Key result
Angiotensin II infusion increased renal vascular resistance more in men with higher initial blood pressure (p<0.002), indicating enhanced renal vascular reactivity in essential hypertension.
Why the study?
Does the renal hemodynamic response to subpressor doses of angiotensin II vary in relation to initial blood pressure in untreated men?
Does the renal hemodynamic response to subpressor doses of angiotensin II vary in relation to initial blood pressure in untreated men?
p-value: p=<0.002
Essential hypertension is associated with an increased reactivity and sensitivity of the renal vascular bed to angiotensin II, which may contribute to reduced sodium excretion and disease progression.
Supports renal vascular hyperreactivity in hypertension but does not establish causality; leaves open implications for progression and therapy.
The renal hemodynamic response to subpressor doses of angiotensin II (AII; 0.1 and 0.5 ng/min/kg) was investigated in untreated 49-year-old men (n = 50) representing a wide blood pressure range. Renal blood flow, renal vascular resistance (RVR), glomerular filtration rate (GFR), filtration fraction (FF), plasma renin activity (PRA), plasma AII, plasma aldosterone, and the urinary excretion of sodium and norepinephrine were studied. The higher the initial blood pressure the greater was the increase in RVR in response to AII infusion (p less than 0.002), indicating an increased renal vascular reactivity with increase in initial blood pressure. The AII infusion gave a significant rise in RVR in both the borderline and hypertensive group, but gave no increase in RVR in the normotensive group, implying an enhanced sensitivity of the renal vasculature in the borderline and hypertensive group. The increase in RVR was greater in the hypertensive than in the borderline group, i.e., the hypertensives had a steeper dose-response curve than the borderline group, which points to the presence of structural vascular changes in the renal vessels in the hypertensives. The increase in RVR in response to AII was positively correlated to sodium intake and plasma aldosterone concentration, indicating that these two factors might modulate the renal vascular reactivity. These factors could, however, only partly explain that RVR increased more the higher the initial blood pressure. Thus, the results indicate that there is an increased reactivity of the renal vascular bed to AII in essential hypertension. The increased reactivity seems to be mediated through an increased sensitivity of the renal vasculature to AII in mild essential hypertension and also through the presence of structural vascular changes in established hypertension. These factors may lead to a reduced excretion of sodium and water and may therefore be of importance in the development and progression of essential hypertension.
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Ljungman et al. (1983) studied Essential hypertension (n=50). Angiotensin II vs. Normotensive group was evaluated on Increase in renal vascular resistance (RVR) in response to AII infusion (p=<0.002). Angiotensin II infusion increased renal vascular resistance more in men with higher initial blood pressure (p<0.002), indicating enhanced renal vascular reactivity in essential hypertension.
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