These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Increased proximal tubular sodium reabsorption in hypertensive patients with type 2 diabetes. Author: Mbanya JC, Thomas TH, Taylor R, Alberti KG, Wilkinson R. Journal: Diabet Med; 1989; 6(7):614-20. PubMed ID: 2527703. Abstract: Hyperinsulinaemia and sodium retention have been studied in 22 Type 2 diabetic patients (10 normotensive, 12 hypertensive) and 10 normal control subjects matched for age, sex, and body mass index. Exchangeable sodium was similar in the three groups. Plasma renin activity and plasma angiotensin II were lower in both groups of diabetic patients than in the normal control subjects (p less than 0.01). Plasma atrial natriuretic peptide was increased in the hypertensive patients (7.3 +/- 1.1 vs normotensive 4.7 +/- 1.1 pmol l-1 and control 4.0 +/- 0.2 pmol l-1, p less than 0.01). Fractional lithium clearance, a measure of sodium clearance from the proximal tubule, was decreased (18.5 +/- 1.4, p less than 0.01) and fractional excretion of sodium in the distal tubule was increased (6.66 +/- 0.66, p less than 0.01) in untreated hypertensive diabetic patients compared with both normotensive diabetic patients (25.3 +/- 1.6 and 3.96 +/- 0.52 respectively) and normal control subjects (25.2 +/- 2.9 and 3.31 +/- 0.38, respectively). Fasting serum insulin was higher in hypertensive than in normotensive diabetic patients (18.5 +/- 3.0 vs 10.7 +/- 1.1 mU l-1, p less than 0.01) and higher in both groups than in normal control subjects (5.6 +/- 0.1 mU l-1, both p less than 0.01). Creatinine clearance was higher in both groups of diabetic patients than in normal control subjects (p less than 0.05). Thus there appears to be increased proximal renal tubular sodium reabsorption in these hypertensive Type 2 diabetic patients, matched by a reduction in distal sodium reabsorption so that net sodium excretion was maintained. This was associated with fasting hyperinsulinaemia.[Abstract] [Full Text] [Related] [New Search]