Intravenous Angiotensin II infusion significantly suppressed plasma renin activity in normotensive and hypertensive controls, but not in patients with Type 2 diabetes and hypertension (p>0.77).
Observational (n=257)
Does intravenous Angiotensin II infusion suppress plasma renin activity differently in patients with Type 2 diabetes and hypertension compared to hypertensive and normotensive controls?
Patients with Type 2 diabetes and hypertension exhibit a blunted suppression of plasma renin activity in response to Angiotensin II infusion, suggesting altered intrarenal RAAS feedback.
p-value: p=> 0.77
We have documented, contrary to expectation, that the renin-angiotensin-aldosterone system (RAAS) is stimulated normally by restriction of sodium intake inpatients with Type 2 diabetes mellitus (DM) and hypertension. Conversely, plasma renin activity (PRA)is suppressed less than in normal subjects by a high-salt diet in these patients. Increasing plasma angiotensin II (Ang II) concentration through intravenous Ang II infusion also suppresses renin release, via the short feedback loop. In this study, we sought to ascertain whether the limited renin suppression in Type 2 diabetes mellitus via high-salt intake is a unique defect or part of a more generalised abnormality of PRA suppression. We studied 38 patients with Type 2 DM and hypertension, 158 hypertensive control patients, and 61 normotensive controls. All patients were studied while in metabolic balance on a 10 mEq sodium (Na) diet. The response to the Ang II infusion at 3 ng/kg/min for 45 minutes was measured. We found that PRA fell significantly in normal subjects, from 4.0 +/- 0.33 to 2.5 +/- 0.23 ngAngI/ml/hr (p=0.0056). In patients with essential hypertension, the Ang II infusion also led to a fall in PRA from 3.51 +/- 0.23 to 2.76 +/- 0.17 ng Angl/ml/hr(p=0.014). In patients with DM, despite a similar basal PRA (3.7 +/- 0.40 ng AngI/ml/hr), the infusion of Ang II did nor influence PRA significantly (3.43 +/- 0.42ng AngI/ml/hr; p > 0.77), though these patients had the most robust mean arterial pressure response. Our data are in complete accord with the concept of high intrarenal Ang II in DM and suggest lower systemic Ang II despite comparable PRA.
Gordon et al. (2000) conducted an observational in Type 2 diabetes mellitus and hypertension (n=257). Intravenous Angiotensin II (Ang II) infusion vs. Hypertensive and normotensive controls was evaluated on Change in plasma renin activity (PRA) (p=> 0.77). Intravenous Angiotensin II infusion significantly suppressed plasma renin activity in normotensive and hypertensive controls, but not in patients with Type 2 diabetes and hypertension (p>0.77).