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Oxonic acid-induced hyperuricemia elevates plasma aldosterone in experimental renal insufficiency.
J Hypertens. 2008 Aug; 26(8):1661-8.JH

Abstract

BACKGROUND

Hyperuricemia is associated with renal insufficiency and may predispose to Na retention and hypertension. Whether hyperuricemia plays a causal role in the pathogenesis of cardiovascular disease remains controversial.

OBJECTIVE

We examined the effects of hyperuricemia on circulating and renal components of the renin-angiotensin-aldosterone system in experimental renal insufficiency.

METHODS

Three weeks after 5/6 nephrectomy or sham-operation, rats were put on 2.0% oxonic acid diet for 9 weeks. Blood pressure was monitored using tail-cuff, and blood, urine, and kidney samples were taken, as appropriate. Kidney angiotensin-converting enzyme, angiotensin-converting enzyme 2 and angiotensin II receptors (AT1R, AT2R) were examined using real-time reverse transcriptase-PCR and autoradiography.

RESULTS

Oxonic acid diet increased plasma uric acid by 80-90 micromol/l, while blood pressure was elevated only in hyperuricemic 5/6 nephrectomy rats (18 mmHg). Creatinine clearance was reduced by 60% in both 5/6 nephrectomy groups and by 25% in hyperuricemic Sham rats. The 5/6 nephrectomy group showed over 90% suppression of plasma renin activity, whereas the Sham + oxonic acid diet group showed 1.2 and 1.4-fold, and 5/6 nephrectomy + oxonic acid diet group 2.5 and 2.3-fold increases in plasma renin activity and plasma aldosterone, respectively. Hyperuricemia increased K and decreased Na excretion in Sham and 5/6 nephrectomy rats, leading to a more than 1.6-fold increase in urine K to Na ratio. No changes in kidney angiotensin-converting enzyme, angiotensin-converting enzyme 2, AT1R or AT2R were detected that could explain the hyperuricemia-induced alteration in Na-K balance.

CONCLUSION

As oxonic acid diet increased plasma renin activity, plasma aldosterone, and urine K to Na ratio, these changes may play a significant role in the harmful cardiovascular actions of hyperuricemia.

Authors+Show Affiliations

Institute of Medical Technology, Department of Internal Medicine, University of Tampere, Tampere, Finland.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18622246

Citation

Eräranta, Arttu, et al. "Oxonic Acid-induced Hyperuricemia Elevates Plasma Aldosterone in Experimental Renal Insufficiency." Journal of Hypertension, vol. 26, no. 8, 2008, pp. 1661-8.
Eräranta A, Kurra V, Tahvanainen AM, et al. Oxonic acid-induced hyperuricemia elevates plasma aldosterone in experimental renal insufficiency. J Hypertens. 2008;26(8):1661-8.
Eräranta, A., Kurra, V., Tahvanainen, A. M., Vehmas, T. I., Kööbi, P., Lakkisto, P., Tikkanen, I., Niemelä, O. J., Mustonen, J. T., & Pörsti, I. H. (2008). Oxonic acid-induced hyperuricemia elevates plasma aldosterone in experimental renal insufficiency. Journal of Hypertension, 26(8), 1661-8. https://doi.org/10.1097/HJH.0b013e328303205d
Eräranta A, et al. Oxonic Acid-induced Hyperuricemia Elevates Plasma Aldosterone in Experimental Renal Insufficiency. J Hypertens. 2008;26(8):1661-8. PubMed PMID: 18622246.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oxonic acid-induced hyperuricemia elevates plasma aldosterone in experimental renal insufficiency. AU - Eräranta,Arttu, AU - Kurra,Venla, AU - Tahvanainen,Anna M, AU - Vehmas,Tuija I, AU - Kööbi,Peeter, AU - Lakkisto,Päivi, AU - Tikkanen,Ilkka, AU - Niemelä,Onni J, AU - Mustonen,Jukka T, AU - Pörsti,Ilkka H, PY - 2008/7/16/pubmed PY - 2008/9/16/medline PY - 2008/7/16/entrez SP - 1661 EP - 8 JF - Journal of hypertension JO - J Hypertens VL - 26 IS - 8 N2 - BACKGROUND: Hyperuricemia is associated with renal insufficiency and may predispose to Na retention and hypertension. Whether hyperuricemia plays a causal role in the pathogenesis of cardiovascular disease remains controversial. OBJECTIVE: We examined the effects of hyperuricemia on circulating and renal components of the renin-angiotensin-aldosterone system in experimental renal insufficiency. METHODS: Three weeks after 5/6 nephrectomy or sham-operation, rats were put on 2.0% oxonic acid diet for 9 weeks. Blood pressure was monitored using tail-cuff, and blood, urine, and kidney samples were taken, as appropriate. Kidney angiotensin-converting enzyme, angiotensin-converting enzyme 2 and angiotensin II receptors (AT1R, AT2R) were examined using real-time reverse transcriptase-PCR and autoradiography. RESULTS: Oxonic acid diet increased plasma uric acid by 80-90 micromol/l, while blood pressure was elevated only in hyperuricemic 5/6 nephrectomy rats (18 mmHg). Creatinine clearance was reduced by 60% in both 5/6 nephrectomy groups and by 25% in hyperuricemic Sham rats. The 5/6 nephrectomy group showed over 90% suppression of plasma renin activity, whereas the Sham + oxonic acid diet group showed 1.2 and 1.4-fold, and 5/6 nephrectomy + oxonic acid diet group 2.5 and 2.3-fold increases in plasma renin activity and plasma aldosterone, respectively. Hyperuricemia increased K and decreased Na excretion in Sham and 5/6 nephrectomy rats, leading to a more than 1.6-fold increase in urine K to Na ratio. No changes in kidney angiotensin-converting enzyme, angiotensin-converting enzyme 2, AT1R or AT2R were detected that could explain the hyperuricemia-induced alteration in Na-K balance. CONCLUSION: As oxonic acid diet increased plasma renin activity, plasma aldosterone, and urine K to Na ratio, these changes may play a significant role in the harmful cardiovascular actions of hyperuricemia. SN - 0263-6352 UR - https://www.unboundmedicine.com/medline/citation/18622246/Oxonic_acid_induced_hyperuricemia_elevates_plasma_aldosterone_in_experimental_renal_insufficiency_ L2 - https://doi.org/10.1097/HJH.0b013e328303205d DB - PRIME DP - Unbound Medicine ER -