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Effects of C‐natriuretic peptide in resistance and conduit arteries of the rat.
Author(s) -
Aaronson Philip,
Teague Bonnie,
Bell Robert,
Lewis Tristan,
Robertson Tom,
Shattock Michael
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1242-a
C‐type natriuretic peptide (CNP) is an endothelium‐derived relaxing factor thought to act on vascular smooth muscle via NPR‐B and/or NPR‐C receptors, although its mechanism of action is controversial. We studied the response to CNP in rat mesenteric resistance arteries (RMA), superior mesenteric arteries (SMA) isolated coronary arteries and the perfused rat heart using the small vessel myograph and the Langendorff isolated heart preparation. CNP (1–1000nM) failed to induce a relaxation in the RMA, and coronary arteries and did not alter perfusion pressure in the perfused rat heart, but caused a substantial transient relaxation in the SMA. Relaxation was insensitive to the combination of TRAM‐34 (1μM) and apamin (100nM) and pre‐treatment with pertussis toxin (400ng/ml) but was antagonized by 25mM K + , the combination of Ba 2+ (10μM) and ouabain (100μM) and the BKCa channel inhibitor iberiotoxin (100nM), which had no effect on ACh‐induced relaxations. The NPR‐C agonist cANF (1μM) had no effect in either the RMA or SMA, suggesting that CNP was acting through the NPR‐B receptor in the SMA. Relaxation was insensitive to the protein kinase G inhibitor KT5823 (2μM) but was abolished by the phospholipase C antagonist U73122 (5μM) and by [Ca 2+ ] i store releasing agent caffeine (0.5mM). The results suggest that CNP relaxes the SMA via the NPR‐B receptor, thereby opening BK Ca channels thus inducing hyperpolarization and relaxation. Activation of the BK Ca channels may occur via vectorial release of Ca 2+ towards the sarcolemma.