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  • Title: Abnormal renal sodium handling in essential hypertension. Relation to failure of renal and adrenal modulation of responses to angiotensin II.
    Author: Hollenberg NK, Moore T, Shoback D, Redgrave J, Rabinowe S, Williams GH.
    Journal: Am J Med; 1986 Sep; 81(3):412-8. PubMed ID: 3752141.
    Abstract:
    This study assessed renal sodium handling in a group of patients with essential hypertension in whom control of the renal blood supply and aldosterone release by angiotensin II is abnormal ("non-modulating") because of recent evidence that these patients have sodium-sensitive hypertension. Sixty-one patients were studied, 25 as balance was achieved with a daily sodium intake of 10 meq and 36 after a shift from a 10 meq to 200 meq sodium intake for five days. Renal and adrenal responsiveness to angiotensin II was assessed by measurement of para-aminohippurate clearance and plasma aldosterone prior to and during the infusion of 3 ng/kg per minute of angiotensin II, to identify the non-modulator group (n = 32). The half-time of the exponential function relating sodium excretion to time during the three to five days when external balance was being achieved with a 10 meq sodium intake was 23.9 +/- 0.3 hours in 60 normal subjects, 24.5 +/- 1.8 hours in the patients with essential hypertension in whom renal responsiveness to angiotensin II was normal, and prolonged (p less than 0.001) to 36.6 +/- 2.1 hours in the non-modulating patients. A prolonged half-time suggests that, with a shift to a high sodium intake, more time will be required to achieve external sodium balance and at the expense of more retained sodium. During the shift from a 10 to 200 meq sodium intake, the non-modulator group showed a delayed rate at which external sodium balance was achieved, greater cumulative positive sodium balance, more weight gain, and a greater frequency of blood pressure rise. The abnormality in the rate at which external sodium balance is achieved in non-modulation results in a difference in total body sodium that varies with sodium intake and that may well contribute to, or cause, sodium-sensitive hypertension.
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