Prostaglandins smooth muscle cells

The secretion of extracellular matrix proteins is also a function of smooth muscle cells but, since it occurs concurrently with other activities, it does not seem to constitute a physiological state. However, the fraction of the cellular resources which are devoted to it must be regulated these regulatory mechanisms are virtually unknown. In addition, it should be anticipated that autocrine activity occurs as well, involving peptides, prostaglandins, cytokines, and nitric oxide. 

Ragolia, L., et al. (2003). Prostaglandin D2 synthase inhibits the exaggerated growth phenotype of spontaneously hypertensive rat vascular smooth muscle cells. J. Biol. Chem. 278, 22175-81. 

SIP induces hsp27 in AlO vascular smooth muscle cells and osteoblasts and amplifies inositol phosphates formation in response to vasopressin and prostaglandin F2c respectively (Kozawa et al, 1999a and b ... 

Fig. 3. Mechanisms of vasocontraction and vasorelaxation in endothelial and smooth muscle cells. COX cyclooxygenase, eNOS endothelial nitric oxide synthase, HO-1 heme oxygenase-1, EET epoxyeicosatrienoic acid, EDHF endothelium-derived hyperpolariz-ing factor, PGI2 prostaglandin I2, NO nitric oxide, CO carbon monoxide, PLC phospholipase C, IP3 inositol 1,4,5-trisphosphate, DAG diacylglycerol, ER/SR endo-plasmic/sarcoplasmic reticulum, AC adenylyl cyclase, cAMP cyclic adenosine monophosphate, sGC soluble guanylyl cyclase, cGMP cyclic guanosine monophosphate.

Asada, Y., Kisanuki, A., Hatakeyama, K., Takahama, S., Koyama, T., et al. 1994. Inhibitory effects of prostacyclin analogue, TFC-132, on aortic neointimal thickening in vivo and smooth muscle cell proliferation in vitro. Prostaglandins Leukotrienes Essent. Fatty Acids 51 245-248. 

Mcainelli TA, Mais DE, Oatis Jr JE, Crumbly III AJ, Halushka PV. Characterization of thromboxane Aj/Prostaglandin H receptos in human vascular smooth muscle cells. Life Sci 1990 46 1765-72... 

Nebigil C, Malik KU. Prostaglandin synthesis elicited by adrenergic stimuli is mediated via a2c and a1A adrenergic-receptors in cultured smooth-muscle cells of rabbit aorta. J Pharmacol Exp Therl992 260 849-858. 

Studies of the pathophysiology of acute renal failure has classically considered both tubular and vascular mechanisms [227,228]. In vitro techniques isolating either the vascular or tubular components have been developed. For example, the use of isolated proximal tubules in suspension or in culture allows the study of tubular mechanisms of injury in the absence of vascular factors [229] [230]. There are both in vitro and in vivo models to study vascular injury in the kidney. In vitro models include the study of vascular smooth muscle cells or endothelial cells in culture. In this section, the in vivo methods to evaluate the renal micro-circulation will be discussed. This is of relevance as many nephrotoxins exert their deleterious effects through pharmacologic actions on the resistance vasculature with parenchymal injury occurring as a consequence of ischemia. In clinical practice nephrotoxins may cause prerenal azotemia as a result of increased renal vascular resistance. Nephrotoxins that cause acute renal failure on a vascular basis include prostaglandin inhibitors e.g. aspirin, non-steroidal anti-... 

Kalyankrishna, S, Parmentier, J H, and Malik, K U, Arachidonic acid-derived oxidation products initiate apoptosis in vascular smooth muscle cells. Prostaglandins Other Lipid Mediat. 70 (2002) 13-29. 

RENAL ACTIONS OF VASOPRESSIN Several actions of vasopressin in the kidney involve both Vj and receptors. Vj receptors mediate contraction of mesangial cells in the glomerulus and vascular smooth muscle cells in the vasa recta and efferent arteriole. Indeed, Vj-receptor-mediated reduction of inner medullary blood flow contributes to the maximum concentrating capacity of the kidney (Figure 29-4). Vj receptors also stimulate prostaglandin synthesis by... 

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