Protective Importance of the Myogenic Response in the Renal Circulation

Abstract

Primary essential hypertension is second only to diabetic nephropathy as a etiology for end-stage renal disease.1 In addition, coexistent/superimposed hypertension plays a major role in the progression of most forms of chronic kidney disease (CKD), including diabetic nephropathy.2–5 Nevertheless, the individual risk is very low, with <1% of the hypertensive population developing end-stage renal disease. Such data indicate that there must be mechanisms that normally protect the kidneys from hypertensive injury of a severity sufficient to result in end-stage renal disease. The following Brief Review summarizes the evidence that indicates that the renal autoregulatory response, primarily mediated by the myogenic mechanism, is largely responsible for such protection. Moreover, the differing patterns of renal damage that are observed in clinical and experimental hypertension are best explained when considered in the context of alterations in the renal autoregulatory capacity. Recent data also indicate that hypertensive renal damage correlates most strongly with systolic blood pressure (BP).6–8 Accordingly, the review further emphasizes the kinetic characteristics of the renal myogenic response to oscillating BP signals that render it particularly capable of providing protection against systolic pressures. Most individuals with primary hypertension develop the modest vascular pathology of benign nephrosclerosis.5 The glomeruli are largely spared, and, therefore, proteinuria is not a prominent feature. Because it progresses fairly slowly with limited ischemic nephron loss, renal function is not seriously compromised, except in some genetically susceptible individuals or groups, such as blacks, in whom a more accelerated course may be seen.2–5 Thus, the slope of the relationship between renal damage and BP through most of the hypertensive range is fairly flat in individuals with benign nephrosclerosis.2–4 However, if the hypertension becomes very severe and exceeds a critical threshold, severe acute disruptive injury of malignant nephrosclerosis to the renal arteries and arterioles develops …