The effects of adenosine and two analogs, L-phenylisopropyladenosine (L-PIA) and 5'-N-ethylcarboxamidoadenosine (NECA), on cAMP production and on platelet-derived growth factor (PDGF)-stimulated initiation of DNA synthesis in growth-arrested cultures of rat arterial smooth muscle cells (SMC) were st
Adenosine receptors, cyclic AMP accumulation, and DNA-synthesis in aortic smooth muscle cell cultures of adult and neonatal rats
✍ Scribed by Valérie Querol-Ferrer; Anna Hultgardh-Nilsson; Nils R. Ringertz; Jan Nilsson; Bror Jonzon
- Publisher
- John Wiley and Sons
- Year
- 1992
- Tongue
- English
- Weight
- 534 KB
- Volume
- 151
- Category
- Article
- ISSN
- 0021-9541
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✦ Synopsis
The effects of two adcnosinc analogs on cyclic AMP (CAMP) accumulation and DNA synthesis were studied in cultured smooth muscle cells (SMCs) isolated from adult and neonatal rat arteries. N-ethylcarboxamido adenosine (NECA) dosedependently increased intracellular CAMP levels and appeared to be more potent in adult than in neonatal SMCs. R-phenylisopropyl adenosine (R-PIA), in nanomolar concentrations, counteracted the increase in CAMP evoked by 10 p, M forskolin in adult but not in neonatal SMCs, indicating that the enhanced "A2" response sccn in adult SMCs was not due to a lack of " A l " receptors in these cultures. Binding experiments performed using the adenosine antagonist XAC did not reveal any differences in the number or affinity of the adenmine receptors between neonatal and adult SMCs. This indicates effects presumably on the G-protein level. A high capacity to spontaneously synthesize I f N A and a weak response to platelet-derived growth factor (PDGF) were seen in the neonatal SMCs. Furthermore, NECA had no effect on PDGF-induced DNA synthesis in these CFIIS. In contrast, adult SMCs presented a low rate of spontaneous DNA synthesis and a marked proliferative response to PDLF, which was inhibited by NECA. This inhibition paralleled the increase in CAMP elicited by NECA. Our findings suggest that neonatal and adult SMCs differ both in their response to growth factors and growth inhibitors. 0 I ~~~W ~I C Y -L ~S , In(
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