Long-term renal consequences of hypertension for normal and diseased kidneys

Abstract

Substantial evidence indicates that the adverse effects of hypertension on the kidney depend on the degree to which systemic blood pressure elevations are transmitted to the renal microvasculature. Such blood pressure transmission and consequent susceptibility to hypertensive renal damage is markedly exacerbated in states characterized by preglomerular vasodilation and an impairment of the normally protective renal autoregulatory mechanisms, e.g. diabetes or chronic renal disease. Moreover, this pathophysiology gives rise to the prediction that prevention of hypertension-induced barotrauma will require blood pressure to be reduced well into the normotensive range in such patients, as is being recognized in the currently recommended blood pressure goals. Agents that block the renin-angiotensin system should be preferred as initial therapy as they may provide additional risk reductions and minimize the potassium and magnesium depletion associated with the diuretic use usually necessary to achieve the lower blood pressure targets. The current failure to achieve optimal blood pressure reductions may be contributing not only to the still escalating incidence of end-stage renal disease in diabetic patients, but also to their greatly increased cardiovascular morbidity and mortality.

Renal autoregulation: new perspectives regarding the protective and regulatory roles of the underlying mechanisms

“…6, the BP threshold for injury in the 5/6 ablation model of CKD, which exhibits impaired autoregulation, is much lower than that of the SD or SHR (16,21). The pattern of injury in this model is predominantly that of focal and segmental glomerulosclerosis, consistent with elevated glomerular pressures (14,15,117). The role of hypertension in this lesion is further demonstrated by the fact that lowering BP results in proportionate reductions in injury (20,59).…”

“…The myogenic response involves a direct vasoconstriction of the afferent arteriole when this vessel is presented with an increase in transmural pressure. The current view is that these two mechanisms act in concert and that their primary role is to stabilize renal function by preventing pressure-induced fluctuations in RBF, GFR, and the delivery of filtrate to the distal tubule (distal delivery).Over the last two decades, evidence has accrued to indicate that this autoregulatory response plays a concurrent role in protecting the kidney from hypertensive injury (14,15). This view is based on the strong link between autoregulatory capacity and susceptibility to hypertensive injury.…”

“…Over the last two decades, evidence has accrued to indicate that this autoregulatory response plays a concurrent role in protecting the kidney from hypertensive injury (14,15). This view is based on the strong link between autoregulatory capacity and susceptibility to hypertensive injury.…”

Podocyte Purinergic P2X4 Channels Are Mechanotransducers That Mediate Cytoskeletal Disorganization

“…[4][5][6] There is also evidence for a damaging effect of hypertension in humans. 7 Until now, it has been completely unknown how podocytes sense the changes in glomerular pressure. It was postulated that TRPC6 channels involved in the pathogenesis of familial FSGS 8,9 may serve as mechanosensors in podocytes.…”

<b>Blood pressure, renal biochemical parameters and histopathology in an original rat model of essential hypertension (SHRSP/Kpo </b><b>strain) </b>

“…Furthermore, the 5-year survival rate of patients undergoing hemodialysis due to hypertensive renal disease is reportedly much lower than the rates of hemodialysis patients with other causes (28). Complications often associated with hypertensive nephropathy include glomerular damage, resulting in inflammatory responses and compromised kidney function that seem to be superimposed on the intrinsic phenotypes of the underlying disease (1). Therefore, the correct management of hypertensive renal disease is very Animal Experimentation of Kinki University.…”