Skip to main content

Advertisement

SpringerLink
Log in

Protection from vascular risk in diabetic hypertension

  • Published:
Current Hypertension Reports Aims and scope Submit manuscript

Abstract

Diabetes mellitus is a metabolic disorder characterized by hyperglycemia and associated with a high incidence of complications affecting both the microvascular and the macrovascular systems. Macrovascular disease affects the coronary arteries, the cerebral vessels, and the large peripheral arteries of the lower extremities. Microangiopathy affects the kidneys, eyes, and nerves. Both forms of complication are major causes of death and disability in diabetes. The precise pathophysiology of these vascular complications is becoming better understood, but specific treatment and prevention remain complex.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Similar content being viewed by others

References and Recommended Reading

  1. The Diabetes Control and Complication Trial Research Group: The effect of intensive treatment of diabetes on the development and progression of long term complications in insulin dependent diabetes mellitus. N Engl J Med 1993, 329:977–986.

    Article  Google Scholar 

  2. Abouna GM, Al-Adnani MS, Kremer GD, et al.: Reversal of diabetic nephropathy in human cadaveric kidneys after transplantation into non-diabetic recipients. Lancet 1983, 2(suppl 8362):1274–1276.

    Article  PubMed  CAS  Google Scholar 

  3. Peterson MR, Vine AK: Progression of retinopathy after pancreas transplantation. The University of Michigan Pancreas Transplant Evaluation Committee. Ophthalmology 1990, 97:496–500.

    Google Scholar 

  4. Tuck ML, Corry DB: Pathophysiology and management of hypertension in diabetes. Annu Rev Med 1991, 42:533–548.

    Article  PubMed  CAS  Google Scholar 

  5. Corry DB, Tuck ML: Hypertension and diabetes. Sem Nephrol 1991, 5:561–570.

    Google Scholar 

  6. Henrion D, Laher I: Insulin potentiates norepinephrineinduced vascular tone by activation of protein kinase C and tyrosine kinase. Can J Physiol Pharmacol 1994, 72:849–854.

    PubMed  CAS  Google Scholar 

  7. Kelleher C, Kingston S, Barry SM, et al.: Hypertension in diabetic clinic patients and their siblings. Diabetologia 1998, 31:76–81.

    Article  Google Scholar 

  8. Ferris JB, O’Hare JA, Kelleher CM, et al.: Diabetic control and the renin-angiotensin system, catecholamines and blood pressure. Hypertension 1985, 7(suppl 2):58–63.

    Google Scholar 

  9. Anderson EA, Mark AL: The vasodilator action of insulin. Implications for the insulin hypothesis of hypertension. Hypertension 1993, 21:136–141.

    PubMed  CAS  Google Scholar 

  10. Yamaguchi T, Omaha K, Takayanagi R, et al.: Enhanced secretion of endothelin-1 by elevated glucose levels from cultured bovine aortic endothelial cells. FEBS Lett 1990, 267:16–18.

    Article  Google Scholar 

  11. Kamal K, Du W, Mills I, Sumpio BE: Antiproliferative effect of elevated glucose in human microvascular endothelial cells. J Cell Biochem 1998, 71:49–501.

    Article  Google Scholar 

  12. Vlassara H. Brownlee M, Monague KR, et al.: Cachectin, TNF, and IL-I induced by glucose modified proteins: role in normal tissue remodeling. Science 1998, 240:1546–1548.

    Article  Google Scholar 

  13. Bucola R, Tracey KJ, Cerami A: Advanced glycosylation products quench nitric oxide and mediate defective endothelium-dependent vasodilatation in experimental diabetes. J Clin Invest 1991, 87:432–438.

    Article  Google Scholar 

  14. Muntzel MS, Hamidou I, Barrett S: Metformin attenuates salt-induced hypertension in spontaneously hypertensive rats. Hypertension 1999, 33:1135–1140.

    PubMed  CAS  Google Scholar 

  15. Stern N, Tuck ML: Diabetes and hypertension. In Diabetes Mellitus: A Fundamental and Clinical Text. Edited by LeRoith D, Olefsky JM, Taylor S. New York: Lippincott-Raven; 1996:357–372.

