Vasopressin in hyponatremia: what stimuli?

In hypoosmolar hyponatremia, vasopressin is commonly observed to be less than maximally suppressed. This is attributed to the presence of nonosmolar vasopressin stimuli. However, the exact relationship of nonsuppressed antidiuretic hormone to specific circulatory parameters is controversial. Therefore, in the present study, we examined this question in 100 hypoosmolar hyponatremic patients in the Department of Medicine. Despite plasma hypoosmolality, vasopressin was found to be measurable in 92% of patients. Seventy patients suffered from edematous disorders (congestive heart failure, cirrhosis) or volume contraction per se; in these patients we observed unequivocal, though indirect, evidence of advanced circulatory alterations. These were associated with hyponatremia and nonsuppressed vasopressin. However, the latter could not be related directly to a specific circulatory parameter such as mean arterial blood pressure, creatinine clearance, plasma renin activity (PRA), norepinephrine, or aldosterone. However, patients with nondetectable vasopressin (n = 8) differed significantly from those with high vasopressin concentrations (n = 8: PADH greater than 9 pg/ml); in the latter, pulse rate (104 +/- 3 vs. 82 +/- 5 beats/min), plasma urea concentration (90 +/- 5 vs. 32 +/- 5 mg/dl), plasma urate concentration (7.2 +/- 0.8 vs. 3.6 +/- 0.8 mg/dl), and PRA (36 +/- 7 vs. 9.5 +/- 4.6 ng AI/ml/h) were all significantly higher than in the former. It is concluded that, in hyponatremia, the relationship between circulatory impairment and vasopressin is complex.