Impaired renal autoregulation: implications for the genesis of hypertension and hypertension-induced renal injury.
In summary, autoregulation of the renal vasculature provides a mechanism by which renal function is maintained relatively constant despite variations in systemic blood pressure. This system also provides a means for changes in blood pressure to occur without causing inappropriate alterations in urinary NaCl excretion. Alterations in the autoregulatory response can have clinical consequences. Increased activity of the TGF mechanism may be causally related to the development of some forms of hypertension. Decreased activity of TGF or an impaired myogenic response may help explain the increased susceptibility that certain patient groups exhibit toward hypertension-induced renal injury. The aggressive treatment of hypertension in patients with impaired renal autoregulation may be associated with an increase in the serum creatinine concentration. As long as this increase is neither excessive nor progressive, physicians should not be dissuaded from trying to achieve newly established blood pressure goals.
Palmer
B F
BF
Department of Internal Medicine, University of Texas Southern Medical School, Dallas 75390, USA. biff.palmer@utsouthwestern.edu
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D005246:Feedback; D006706:Homeostasis; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D007668:Kidney / Q000293:injuries / Q000503:physiopathology*; D007676:Kidney Failure, Chronic / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D007678:Kidney Glomerulus / Q000503:physiopathology; D007684:Kidney Tubules / Q000503:physiopathology; D019001:Nitric Oxide Synthase / Q000502:physiology; D052248:Nitric Oxide Synthase Type I; D012018:Reflex / Q000502:physiology; D012084:Renin-Angiotensin System / Q000502:physiology
D000806:Angiotensin-Converting Enzyme Inhibitors; C496320:NOS1 protein, human; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I