    Google Scholar 

  16. Marre M, Bernadet P, Gallois Y, et al.: Relationship between angiotensin 1 converting enzyme gene polymorphism, plasma levels and diabetic retinal and renal complications. Diabetes 1994, 48:384–388.

    Article  Google Scholar 

  17. UK Prospective Diabetes Study Group: Tight blood pressure control and risk of macrovascular complications in type 2 diabetes: UKPDS 38. Br Med J 1998, 317:703–713.

    Google Scholar 

  18. Hansson L, Zanchetti A, Carruters SG, et al.: Effects of intensive blood pressure lowering and low dose aspirin in patients with hypertension: principal results of the Hypertension Optimal Treatment (HOT) randomized trial. Lancet 1998, 351:1755–1762.

    Article  PubMed  CAS  Google Scholar 

  19. Tuomilehto J, Rastenyte D, Birkenhager WH, et al.: Effects of calcium-channel blockade in older patients with diabetes and systolic hypertension. Systolic Hypertension in Europe Trial Investigators. N Engl J Med 1999, 340:677–684.

    Article  PubMed  CAS  Google Scholar 

  20. Okubo S, Niimura F, Matsuoka T, et al.: Angiotensinogen gene null-mutant mice lack homeostatic regulation of glomerular filtration and tubular reabsorption. Kidney Int 1998, 53:617–625.

    Article  PubMed  CAS  Google Scholar 

  21. Danser AH, Derkx FH, Admiraal PJ, et al.: Angiotensin levels in the eye. Invest Ophthalmol Vis Sci 1994, 35:1008–1018.

    PubMed  CAS  Google Scholar 

  22. Wagner J, Jan Danser AH, Derkx FH, et al.: Demonstration of renin mRNA, angiotensinogen mRNA and angiotensin converting enzyme mRNA expression in the human eye: evidence for an intraocular renin-angiotensin system. Br J Ophthalmol 1996, 80:159–163. This study emphasizes the fact that the full renin angiotensin system is present in tissues of the eye.

    PubMed  CAS  Google Scholar 

  23. Makimattila S, Summanen P, Matinlauri I, et al.: Serum total renin: an independent marker of the activity and severity of retinopathy in patients with IDDM. Br J Ophtalmol 1998, 82:939–944.

    CAS  Google Scholar 

  24. Chase HP, Garg SK, Harris S, et al.: Angiotensin-converting enzyme inhibitor treatment of young normotensive diabetic subjects: a two-year trial. Ann Ophthalmol 1993, 25:284–289.

    PubMed  CAS  Google Scholar 

  25. Larsen M, Hommel E, Parving HH, Lund-Handersen H: Protective effect of captopril on the blood-retina barrier in normotensive insulin-dependent patients with nephropathy and background retinopathy. Graefes Arch Clin Exp Ophthalmol 1990, 228:505–509.

    Article  PubMed  CAS  Google Scholar 

  26. Ravid M, Savin H, Jutrin I, et al.: Long-term stabilizing effect of angiotensin-converting enzyme inhibition on plasma creatinine and on proteinuria in normotensive type II diabetic patients. Ann Intern Med 1993, 118:577–581.

    PubMed  CAS  Google Scholar 

  27. Chaturvedi N, Sjolie AK, Stephenson JM, et al.: Effect of lisinopril on progression of retinopathy in normotensive people with type 1 diabetes. Lancet 1998, 351:28–31. First study to show significant prevention of diabetic retinopathy by documented retinal photographs using an ACE inhibitor lisinopril 10–20 mg/d in normotensive type 1 diabetic patients treated for two years.

    Article  PubMed  CAS  Google Scholar 

  28. Poulsen PL, Bek T, Ebbehloj E, et al.: 24-h ambulatory blood pressure and retinopathy in normoalbuminuric IDDM patients. Diabetologia 1998, 41:105–110.

    Article  PubMed  CAS  Google Scholar 

  29. The United States Renal Data System: USRDS Annual Data Report. Bethesda: The National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases; 1995.

