ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2017) 50 OC4.4 | DOI: 10.1530/endoabs.50.OC4.4

The role of [ldquo]stress[rdquo] in aldosterone-mediated hypertension: circumstantial evidence from the [ldquo]stress subtraction[rdquo] experiment of adrenal vein sampling

Gregory Kline1, Pol Darras2, Alexander Leung1, Alex Chin1, Benny So1 & Daniel Holmes2

1University of Calgary, Calgary, Canada; 2University of British Columbia, Vancouver, Canada.

Background: Primary aldosteronism (PA) accounts for a significant proportion of patients with hypertension. There has been a focus on ACTH in the pathogenesis of aldosterone secretion even with suppressed renin. With the link between psychological stress and cardiovascular disease as well as the association between anxiety and PA, there may be broader neurohormonal “stress” stimuli that modulate aldosterone production in PA patients, beyond the HPA axis. PA patients who undergo adrenal venous sampling (AVS) receive sedation with narcotic and benzodiazepine. This induces a state of relaxation (“stress subtraction”) and permits observation of plasma aldosterone levels in such a setting.

Hypothesis: Dampening the neurohormonal stress response via narcotic/benzodiazepine results in a decrease in aldosterone production even among PA patients.

Patients: One hundred and thirty-one subjects undergoing AVS for PA (University of Calgary). 78 PA-AVS patients from University of British Columbia served as an independent confirmatory cohort.

Methods: Post narcotic/benzodiazepine morning IVC aldosterone (IVC-A) levels were compared to morning aldosterone levels drawn as an outpatient for the diagnosis of PA. IVC-A levels were correlated with IVC cortisol levels pre and post cosyntropin.

Results: Median AVS-IVC-A levels were significantly lower than outpatient measures (278 pmol/l vs 468 pmol/l, P<0.001). 72% of PA subjects had IVC-A levels more than 30% lower than outpatient measures. While the correlation between IVC-A and IVC cortisol was poor at baseline and post cosyntropin, the proportional rise in IVC-A and IVC- cortisol was modestly correlated (r=0.32, P<0.001). Repeat analysis on the UBC cohort produced nearly identical results (median 210 pmol/l vs 568 pmol/l, P<0.001) with 88% having IVC-A > 30% lower than the outpatient aldosterone.

Conclusions: Most PA patients have markedly lower IVC-A levels during AVS compared to those found during first outpatient diagnosis. In the absence of confounding medications, hypokalemia, circadian timing, postural variation and with low correlation to cortisol, this suggests alternate input from the CNS upon aldosterone secretion in PA.

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