Moment-to-moment characteristics of the relationship between arterial pressure and renal interstitial hydrostatic pressure.
The kidney is a key controller of the long-term level of arterial pressure, in part through pressure-natriuresis. Although direct coupling of changes in renal arterial pressure to renal interstitial hydrostatic pressure (RIHP) and consequent sodium excretion is well established, few studies have characterized the moment-to-moment aspects of this process. These studies characterized the short-term hemodynamic component of pressure-natriuresis in vivo before and after autonomic nervous system and renin-angiotensin system inhibition. Changes in RIHP were determined over a range of renal arterial pressures in Wistar rats receiving no treatment, a ganglionic blocker (hexamethonium; 20 mg/kg per hour IV), or an angiotensin II type 1 receptor blocker (losartan; 10 mg/kg per hour IV). After a series of changes in renal arterial pressure, a delay of only ≈1 second was found for the onset of RIHP responses that was independent of the stimulus magnitude and neurohumoral manipulation; however, completion of the full RIHP response was within ≈15 seconds for renal arterial pressure changes of ≤30 mm Hg. The overall slope of the renal arterial pressure- RIHP relationship (0.09±0.01) was also not affected by autonomic nervous system and renin-angiotensin system inhibition despite decreasing renal arterial pressure (↓40% and ↓28%, respectively). Separate assessment of this relationship above and below the prevailing arterial pressure revealed that the pressor versus the depressor portion was blunted (P<0.001), a difference that was abolished after autonomic nervous system and renin-angiotensin system inhibition. The results suggest that spontaneous changes in arterial pressure are coupled to moment-to-moment changes in RIHP over a wide range of pressures, emphasizing a likely role for the dynamic component of the renal arterial pressure-RIHP relationship in the modulation of sodium excretion and, hence, arterial pressure.
Komolova
Marina
M
Department of Pharmacology and Toxicology, Queen's University, Kingston, Ontario K7L3N6, Canada.
Adams
Michael A
MA
D000704:Analysis of Variance; D000804:Angiotensin II / Q000494:pharmacology; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D000818:Animals; D001341:Autonomic Nervous System / Q000187:drug effects / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology*; D005730:Ganglionic Blockers / Q000494:pharmacology; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D018738:Hexamethonium / Q000494:pharmacology; D006874:Hydrostatic Pressure; D007668:Kidney / Q000098:blood supply / Q000502:physiology*; D019808:Losartan / Q000494:pharmacology; D008297:Male; D009318:Natriuresis / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D012079:Renal Circulation / Q000187:drug effects / Q000502:physiology*; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology; D013997:Time Factors; D014662:Vasoconstrictor Agents / Q000494:pharmacology
D047228:Angiotensin II Type 1 Receptor Blockers; D005730:Ganglionic Blockers; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D018738:Hexamethonium; D019808:Losartan