Role of nitric oxide and prostanoids in attenuation of rapid baroreceptor resetting

Because the regulation of vascular function involves complex mutual interactions between nitric oxide (NO) synthase (NOS) and cyclooxygenase (COX) products, we examined the contribution of NO and prostanoids derived from the COX pathway in modulating aortic baroreceptor resetting during an acute (30...

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Veröffentlicht in:American journal of physiology. Heart and circulatory physiology 2006-03, Vol.59 (3), p.H1059
Hauptverfasser: Salgado, Maria Cristina O, Soraia V S Justo, Joaquim, Luis F, Fazan, Rubens, Salgado, Helio C
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Sprache:eng
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Zusammenfassung:Because the regulation of vascular function involves complex mutual interactions between nitric oxide (NO) synthase (NOS) and cyclooxygenase (COX) products, we examined the contribution of NO and prostanoids derived from the COX pathway in modulating aortic baroreceptor resetting during an acute (30 min) increase in arterial pressure in anesthetized rats. Increase in pressure was induced either by administration of the nonselective NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME) or aortic coarctation (COA) with or without treatment with the COX inhibitor indomethacin (INDO) or the selective neuronal NOS inhibitor 1-(2-trifluoromethylphenyl)imidazole (TRIM). The activity of the aortic depressor nerve and arterial pressure were simultaneously recorded, and the degree of resetting was determined by the shift of the pressure-nerve activity curve using the ratio [{Delta} systolic pressure at 50% of maximum baroreceptor activity/{Delta} systolic pressure] x 100. The magnitude of pressure rise was similar in the different groups (59 plus or minus 6, 53 plus or minus 5, 53 plus or minus 5, 45 plus or minus 5, 49 plus or minus 3, and 41 plus or minus 3 mmHg for COA, L-NAME, INDO+COA, INDO+L-NAME, TRIM+COA, and TRIM+INDO+COA, respectively, P = 0.27). The degree of resetting that occurred with L-NAME or COA combined with treatment with TRIM was attenuated compared with COA alone (7 plus or minus 4, 5 plus or minus 2, and 31 plus or minus 6%, respectively, P = 0.04). INDO failed to influence baroreceptor resetting to higher pressure but prevented L-NAME- and TRIM-induced effects (20 plus or minus 7, 21 plus or minus 8, and 32 plus or minus 6% for INDO+COA, INDO+L-NAME, and INDO+TRIM+COA, respectively; P = 0.38). Baroreceptor gain was affected only by L-NAME. These findings indicate that NO, probably from neuronal origin, may exert stimulatory influence on the degree of rapid baroreceptor resetting to hypertension that involves COX-derived prostanoids.[PUBLICATION ABSTRACT]
ISSN:0363-6135
1522-1539