Moment-to-moment characteristics of the relationship between arterial pressure and renal interstitial hydrostatic pressure.

نویسندگان

  • Marina Komolova
  • Michael A Adams
چکیده

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.

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عنوان ژورنال:
  • Hypertension

دوره 56 4  شماره 

صفحات  -

تاریخ انتشار 2010