  30. Nelson RG, Bennett PH, Beck GJ et al.: Development and progression of diabetic nephropathy in Pima Indians with non-insulin-dependent diabetes mellitus. N Engl J Med 1996, 335:1636–1642.

    Article  PubMed  CAS  Google Scholar 

  31. Neil AM, Hawkins M, Potock M, et al.: A prospective population-based study of microalbuminuria as a predictor of mortality in NIDDM. Diabetes Care 1993, 16:996–1003.

    Article  PubMed  CAS  Google Scholar 

  32. Ibrahim HN, Rosenberg ME, Greene EL, et al.: Aldosterone is a major factor in the progression of renal disease. Kidney Int 1997, 52 (suppl 63):S115-S118.

    Google Scholar 

  33. Jacobsen P, Rossing K, Rossing P, et al.: Angiotensin converting gene polymorphism and ACE inhibition in diabetic nephropathy. Kidney Int 1998, 53:1002–1006.

    Article  PubMed  CAS  Google Scholar 

  34. Freire MBS, Ji L, Onuma T, et al.: Gender-specific association of M235T polymorphism in angiotensinogen gene and diabetic nephropathy in NIDDM. Hypertension 1998, 31:896–899.

    PubMed  CAS  Google Scholar 

  35. Brazy PC, Fitzwilliam JF: Progressive renal disease: role of race and antihypertensive medications. Kidney Int 1990, 37:1113–1119.

    PubMed  CAS  Google Scholar 

  36. Parving HH, Tarnow L, Rossing P: Renal protection in diabetes: an emerging role for calcium antagonists. Cardiology 1997, 88(Suppl 3):56–62.

    Article  PubMed  CAS  Google Scholar 

  37. US department of Health and Human Services, Public Health Service Centers for Disease Control: Surveillance for Diabetes Mellitus--United States, 1980–1989. MMWR CDC Surveill Summ 1993, 42:334(suppl 2):1–20.

    Google Scholar 

  38. Miller JA, Anacta LA, Cattran DC: Impact of gender on the renal response to angiotensin II. Kidney Int 1999, 55:278–285. This study indicates there may be different responses of renal hemodynamics to angiotensin II in men and woman. The findings could imply sex differences in the effects of the renin angiotensin system in the kidney and perhaps differences in responses to agents that inhibit the renin angiotensin system.

    Article  PubMed  CAS  Google Scholar 

  39. Koya D, King GL: Protein kinase C in diabetic renal involvement: the perspective of its inhibition. In The Kidney and Hypertension in Diabetes Mellitus. edn 4. Edited by Morgenson CE. Boston: Kluwer Academic Publishers; 1998: 263. Protein kinase C is emerging as one of the most important mediators of diabetic complications and its activity is stimulated by high glucose.

    Google Scholar 

  40. Murphy M, McGinty A, Godson C: Protein kinases C: potential targets for intervention in diabetic nephropathy. Curr Opin Nephrol Hypertens 1998, 7(suppl 5):563–570.

    PubMed  CAS  Google Scholar 

  41. Ishii H, Tada H, Isogai S: An aldose reductase inhibitor prevents glucose-induced increase in transforming growth factor-b and protein kinase C activity in cultured human mesangial cells. Diabetologia 1998, 41:362–364.

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Division of Nephrology, Olive View UCLA Medical Center, 14111 Olive View Drive, 91342, Sylmar, CA, USA

    Dalila B. Corry MD

  2. Division of Endocrinology, Veterans Affairs Greater Los Angeles Clinics, 91343, Sepulveda, CA, USA

    Michael L. Tuck MD

Authors
  1. Dalila B. Corry MD
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Michael L. Tuck MD
    View author publications

    You can also search for this author in PubMed Google Scholar

Rights and permissions

Reprints and permissions

About this article

Cite this article

Corry, D.B., Tuck, M.L. Protection from vascular risk in diabetic hypertension. Current Science Inc 2, 154–159 (2000). https://doi.org/10.1007/s11906-000-0075-2

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1007/s11906-000-0075-2

Keywords

Search

Navigation