Intrarenal pressures during direct inhibition of sodium transport

A. A. Khraibi, J. P. Granger, J. A. Haas, John C Jr. Burnett, F. G. Knox

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Renal interstitial hydrostatic pressure (RIHP) has been implicated in the regulation of sodium excretion. Studies using vasodilators and other maneuvers to increase RIHP have found a significant correlation between RIHP and sodium excretion. Since correlative studies do not prove a cause-and- effect relationship, it is not known whether the rise in sodium excretion in these studies is the result of increases in RIHP or if RIHP is elevated as a result of decreases in sodium and water reabsorption and increases in intratubular pressure. Therefore, the purpose of the present study was to determine whether elevation of intratubular hydrostatic pressures in response to direct inhibition of tubule transport with loop diuretics results in increases in RIHP in dogs and rats. Intrarenal hydrostatic pressures, renal hemodynamics, and sodium and water excretion were examined in dogs during intravenous administration of furosemide (3 mg/kg bolus followed by 0.03 mg · kg-1 · min-1) or bumetanide (60 μg/kg bolus followed by 1 μg · kg-1 · min-1). Furosemide administration increased urinary flow rate (V̇; 0.10 ± 0.02 to 4.6 ± 0.97 ml/min), urinary sodium excretion (U(Na)V̇; 16 ± 5 to 549 ± 123 μeq/min), and proximal tubule hydrostatic pressure (P(T); 21 ± 1 to 28 ± 1 mmHg) but had no effect on RIHP (7.2 ± 0.6 to 7.4 ± 0.7 mmHg) or peritubular capillary hydrostatic pressure (14 ± 1 to 14 ± 1 mmHg). Bumetanide also had no effect on RIHP (6.5 ± 0.3 to 6.8 ± 0.3 mmHg) despite large increases in U(Na)V̇ (12 ± 4 to 313 ± 75 μeq/min), V̇ (0.09 ± 0.02 to 2.8 ± 0.6 ml/min), and P(T) (20 ± 1.0 to 31 ± 0.4 mmHg). Similarly, administration of furosemide in Sprague-Dawley rats resulted in a significant increase in U(Na)V̇, V̇, and P(T), but had no effect on RIHP. In summary, significant increases in intratubular hydrostatic pressures during administration of the loop diuretics furosemide or bumetanide are not associated with increases in RIHP. We conclude that increases in intratubular hydrostatic pressures in response to direct inhibition of tubule transport with loop diuretics are not transmitted into the renal interstitium.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume263
Issue number6 32-6
StatePublished - 1992

Fingerprint

Hydrostatic Pressure
Sodium
Pressure
Kidney
Furosemide
Sodium Potassium Chloride Symporter Inhibitors
Bumetanide
Dogs
Water
Vasodilator Agents

Keywords

  • bumetanide
  • dog
  • furosemide
  • intrarenal hydrostatic pressures
  • sodium excretion
  • Sprague-Dawley rat

ASJC Scopus subject areas

  • Physiology

Cite this

Intrarenal pressures during direct inhibition of sodium transport. / Khraibi, A. A.; Granger, J. P.; Haas, J. A.; Burnett, John C Jr.; Knox, F. G.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 263, No. 6 32-6, 1992.

Research output: Contribution to journalArticle

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AU - Khraibi, A. A.

AU - Granger, J. P.

AU - Haas, J. A.

AU - Burnett, John C Jr.

AU - Knox, F. G.

PY - 1992

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N2 - Renal interstitial hydrostatic pressure (RIHP) has been implicated in the regulation of sodium excretion. Studies using vasodilators and other maneuvers to increase RIHP have found a significant correlation between RIHP and sodium excretion. Since correlative studies do not prove a cause-and- effect relationship, it is not known whether the rise in sodium excretion in these studies is the result of increases in RIHP or if RIHP is elevated as a result of decreases in sodium and water reabsorption and increases in intratubular pressure. Therefore, the purpose of the present study was to determine whether elevation of intratubular hydrostatic pressures in response to direct inhibition of tubule transport with loop diuretics results in increases in RIHP in dogs and rats. Intrarenal hydrostatic pressures, renal hemodynamics, and sodium and water excretion were examined in dogs during intravenous administration of furosemide (3 mg/kg bolus followed by 0.03 mg · kg-1 · min-1) or bumetanide (60 μg/kg bolus followed by 1 μg · kg-1 · min-1). Furosemide administration increased urinary flow rate (V̇; 0.10 ± 0.02 to 4.6 ± 0.97 ml/min), urinary sodium excretion (U(Na)V̇; 16 ± 5 to 549 ± 123 μeq/min), and proximal tubule hydrostatic pressure (P(T); 21 ± 1 to 28 ± 1 mmHg) but had no effect on RIHP (7.2 ± 0.6 to 7.4 ± 0.7 mmHg) or peritubular capillary hydrostatic pressure (14 ± 1 to 14 ± 1 mmHg). Bumetanide also had no effect on RIHP (6.5 ± 0.3 to 6.8 ± 0.3 mmHg) despite large increases in U(Na)V̇ (12 ± 4 to 313 ± 75 μeq/min), V̇ (0.09 ± 0.02 to 2.8 ± 0.6 ml/min), and P(T) (20 ± 1.0 to 31 ± 0.4 mmHg). Similarly, administration of furosemide in Sprague-Dawley rats resulted in a significant increase in U(Na)V̇, V̇, and P(T), but had no effect on RIHP. In summary, significant increases in intratubular hydrostatic pressures during administration of the loop diuretics furosemide or bumetanide are not associated with increases in RIHP. We conclude that increases in intratubular hydrostatic pressures in response to direct inhibition of tubule transport with loop diuretics are not transmitted into the renal interstitium.

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