Efferent glomerular arteriolar constriction: a possible intrarenal hemodynamic defect in hypertension.
A variety of mechanisms involving the kidney subserve the control of arterial pressure and the development and maintenance of hypertension. The precise and direct delineation of intrarenal hemodynamic mechanisms has been possible only by micropuncture techniques. Since these methods can be used only in the anesthetized animal, intrarenal hemodynamic assessment in conscious intact experimental animals or patients with essential hypertension must be indirect. Using indirect methods, calculated pressures in our laboratory have demonstrated differences in intrarenal hemodynamics between SHR and normotensive WKY rats, notably enhanced responsiveness of the efferent arteriole to alpha adrenergic agonist stimulation. When the calcium antagonist diltiazem was administered to the SHR or to patients with essential hypertension, it effected an increased renal blood flow and a well-maintained glomerular filtration rate without hyperfiltration. These indirect data suggest that there may be an efferent arteriolar abnormality in genetically mediated hypertension that may be reversed with certain calcium antagonists.
Frohlich
E D
ED
Alton Ochsner Medical Foundation, New Orleans, Louisiana 70121.
D000818:Animals; D001160:Arterioles; D001783:Blood Flow Velocity; D001794:Blood Pressure; D004110:Diltiazem / Q000627:therapeutic use; D005260:Female; D005919:Glomerular Filtration Rate; D006339:Heart Rate; D006439:Hemodynamics; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D007678:Kidney Glomerulus / Q000098:blood supply* / Q000503:physiopathology; D008297:Male; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D014655:Vascular Resistance; D014661:Vasoconstriction
D004110:Diltiazem