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Cyclooxygenase-1 inhibition attenuates angiotensin II-salt hypertension and neurogenic pressor activity in the rat.
Am J Physiol Heart Circ Physiol. 2013 Nov 15; 305(10):H1462-70.AJ

Abstract

Cyclooxygenase (COX)-derived prostanoids contribute to angiotensin II (ANG II) hypertension (HTN). However, the specific mechanisms by which prostanoids act are unclear. ANG II-induced HTN is caused partly by increased sympathetic nervous system activity, especially in a setting of high dietary salt intake. This study tested the hypothesis that COX-derived prostanoids cause ANG II-salt sympathoexcitation and HTN. Experiments were conducted in conscious rats. Infusion of ANG II (150 ng·kg(-1)·min(-1) sc) caused a marked HTN in rats on 2% salt diet, but a much smaller increase in blood pressure in rats on 0.4% salt diet. The nonselective COX inhibitor ketoprofen (2 mg/kg sc) given throughout the ANG-II infusion period attenuated HTN development in rats on 2% NaCl diet, but not in rats on 0.4% NaCl diet. The acute depressor response to ganglion blockade was used to assess neurogenic pressor activity in rats on 2% NaCl diet. Ketoprofen-treated rats showed a smaller fall in arterial pressure in response to ganglion blockade during ANG-II infusion than did nontreated controls. In additional experiments, ketoprofen-treated rats exhibited smaller increases in plasma norepinephrine levels and whole body norepinephrine spillover than we previously reported in ANG II-salt HTN. Finally, the effects of the selective COX-1 inhibitor SC560 (10 mg·kg(-1)·day(-1) ip) and the selective COX-2 inhibitor nimesulide (10 mg·kg(-1)·day(-1) ip) were investigated. Treatment with SC560 but not nimesulide significantly reduced blood pressure and the depressor response to ganglion blockade in ANG II-salt HTN rats. The results suggest that COX-1 products are critical for sympathoexcitation and the full development of ANG II-salt HTN in rats.

Authors+Show Affiliations

Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

24014677

Citation

Asirvatham-Jeyaraj, Ninitha, et al. "Cyclooxygenase-1 Inhibition Attenuates Angiotensin II-salt Hypertension and Neurogenic Pressor Activity in the Rat." American Journal of Physiology. Heart and Circulatory Physiology, vol. 305, no. 10, 2013, pp. H1462-70.
Asirvatham-Jeyaraj N, King AJ, Northcott CA, et al. Cyclooxygenase-1 inhibition attenuates angiotensin II-salt hypertension and neurogenic pressor activity in the rat. Am J Physiol Heart Circ Physiol. 2013;305(10):H1462-70.
Asirvatham-Jeyaraj, N., King, A. J., Northcott, C. A., Madan, S., & Fink, G. D. (2013). Cyclooxygenase-1 inhibition attenuates angiotensin II-salt hypertension and neurogenic pressor activity in the rat. American Journal of Physiology. Heart and Circulatory Physiology, 305(10), H1462-70. https://doi.org/10.1152/ajpheart.00245.2013
Asirvatham-Jeyaraj N, et al. Cyclooxygenase-1 Inhibition Attenuates Angiotensin II-salt Hypertension and Neurogenic Pressor Activity in the Rat. Am J Physiol Heart Circ Physiol. 2013 Nov 15;305(10):H1462-70. PubMed PMID: 24014677.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cyclooxygenase-1 inhibition attenuates angiotensin II-salt hypertension and neurogenic pressor activity in the rat. AU - Asirvatham-Jeyaraj,Ninitha, AU - King,Andrew J, AU - Northcott,Carrie A, AU - Madan,Shivanshu, AU - Fink,Gregory D, Y1 - 2013/09/06/ PY - 2013/9/10/entrez PY - 2013/9/10/pubmed PY - 2014/1/10/medline KW - angiotensin II KW - cyclooxygenase KW - hypertension KW - salt KW - sympathetic SP - H1462 EP - 70 JF - American journal of physiology. Heart and circulatory physiology JO - Am. J. Physiol. Heart Circ. Physiol. VL - 305 IS - 10 N2 - Cyclooxygenase (COX)-derived prostanoids contribute to angiotensin II (ANG II) hypertension (HTN). However, the specific mechanisms by which prostanoids act are unclear. ANG II-induced HTN is caused partly by increased sympathetic nervous system activity, especially in a setting of high dietary salt intake. This study tested the hypothesis that COX-derived prostanoids cause ANG II-salt sympathoexcitation and HTN. Experiments were conducted in conscious rats. Infusion of ANG II (150 ng·kg(-1)·min(-1) sc) caused a marked HTN in rats on 2% salt diet, but a much smaller increase in blood pressure in rats on 0.4% salt diet. The nonselective COX inhibitor ketoprofen (2 mg/kg sc) given throughout the ANG-II infusion period attenuated HTN development in rats on 2% NaCl diet, but not in rats on 0.4% NaCl diet. The acute depressor response to ganglion blockade was used to assess neurogenic pressor activity in rats on 2% NaCl diet. Ketoprofen-treated rats showed a smaller fall in arterial pressure in response to ganglion blockade during ANG-II infusion than did nontreated controls. In additional experiments, ketoprofen-treated rats exhibited smaller increases in plasma norepinephrine levels and whole body norepinephrine spillover than we previously reported in ANG II-salt HTN. Finally, the effects of the selective COX-1 inhibitor SC560 (10 mg·kg(-1)·day(-1) ip) and the selective COX-2 inhibitor nimesulide (10 mg·kg(-1)·day(-1) ip) were investigated. Treatment with SC560 but not nimesulide significantly reduced blood pressure and the depressor response to ganglion blockade in ANG II-salt HTN rats. The results suggest that COX-1 products are critical for sympathoexcitation and the full development of ANG II-salt HTN in rats. SN - 1522-1539 UR - https://www.unboundmedicine.com/medline/citation/24014677/Cyclooxygenase_1_inhibition_attenuates_angiotensin_II_salt_hypertension_and_neurogenic_pressor_activity_in_the_rat_ L2 - http://journals.physiology.org/doi/full/10.1152/ajpheart.00245.2013?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -