Mechanisms affecting the development of renal cystic disease induced by diphenylthiazole

Kidney Int. 1988 Jun;33(6):1130-9. doi: 10.1038/ki.1988.121.

Abstract

To provide information on the possible influence that hypertension or its treatment might have on the development of cysts in autosomal dominant polycystic kidney disease, we studied the effects of the sodium content of the diet, DOCA-salt hypertension, renovascular hypertension, and the administration of enalapril or furosemide on the development of 2-amino-4-5-diphenylthiazole (DPT)-induced renal cystic disease. DOCA-salt hypertension caused vascular and glomerular lesions and proteinuria, but it did not enhance the development of cysts. Cytogenesis was enhanced in experimental conditions where the renin-angiotensin system is known to be activated. On the other hand, interventions known to suppress the renin-angiotensin system lessened the development of cysts. We hypothesize that this effect might be mediated by intrarenal angiotensin II and its capacity to promote cell growth and to control the postglomerular vascular resistances and the compliance of the renal interstitium.

MeSH terms

  • Animals
  • Desoxycorticosterone / toxicity
  • Enalapril / toxicity
  • Furosemide / toxicity
  • Hypertension / complications
  • Hypertension, Renovascular / complications
  • Male
  • Polycystic Kidney Diseases / chemically induced*
  • Polycystic Kidney Diseases / genetics
  • Rats
  • Rats, Inbred Strains
  • Renin-Angiotensin System
  • Sodium, Dietary / pharmacology
  • Thiazoles / toxicity*

Substances

  • Sodium, Dietary
  • Thiazoles
  • Desoxycorticosterone
  • Bax 439
  • Enalapril
  • Furosemide