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Blood Pressure Control Early In Diabetes: A Balance Between Angiotensin Ii And Nitric Oxide
Author(s) -
Brands Michael W,
Fitzgerald Sharyn M
Publication year - 2002
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.2002.03619.x
Subject(s) - medicine , diabetes mellitus , blood pressure , endocrinology , nitric oxide , angiotensin ii , vasoconstriction , natriuresis , renin–angiotensin system , renal function
SUMMARY 1. Hyperglycaemia can lead to hypertension in long‐ standing diabetes through cumulative effects to cause progressive glomerular injury. However, it is not known how hyperglycaemia directly affects blood pressure control. Moreover, it has been difficult to isolate the actions of hyperglycaemia from other factors that can influence blood pressure. Recent studies at the earliest stages of type I diabetes have started to address these issues. 2. In humans and in animal models of type I diabetes, there is evidence that onset of hyperglycaemia can increase blood pressure. The increase is mild and has been linked to angiotensin (Ang) II, possibly due to slight overstimulation of the system in response to hyperglycaemia. 3. We have reported recently that onset of hyperglycaemia causes severe hypertension in rats that are treated chronically with N G ‐nitro‐ L ‐arginine methyl ester and the hypertension is accompanied by a progressive increase in AngII and absence of hyperfiltration. This suggests that nitric oxide (NO), at the early stages of diabetes, is important in mediating the increase in glomerular filtration rate and in preventing hypertension. 4. We propose a hypothesis based on these results that hyperglycaemia at the earliest stages of diabetes induces hyperfiltration and natriuresis and also activates a compensatory hypertensive stimulus (likely AngII) in an attempt to maintain normal blood pressure. A critical balance exists between these forces and NO plays a pivotal role by attenuating AngII‐ mediated renal vasoconstriction and facilitating the increase in glomerular filtration rate.