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Simonson DC. Etiology and prevalence of hypertension in diabetic patients. Diabetes Care. 1988;11(10):821-7doi: 10.2337/diacare.11.10.821.
Simonson, D. C. (1988). Etiology and prevalence of hypertension in diabetic patients. Diabetes care, 11(10), 821-7. https://doi.org/10.2337/diacare.11.10.821
Simonson, D C. "Etiology and prevalence of hypertension in diabetic patients." Diabetes care vol. 11,10 (1988): 821-7. doi: https://doi.org/10.2337/diacare.11.10.821
Simonson DC. Etiology and prevalence of hypertension in diabetic patients. Diabetes Care. 1988 Nov-Dec;11(10):821-7. doi: 10.2337/diacare.11.10.821. PMID: 3073072.
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Diabetes Care. 1988 Nov-Dec;11(10):821-7. doi: 10.2337/diacare.11.10.821.

Etiology and prevalence of hypertension in diabetic patients.

Diabetes care

D C Simonson

Affiliations

  1. Department of Internal Medicine, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215.

PMID: 3073072 DOI: 10.2337/diacare.11.10.821

Abstract

Data from several epidemiologic studies have suggested that the prevalence of hypertension in patients with diabetes mellitus is approximately 1.5-2.0 times greater than in an appropriately matched nondiabetic population. In patients with insulin-dependent diabetes mellitus (IDDM), hypertension is generally not present at the time of diagnosis. As renal insufficiency develops, blood pressure rises and may exacerbate the progression to end-stage renal failure. In non-insulin-dependent diabetes mellitus (NIDDM), many patients are hypertensive at the time of diagnosis. The incidence of hypertension in NIDDM is related to the degree of obesity, advanced age, and extensive atherosclerosis that is typically present, and it probably includes many patients with essential hypertension. Several other pathophysiologic mechanisms also contribute to the genesis and maintenance of hypertension in the patient with diabetes. Hyperglycemia and increases in total-body exchangeable sodium may lead to extracellular fluid accumulation and expansion of the plasma volume. In some patients, alterations in the function of the renin-angiotensin-aldosterone system and vascular sensitivity to vasoactive hormones may also play a role. It has recently been suggested that hyperinsulinemia and insulin resistance may also contribute to the maintenance of an elevated blood pressure because insulin is known to promote sodium retention and enhance sympathetic nervous system activity. The evidence for these hypotheses and their respective contributions to the etiology of hypertension in IDDM and NIDDM are discussed.

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