Autoregulation versus other vasoconstrictors in hypertension. A critical review.

SUMMARY Hypertension is a disease of relatively normal blood flow and increased vascular resistance. The search for neural and humoral vasoconstrictors to explain this pattern has not produced convincing evidence in most cases. Autoregulatory vasoconstriction is an alternative explanation supported by Borst, Ledingbam and others; the validity of this idea is strengthened by frequent observations of relatively normal cardiac output and blood flow distribution in hypertension. Autoregulatory vasoconstriction has been combined with concepts of renal excretory function to form the following theory: Renal excretion is determined by arterial pressure − pressure must be high enough to maintain salt and water balance − and autoregulation provides the hemodynamic pattern of vasoconstriction with normal flow. Several different types of experiments point to the kidney as the long-term controller of blood pressure. However, data relevant to the autoregulatory part of the theory are conflicting. In some experiments, autoregulation is suggested by changes in flow that precede changes in resistance. In other experiments, no change in flow has been observed. In some experiments, volume expansion appears to be an intermediary between kidney dysfunction and the autoregulatory response. In other instances, volumes are normal or low. Flow relative to metabolic needs, venous capacity, and the abruptness of the hypertension-producing perturbation become important considerations in understanding these results. The argument that autoregulation supplies vasoconstriction in most cases of hypertension is based on interpretation of many different observations that are unfortunately relatively indirect. Controversy over vasoconstrictor mechanisms in hypertension is fostered by a lack of direct experimental results either supporting or refuting the various possibilities.