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Tuesday, 17 December 2013

The Effects of Hormone Prostacyclin(1)

Prostacyclin
Prostacyclin (or PGI2), also known as known as eicosanoids, a member of the family prostaglandins as a metabolite of arachidonic acid, inhibits platelet aggregation, and dilates blood vessels and is released by healthy endothelial cells and performs its function through a paracrine signaling cascade that involves G protein-coupled receptors on nearby platelets and endothelial cells(a).

1. Obesity and endothelial dysfunction
Obesity is frequently associated with endothelial dysfunction. In the study to investigate the role of the 'endothelial' MR in obesity-induced endothelial dysfunction, the earliest stage in atherogenesis, with C57BL/6 mice exposed to a normal chow diet (ND) or a high-fat diet (HFD) alone or in combination with the MR antagonist eplerenone (200 mg/kg/day) for 14 weeks, showed that Obesity-induced endothelial dysfunction depends on the 'endothelial' mineralocorticoid receptor (MR) and is mediated by an imbalance of oxidative stress-modulating mechanisms. Therefore, MR antagonists may represent an attractive therapeutic strategy in the increasing population of obese patients to decrease vascular dysfunction and subsequent atherosclerotic complications(1).

2.  Caloric restriction reverses high-fat diet-induced endothelial dysfunction
In the study to examine whether caloric restriction could reverse the detrimental vascular effects related to obesity with male C57Bl/6 mice were fed with normal-fat diet (fat 17%) or high-fat diet (fat 60%) for 150 days. After establishment of obesity at day 100, a subgroup of obese mice were put on caloric restriction (CR) (70% of ad libitum energy intake) for an additional 50 days. At day 100, aortic rings from obese mice receiving high-fat diet showed impaired endothelium-dependent vasodilation in response to acetylcholine (ACh), showed that Caloric restriction markedly attenuated vascular superoxide production. In obese mice on CR, endothelial denudation increased superoxide formation whereas vascular superoxide production was unaffected by L-NAME. Western blot analysis revealed decreased phosphorylated eNOS (Ser1177)-to-total eNOS expression ratio in obese mice as compared to lean controls, whereas the phospho-eNOS/NOS ratio in obese mice on CR did not differ from the lean controls. In conclusion, the present study suggests that caloric restriction reverses obesity induced endothelial dysfunction and vascular oxidative stress, and underscores the importance of uncoupled eNOS in the pathogenesis(2).

3. Prostacyclin receptor (IP-receptor) agonists anti-inflammatory and antiviral activity
Prostacyclin receptor (IP-receptor) agonists display anti-inflammatory and antiviral activity in cell-based assays and in preclinical models of asthma and chronic obstructive pulmonary disease. In the study to  extended these observations by demonstrating that IP-receptor activation also can enhance the ability of glucocorticoids to induce genes with anti-inflammatory activity, found that IP-receptor agonists can augment the ability of glucocorticoids to induce anti-inflammatory genes in human airway epithelial cells by activating a cAMP/PKA-dependent mechanism. This observation may have clinical relevance in the treatment of airway inflammatory diseases that are either refractory or respond suboptimally to glucocorticoids(3).

4. Synthesis of prostacyclin effect on the contractile activity of the inflamed porcine uterus
In the study to estimate the content of prostacyclin (PGI(2)), the levels of PGI synthase (PTGIS) and receptor (PTGIR) protein expression, and the cellular localization of these factors in the inflammatory-changed porcine uterus, showed that inflammation of the porcine uterus upregulates PGI(2) synthesis and that PGI(2) increases contractility, which suggests that PGI(2) might be essential for the course of uterine inflammation(4).

5. Rosuvastatin and PGI(2)-peroxisome proliferator-activated receptor
Statins are reported to alleviate renal fibrosis in animal models with ureteral obstruction.  Pressure force is an important mechanism contributing to induction and progression of tubulointerstitial fibrogenesis in ureteric obstruction. In the study to assess whether the influence of rosuvastatin on pressure-induced fibrotic responses in rat renal tubular cells (NRK-52E). We established an in vitro pressure culture system to study pressure-induced fibrotic responses in NRK-52E cells, indicated that rosuvastatin reduces pressure-induced fibrotic responses in renal tubular cells by enhancing the PGI(2)-peroxisome proliferator-activated receptor α pathway and reducing PGE(2) generation(5).

6. Prostacyclin and its prostacyclin receptor and cardio-protective effects
Prostacyclin and its prostacyclin receptor, the I Prostanoid (IP), play essential roles in regulating hemostasis and vascular tone and have been implicated in a range cardio-protective effects. In the study to investigate the influence of cholesterol on human IP [(h)IP] gene expression  in cultured vascular endothelial and platelet-progenitor megakaryocytic cells, showed that cholesterol can regulate hIP expression, which may, at least in part, account for the combined cardio-protective actions of low serum cholesterol through its regulation of IP expression within the human vasculature(6).

7. Thromboxane A2 and prostacyclin and endothelial dysfunction
Endothelial dysfunction participates in the pathogenesis of many cardiovascular disorders. In the study to assess whether cyclooxygenase-2 (COX-2) activation is involved in the effects of chronic aldosterone treatment on endothelial function of mesenteric resistance arteries (MRA) from Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR), showed that Aldosterone reduced acetylcholine relaxation in MRA from both strains. In MRA from both aldosterone-treated strains the COX-1/2 or COX-2 inhibitor (indomethacin and NS-398, respectively), TxA2 synthesis inhibitor (furegrelate), prostacyclin synthesis inhibitor (tranylcypromine) or TxA2/ PGH2 receptor antagonist (SQ 29 548), but not COX-1 inhibitor SC-560, increased acetylcholine relaxation. In untreated rats this response was increased only in SHR. Prostacyclin elicited a biphasic vasomotor response: lower concentrations elicited relaxation, whereas higher concentrations elicited contraction that was reduced by SQ 29 548. Aldosterone increased the acetylcholine-stimulated production of 6-oxo-PGF(1alpha) and TxB2 in MRA from both strains. COX-2 expression was higher in both strains of rats treated with aldosterone(7).

8. Prostacyclin in endothelial dysfunction
In the study to analyze the possible involvement of vasoconstrictors prostanoids on the reduced endothelium-dependent relaxations produced by chronic administration of aldosterone in Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR), indicated that chronic treatment with aldosterone was able to produce endothelial dysfunction through COX-2 activation in normotensive and hypertensive conditions. PGI2 seems to be the main factor accounting for endothelial dysfunction in hypertensive rats, whereas other prostanoids besides PGI2 appear to be involved in endothelial dysfunction under normotensive conditions(8).

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Sources
(a) http://en.wikipedia.org/wiki/Prostacyclin
(1) http://www.ncbi.nlm.nih.gov/pubmed/23594590
(2) http://www.ncbi.nlm.nih.gov/pubmed/20512454
(3) http://www.ncbi.nlm.nih.gov/pubmed/19880449
(4) http://www.ncbi.nlm.nih.gov/pubmed/23218395
(5) http://www.ncbi.nlm.nih.gov/pubmed/23276663
(6) http://www.ncbi.nlm.nih.gov/pubmed/22969152
(7) http://www.ncbi.nlm.nih.gov/pubmed/18500359
(8) http://www.ncbi.nlm.nih.gov/pubmed/15956108