Renal mechanisms of hypertension
- David L. Mattson(corresponding author),
- Allen W. Cowley
- Medical College of Wisconsin
Abstract
Overwhelming evidence has demonstrated that the kidney is an important regulator of arterial pressure, and that an abnormality in renal function is critical in the development and maintenance of arterial hypertension. Renal transplant studies between normotensive and hypertensive animals (and patients) have convincingly shown that the level of blood pressure is determined by an intrinsic property of the kidney. Further experimental evidence indicates that the kidney regulates blood pressure by controlling extracellular fluid volume through the pressure-natriuretic-diuretic relationship, the relationship between renal perfusion pressure and sodium and water excretion. Normally, an increase in arterial pressure leads to increased urinary output through pressure natriuresis, a decrease in extracellular volume, and normalization of blood pressure. In hypertensives, the pressure natriuretic response is shifted to increased levels of arterial pressure, indicating that the kidney controls extracellular fluid volume at an elevated level of arterial pressure. Data are presented which indicate that a transmission of renal perfusion pressure to the vasa recta capillaries in the renal medulla is a critical mediator in the pressure-natriuretic response. Finally, additional evidence demonstrates that selective manipulation of renal medullary blood flow leads to parallel alterations in sodium and water excretion, and that chronic manipulation of renal medullary blood flow leads to alterations in fluid and electrolyte balance and blood pressure in both normotensive and hypertensive animals.
Publication Information
Output type
Original language
English (US)Pages from-to (Number of pages)
Pages 217-224 (8 pages)Journal (Volume, Issue Number)
Current opinion in nephrology and hypertension (Volume 8, Issue 2)Publication milestones
- Published - 03/1999
Publication status
ISSN
1062-4821Publication IDs
- Scopus: 0033008745
