Renal effects of converting enzyme inhibitors in hypertension and diabetes

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Recent studies in animal models suggest that glomerular capillary hyperperfusion and hypertension, rather than ischemia, cause renal injury. Interventions that control glomerular capillary hypertension may protect against progressive injury, even in the presence of continued systemic hypertension. In the absence of systemic hypertension, diabetes mellitus is a prominent clinical example of glomerular hypertension. Animal studies have shown that glomerular hemodynamic abnormalities, especially elevations in glomerular pressure, play an important role in the pathogenesis of diabetic glomerulopathy. A number of clinical observations suggest that angiotensin converting enzyme (ACE) inhibitors may delay the progression of diabetic nephropathy by their effects on renal hemodynamics. In experimental animals, comparisons between calcium channel blockers and ACE inhibitors have shown the latter to be more effective in protecting the kidneys. Preliminary clinical studies indicate that ACE inhibitors may have advantages in preserving renal function in hypertensive and diabetic patients with renal failure.

Original languageEnglish (US)
Pages (from-to)S11-S15
JournalJournal of Cardiovascular Pharmacology
Volume15
StatePublished - 1990
Externally publishedYes

Fingerprint

Enzyme Inhibitors
Hypertension
Kidney
Angiotensin-Converting Enzyme Inhibitors
Hemodynamics
Wounds and Injuries
Calcium Channel Blockers
Diabetic Nephropathies
Renal Insufficiency
Diabetes Mellitus
Ischemia
Animal Models
Pressure

Keywords

  • Angiotensin converting enzyme inhibitors
  • Diabetes mellitus
  • Hypertension
  • Renal disease

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Pharmacology

Cite this

Renal effects of converting enzyme inhibitors in hypertension and diabetes. / Anderson, Sharon.

In: Journal of Cardiovascular Pharmacology, Vol. 15, 1990, p. S11-S15.

Research output: Contribution to journalArticle

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