29 ± 5{\%}) as TPR rose further (+31 ± 10{\%}). In conclusion, hemodynamic responses to ANF vary according to both the dose and the mechanisms sustaining hypertension. Lower doses of ANF appear to preferentially reduce BP by antagonizing the action of vasoconstrictors such as angiotensin II.",
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T1 - Differing hemodynamic responses to atrial natriuretic factor in two models of hypertension

AU - Volpe, M.

AU - Sosa, R. E.

AU - Muller, F. B.

AU - Camargo, M. J.

AU - Glorioso, N.

AU - Laragh, J. H.

AU - Maack, T.

AU - Atlas, S. A.

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N2 - Hemodynamic responses to synthetic atrial natriuretic factor (ANF), were studied in renin-dependent two-kidney, one-clip (2K,1C) and deoxycorticosterone (DOC) salt-treated hypertensive rats as well as normotensive controls. ANF infusion (800 pmol/kg prime, 120 pmol·kg-1·min-1 for 60 min) decreased blood pressure (BP) more in conscious 2K,1C (-24 ± 4%) than in DOC salt-treated (-12 ± 4%, P <0.05) or control rats. Hemodynamic parameters were also evaluated during graded infusion of three doses, each for 30 min. At 24 and 120 pmol·kg-1·min-1, ANF lowered BP in 2K,1C rats, both conscious (from 156 ± 6 to 144 ± 7, P <0.05 and 135 ± 5 mmHg, P <0.05) and anesthetized (from 148 ± 7 to 138 ± 7, P <0.05 and 128 ± 7, P <0.05). In anesthetized 2K,1C, BP changes were associated with reduction in total peripheral resistance (TPR) that became significant at 120 pmol·kg-1·min-1 (-10 ± 2%), whereas cardiac output (CO) and stroke volume (SV) were unchanged. In DOC-salt-treated rats these doses did not lower BP despite progressive falls in CO (-7 ± 3% and -24 ± 5%, P <0.05) and SV (-8 ± 2% and -23 ± 5%, P <0.05), which were balanced by a simultaneous rise in TPR (+12 ± 4% and +26 ± 10%, P <0.05). At 600 pmol·kg-1·min-1, ANF reduced BP in both conscious and anesthetized 2K,1C (-19 ± 2% and -17 ± 2%), DOC-salt-treated rats (-10 ± 2%, -16 ± 2%), and control rats (-9 ± 3%, -14 ± 3%). At this dose, ANF lowered CO in anesthetized 2K,1C (-17 ± 2%) as well as DOC-salt-treated rats (-33 ± 6%), but SV fell significantly only in DOC-salt-treated rats (-29 ± 5%) as TPR rose further (+31 ± 10%). In conclusion, hemodynamic responses to ANF vary according to both the dose and the mechanisms sustaining hypertension. Lower doses of ANF appear to preferentially reduce BP by antagonizing the action of vasoconstrictors such as angiotensin II.

AB - Hemodynamic responses to synthetic atrial natriuretic factor (ANF), were studied in renin-dependent two-kidney, one-clip (2K,1C) and deoxycorticosterone (DOC) salt-treated hypertensive rats as well as normotensive controls. ANF infusion (800 pmol/kg prime, 120 pmol·kg-1·min-1 for 60 min) decreased blood pressure (BP) more in conscious 2K,1C (-24 ± 4%) than in DOC salt-treated (-12 ± 4%, P <0.05) or control rats. Hemodynamic parameters were also evaluated during graded infusion of three doses, each for 30 min. At 24 and 120 pmol·kg-1·min-1, ANF lowered BP in 2K,1C rats, both conscious (from 156 ± 6 to 144 ± 7, P <0.05 and 135 ± 5 mmHg, P <0.05) and anesthetized (from 148 ± 7 to 138 ± 7, P <0.05 and 128 ± 7, P <0.05). In anesthetized 2K,1C, BP changes were associated with reduction in total peripheral resistance (TPR) that became significant at 120 pmol·kg-1·min-1 (-10 ± 2%), whereas cardiac output (CO) and stroke volume (SV) were unchanged. In DOC-salt-treated rats these doses did not lower BP despite progressive falls in CO (-7 ± 3% and -24 ± 5%, P <0.05) and SV (-8 ± 2% and -23 ± 5%, P <0.05), which were balanced by a simultaneous rise in TPR (+12 ± 4% and +26 ± 10%, P <0.05). At 600 pmol·kg-1·min-1, ANF reduced BP in both conscious and anesthetized 2K,1C (-19 ± 2% and -17 ± 2%), DOC-salt-treated rats (-10 ± 2%, -16 ± 2%), and control rats (-9 ± 3%, -14 ± 3%). At this dose, ANF lowered CO in anesthetized 2K,1C (-17 ± 2%) as well as DOC-salt-treated rats (-33 ± 6%), but SV fell significantly only in DOC-salt-treated rats (-29 ± 5%) as TPR rose further (+31 ± 10%). In conclusion, hemodynamic responses to ANF vary according to both the dose and the mechanisms sustaining hypertension. Lower doses of ANF appear to preferentially reduce BP by antagonizing the action of vasoconstrictors such as angiotensin II.

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