Effects of C-type natriuretic peptide on vascular reactivity in hypertension. Participation of nitric oxide system and potassium channels

COSTA A.; CANIFFI C.; SUEIRO L; CERNIELO M; SUAREZ DI SALVO D; MENDES GARRIDO F; WENK S; ARRANZ C.

Londres

Congreso; 22nd European Meeting on Hypertension and Cardiovascular Prevention; 2012

European Society of Hypertension

The aim was to study the mechanisms involved in vascular relaxation induced by CNP and NO system participation in spontaneously hypertensive rats (SHR). Methods: Aorta segments of 3–5 mm from Wistar (W) and SHR, were suspended in Krebs solution (37°C, gassed 95% O2-5% CO2, pH: 7.4). The aortic rings were allowed to equilibrate for 60 min and readjusted to basal tension 1 g. Isometric tension (g) was recorded by a force-transducer, in presence of:  phenylephrine (PE, 10-7-10-5 M), CNP (10-12-10-6 M), L-NAME (NOS inhibitor, 10−5 M), indomethacin (Indo, cyclooxygenase inhibitor, 10−5 M) and tetraethylammonium (TEA, non selective K+ channel blocker, 1 mM) and/or in absence of endothelium (NoE). Endothelium integrity was verified with acetylcholine. Aortic NOS activity (pmol 14C L-citrulline/g tissue·min) was determined. Results: NOS activity was higher in SHR, and CNP increases NOS activity in both groups (W-basal: 202 ± 5; W-CNP: 315 ± 9*; SHR-basal: 356 ± 9*; SHR-CNP: 432 ± 10#; *p < 0.01 vs. W-basal, #p < 0.01 vs. SHR-basal) but the increase in SHR was lower than W (W(CNP-basal) = 113 ± 4 vs. SHR(CNPbasal) = 76 ± 6; p < 0.01; n = 8 rats/group). NOS blockade with L-NAME diminished basal NOS activity and revert CNP effects (data not shown). ANOVA followed by Bonferroni’s post hoc test.