title: Deficient production of nitric oxide induces volume-dependent hypertension.
abstract: OBJECTIVE
  To study the influence of nitric oxide on renal function.
  
  
  METHODS
  Nitric oxide synthesis was inhibited and the effects on renal parameters were determined.
  
  
  METHODS
  Nitric oxide synthesis was progressively blocked by the intravenous administration of increasing doses of NG-nitro-arginine methylester (L-NAME) and then (c)GMP was administered.
  
  
  RESULTS
  The blockade of nitric oxide synthesis first induced a marked fall in urinary sodium excretion, and later, a sustained increase in mean arterial pressure. These effects were reversed by 8-bromide cGMP. Nitric oxide-dependent cGMP formation was higher in the inner medulla than in any other part of the renal parenchyma, and the inhibition of nitric oxide synthesis significantly decreased both pressure- and volume expansion-induced natriuresis.
  
  
  CONCLUSIONS
  Both the natriuretic and vasodilator tone maintained by nitric oxide are ultimately due to the production of cGMP. Nitric oxide-induced formation of cGMP appears to be the major factor that links changes in renal medullary circulation to those of sodium excretion. Sufficient inhibition of nitric oxide synthesis to decrease sodium excretion without altering blood pressure induces volume-dependent hypertension because blood pressure is elevated by an increased sodium intake.
authors.affiliation: Department of Physiology and Biophysics, Mayo School of Medicine, Rochester, Minnesota.
authors.forename: V
authors.initials: V
authors.lastname: Lahera
authors.forename: J
authors.initials: J
authors.lastname: Salazar
authors.forename: M G
authors.initials: MG
authors.lastname: Salom
authors.forename: J C
authors.initials: JC
authors.lastname: Romero
mesh_terms: D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000378:metabolism; D005919:Glomerular Filtration Rate / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology; D007668:Kidney / Q000503:physiopathology; D019331:NG-Nitroarginine Methyl Ester; D009318:Natriuresis / Q000502:physiology; D009569:Nitric Oxide / Q000037:antagonists & inhibitors / Q000378:metabolism* / Q000502:physiology; D012079:Renal Circulation / Q000502:physiology
chemical_list: D009569:Nitric Oxide; D001120:Arginine; D019331:NG-Nitroarginine Methyl Ester