Researchers found racial differences in a biochemical driver of hypertension that could be part of the explanation for the latter's higher prevalence in Black Americans.
Copeptin concentration -- a surrogate for vasopressin level -- was higher in Black Americans (median 7.4 vs 5.4 pmol/L for whites, P<0.001), a finding that persisted after adjustment for urine sodium and calculated osmolality (P=0.0012), according to a group led by Ronstan Lobo, MB, of the Mayo Clinic in Rochester, Minnesota, reporting during a poster session at this year's virtual Hypertension meeting of the American Heart Association.
"Higher copeptin values in Blacks could mean that they may have lower sodium excretion, which exacerbates the volume retention," according to the poster. "Their high volume state is corroborated by the significantly lower renin seen in Blacks vs whites."
Indeed, Black patients had less than half the renin activity of white people in the study (0.5 vs 1.2 ng/mL/h, P<0.001). They also had lower calculated plasma osmolality (280.8 vs 282.5 mOsm/kg, P<0.001).
Those with low renin hypertension are said to need a volume-depleting strategy to achieve blood pressure (BP) control.
Ultimately, differences in vasopressin apparently help to explain the differences in hypertensive phenotypes between racial groups, Lobo and colleagues concluded. "The underlying mechanisms require further study."
Samples for the study came from the older GERA I study. Participants included 230 Black and 206 white patients. Those with renal disease were excluded.
Lobo's team had frozen blood samples thawed and copeptin measured on an assay.
The antidiuretic hormone vasopressin increases water permeability via the aquaporin-2 channel and increases activity of the epithelial sodium channel in distal nephrons, favoring increased sodium retention. Copeptin is a fragment of pre-pro-arginine vasopressin that is larger and has a prolonged half-life -- thus easier to measure in the lab than vasopressin itself.
Investigators previously confirmed that concentration of copeptin matches that of vasopressin.
Based on this study, vasopressin appears to be one more way in which Black people would be more likely to have high BP caused by fluid retention, agreed J. David Spence, MD, of the Robarts Research Institute at University of Western Ontario, London, who was not involved with the study.
What's more, Spence said, it adds to two other known mechanisms for the lower plasma renin in Black patients: excess aldosterone secretion, and excess renal tubular absorption of sodium (due to changes in the function of the renal tubular epithelial sodium channel).
Genetics may explain why vasopressin values are higher in Blacks, Lobo's group suggested. One theory is that their ancestors evolved in warmer climates where dehydration is more common, so volume retention would be helpful. Faced with the contemporary American diet of high salt intake, however, this results in more sodium and water retention in Black people today.
That the study relied on frozen samples from nearly 20 years ago was a limitation of the present analysis. Additionally, the researchers calculated osmolality and not blood urea nitrogen.
![author['full_name']](https://clf1.medpagetoday.com/media/images/author/nicoleLou_188.jpg)
Disclosures
Lobo had no disclosures.
One study co-author reported consulting for most of the major diagnostic companies.
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