Abstract
Alterations in glomerular hemodynamics may play an important role in the progression of renal dysfunction. Accordingly, treating not only systemic hypertension, but also glomerular hypertension is important for conservation of renal function in patients with renal disease. However, glomerular capillary pressure does not necessarily change in parallel with systemic blood pressure due to unique mechanisms that control the resistance of glomerular afferent and efferent arterioles. While myogenic response and tubuloglomerular feedback play an important role in controlling afferent arteriolar resistance, angiotensin II is a major determinant of efferent arteriolar tone. Calcium antagonists block almost all mechanisms that constrict the afferent arteriole, rendering glomerular capillary pressure dependent on systemic pressure. On the other hand, angiotensin-converting enzyme inhibitors dilate efferent arterioles, thereby lowering glomerular capillary pressure. Such differences should be taken into account when selecting adequate drugs for the treatment of hypertension with various degrees of renal dysfunction.
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