{'fraction_non_alphanumeric': 0.08133669609079446, 'fraction_numerical': 0.05485498108448928, 'mean_word_length': 4.588028169014085, 'pattern_counts': {'":': 0, '<': 3, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Nitric oxide (NO) released from a new NO donor has lower activity in vascular smooth muscle cells from renal hypertensive rat

Increased production of superoxide anion (O2−) reduces the biovailability of NO released by the new NO donor cis‐[Ru(bpy)2(py)NO](PF6)2 (RUNOCL) in rat aortic smooth muscle cells (SMC). NO is a messenger molecule that plays an important role in the control of vascular tone due to the activation of soluble guanylyl cyclase (sGC)‐ cGMP‐ protein kinase G pathway that causes the decrease of cytosolic Ca2+concentration ([Ca2+]c). This study aimed to investigate the effect of the NO released from RUNOCL on the [Ca2+]c in SMC from normotensive (2K) and renal hypertensive rats (2K‐1C). [Ca2+]c, [NO]c and [O2−]c were measured with fluorescent probes FLUO‐3AM (510 nm), DAF‐2DA (545 nm) and DHE (595 nm), respectively, excited by 488 nm using a laser scanning confocal microscopy. [NO]c released from RUNOCL (10 μmol/L) was greater in 2K cells (15.9±0.6%) than in 2K‐1C cells (10.9±1.1%, n=3, P<0.001). On the other hand, in 2K‐1C cells the basal [O2−] was 2.6 times greater than in 2K cells (P<0.05). RUNOCL decreased [Ca2+]c from 100% to 60.0±10%, n=3) in 2K cells and from 100% to 77.2 ± 2%, n=3 (P<0.001) in 2K‐1C cells. These results indicate that the NO donor RUNOCL has greater effect in reducing [Ca2+]c in 2K than in 2K‐1C cells. This impaired effect of the NO donor is related to the lower [NO]c available in 2K‐1C cells. It could be due to an increased production of O2− that reacts with NO reducing its bioavailability. Supported by FAPESP and CNPq.