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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors studied the effect of sodium salicylate administered into different parts of the circulatory system on various cardiovascular, respiratory and glottic parameters in Pentobarbital-anaesthetized rabbits. The results show that apnoea, bradycardia and hypotension, followed by hypertension, can also be caused by the extrathoracic action of salicylate. Cardiovascular responses induced by injecting salicylate into the carotid circulation are qualitatively the same, even after vagotomy, as in injection into the femoral vein. Salicylate injected into the common carotid artery, the internal carotid artery or the femoral vein causes inspiratory apnoea in rabbits, with powerful electrical activity of the diaphragm and an intrapleural pressure shift to marked inspiratory values. Laryngoconstriction occurs simultaneously, despite inspiratory apnoea. The injection of salicylate into the common carotid artery after bilateral vagotomy induces expiratory (not inspiratory) apnoea, indicating that the vagi play an important role in the origination of inspiratory apnoea in rabbits.
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PMID:Cardiovascular, respiratory and glottic effects of sodium salicylate administered into different parts of the circulation in rabbits. 12 83

The expression of inducible nitric oxide synthase (iNOS) is a characteristic response to inflammation and can be inhibited with sodium salicylate. We used the cytokine-induced iNOS induction in cardiac fibroblasts as a model system in which to test the hypothesis that effects on mitogen-activated protein kinases (MAPKs) may explain the mechanism by which salicylate exerts its anti-inflammatory effects. Tumor necrosis factor-alpha (TNF-alpha) alone can induce extracellular signal-regulated kinase (ERK), p38 MAPK, and c-Jun N-terminal kinase activity in a rapid and transient manner, whereas interferon-gamma (IFN-gamma) can induce only ERK. The inhibition of either the ERK pathway or p38 MAPK activity with selective inhibitors blocked cytokine-induced iNOS protein and nitrite production. Salicylate treatment inhibited iNOS expression induced by TNF-alpha and IFN-gamma and attenuated the phosphorylation of ERK by TNF-alpha and IFN-gamma either alone or in combination. Salicylate had no obvious effect on the activation of p38 MAPK or c-Jun N-terminal kinase. The results showed that salicylate inhibited the phosphorylation of ERK and iNOS expression induced by cytokines in a dose-dependent manner and suggested that salicylate exerts its anti-inflammatory action in part through inhibition of the ERK pathway and iNOS induction.
Hypertension 1999 Dec
PMID:Salicylate inhibition of extracellular signal-regulated kinases and inducible nitric oxide synthase. 1060 Nov 28

-The anti-inflammatory effects of salicylate are well known, but the intracellular mechanisms underlying those effects remain to be clarified and are not explained solely by an influence on cyclooxygenase activity. In the present study, we have used cardiac fibroblasts stimulated by either angiotensin II (Ang II) or platelet-derived growth factor (PDGF) to demonstrate an inhibitory effect of salicylate on the phosphorylation of the nonreceptor tyrosine kinases, proline-rich tyrosine kinase 2 (PYK2) and c-Src, by immunoprecipitation and immunoblotting methods. This inhibition was dose dependent, with a clear effect observed at concentrations between 5 and 20 mmol/L salicylate. Intracellular Ca(2+) chelation and protein kinase C (PKC) inhibition reduced Ang II and PDGF-induced PYK2 and c-Src phosphorylation. Salicylate significantly inhibited the phosphorylation of both of the tyrosine kinases activated by either ionophore A23187 or thapsigargin treatment, which led to an elevation of cytosolic Ca(2+). Activation of PKC by phorbol ester phosphorylated both PYK2 and Src, and this effect also was attenuated by salicylate. In contrast, salicylate had no effect on either the transactivation of the epidermal growth factor receptor by Ang II or the phosphorylation of phospholipase C-gamma by PDGF. These studies indicate a novel site of action for salicylate on PYK2 and c-Src phosphorylation and suggest that this inhibitory effect on these important signaling intermediates may be through a Ca(2+)- and PKC-dependent mechanism.
Hypertension 2001 Jan
PMID:Salicylate Inhibits Phosphorylation of the Nonreceptor Tyrosine Kinases, Proline-Rich Tyrosine Kinase 2 and c-Src. 1120 70