原创力文档role of 20-hydroxyeicosatetraenoic acid in mediating hypertension in response to chronic renal medullary endothelin type b receptor blockade20-hydroxyeicosatetraenoic酸的作用在调节高血压应对慢性肾髓内皮素b型受体封锁.pdfVIP
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role of 20-hydroxyeicosatetraenoic acid in mediating hypertension in response to chronic renal medullary endothelin type b receptor blockade20-hydroxyeicosatetraenoic酸的作用在调节高血压应对慢性肾髓内皮素b型受体封锁
Role of 20-Hydroxyeicosatetraenoic Acid in Mediating
Hypertension in Response to Chronic Renal Medullary
Endothelin Type B Receptor Blockade
Joshua S. Speed1,2, Eric M. George1,2, Marietta Arany1,2, Kathy Cockrell1,2, Joey P. Granger1,2*
1 Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, United States of America, 2 Center for Excellence in
Cardiovascular–Renal Research, University of Mississippi Medical Center, Jackson, Mississippi, United States of America
Abstract
Background: The renal medullary endothelin (ET-1) system plays an important role in the control of sodium excretion and
arterial pressure (AP) through the activation of renal medullary ET-B receptors. We have previously shown that blockade of
endothelin type B receptors (ET-B) leads to salt-sensitive hypertension through mechanisms that are not fully understood.
One possible mechanism is through a reduction in renal medullary production of 20-hydroxyeicosatetraenoic acid (20-
HETE). 20-HETE, a metabolite of arachidonic acid, has natriuretic properties similar to ET-B activation. While these findings
suggest a possible interaction between ET-B receptor activation and 20-HETE production, it is unknown whether blockade
of medullary ET-B receptors in rats maintained on a high sodium intake leads to reductions in 20-HETE production.
Methodology/Principal Findings: The effect of increasing sodium intake from low (NS = .8%) to high (HS = 8%) on renal
medullary production of 20-HETE in the presence and absence of renal medullary ET-B receptor antagonism was examined.
Renal medullary blockade of ET-B receptors resulted in salt sensitive hypertension. In control rats, blood pressure rose from
112.862.4 mmHg (NS) to 120.769.3 mmHg (HS). In contrast, when treated with an ET-B receptor blocker, blood pressure
was significantly elevated from 123.7 63.2 (NS) to 1
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