There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.
Abstract
1. This study explored the hypothesis that atrial natriuretic peptide (ANP), brain
natriuretic peptide (BNP), and C-natriuretic peptide (CNP) have differing antiproliferative
and antihypertrophic effects on pulmonary artery (PA) and thoracic aorta (TA) smooth-muscle
cells (SMCs). 2. Cultured cells were exposed to 5% fetal calf serum (FCS) and angiotensin
II (A-II) to induce DNA and protein synthesis, respectively. 3. ANP (10(-7) M) significantly
reduced thymidine uptake in TA by 31% +/- 2% (P < or = 0.01) but not in PA (P > or
= 0.05). 4. In parallel experiments, BNP (10(-7) M) significantly reduced thymidine
uptake in TA (-22% +/- 5%, P < or = 0.01), but not in PA cells (P > or = 0.05). 5.
CNP (10(-7) M) did not significantly alter thymidine uptake in TA cells exposed to
FCS, but it did significantly reduce uptake in PA (-28.5% +/- 4%) 2(P < or = 0.05).
6. Blunting by ANP (10(-7) M) of the A-II (10(-8) M)-induced increase in protein synthesis
was significantly greater in PA than in TA cells. 7. However, BNP and CNP (10(-7)
M) exerted similar antihypertrophic effects on TA and PA cells exposed to A-II. 8.
The antiproliferative effects of BNP and ANP exceed those of CNP in TA SMCs, but CNP
appears to be the most effective antiproliferative agent in PA SMCs. In addition,
PA-derived SMCs are more sensitive to the antihypertrophic effects of ANP than TA-derived
cells, suggesting phenotypic differences. The findings indicate that the natriuretic
peptides may play complementary roles in modulating SMC proliferation and protein
synthesis.