Renal medullary mechanisms in hypertension.

The emergence of laser-Doppler and videomicroscopy techniques has renewed interest in study of the renal medullary circulation in the control of sodium excretion, pressure-natriuresis and arterial pressure. In this regard, elevations in renal perfusion pressure increase papillary blood flow and vasa recta capillary pressure which increase renal interstitial pressure (RIHP) and dissipate the medullary osmotic gradient. These factors act together to inhibit sodium reabsorption in the proximal tubule and the loop of Henle, particularly in deep nephrons. Changes in medullary hemodynamics also participate in alterating sodium reabsorption following volume expansion and administration of vasoactive agents. For example, administration of antihypertensive compounds such as ANF, captopril, calcium channel blockers, and kinins all increase papillary blood flow, RIHP and promote sodium excretion; whereas, inhibitors of NO and PGE2, or stimulation of the renal nerves lowers medullary blood flow, RIHP and sodium excretion. More recently, compounds have been infused directly into the renal medulla of rats to determine whether changes in medullary hemodynamics are sufficient to alter arterial pressure. Infusion of LNAME or a V1 agonist lowered medullary blood flow and produced sustained hypertension; whereas, medullary infusion of captopril increased medullary blood flow and lowered arterial pressure in SHR. These studies further support the view that the medullary circulation plays an important role in the regulation of sodium excretion and the control of arterial pressure.