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At least 1,117 records · Page 62Linked to original sources
PubMed2003

Dual effects of hexanol and halothane on the regulation of calcium sensitivity in airway smooth muscle.

BACKGROUND: Contraction of airway smooth muscle is regulated by receptor-coupled mechanisms that control the force developed for a given cytosolic calcium concentration (i.e., calcium sensitivity). Halothane antagonizes acetylcholine-induced increases in calcium sensitivity by inhibiting GTP-binding (G)-protein pathways. The authors tested the hypothesis that hexanol, like halothane, inhibits agonist-induced increases in calcium sensitivity in airway smooth muscle by inhibiting G-protein pathways. METHODS: Calcium sensitivity was assessed using alpha-toxin-permeabilized canine tracheal smooth muscle. In selected experiments, regulatory myosin light chain phosphorylation was also determined by Western blotting in the presence and absence of 10 mm hexanol and/or 100 microm acetylcholine. RESULTS: Hexanol (10 mm) and halothane (0.76 mm) attenuated acetylcholine-induced calcium sensitization by decreasing regulatory myosin light chain phosphorylation during receptor stimulation. Hexanol also inhibited increases in calcium sensitivity due to direct stimulation of heterotrimeric G-proteins with tetrafluoroaluminate but not with 3 microm GTPgammaS, consistent with prior results obtained with halothane. In contrast, in the absence of receptor stimulation, both compounds produced a small increase in calcium sensitivity by a G-protein-mediated increase in regulatory myosin light chain phosphorylation that was not affected by pertussis toxin treatment. CONCLUSIONS: The authors noted dual effects of hexanol and halothane. In the presence of muscarinic receptor stimulation, hexanol, like halothane, decreases calcium sensitivity by interfering with heterotrimeric G-protein function. However, in the absence of muscarinic receptor stimulation, hexanol and halothane slightly increase calcium sensitivity by a G-protein-mediated process not sensitive to pertussis toxin. Hexanol may represent a useful experimental tool to study the effect of anesthetics on heterotrimeric G-protein function.

Aluminum Compounds↗
PubMed1997

Nitric oxide induces heme oxygenase-1 gene expression and carbon monoxide production in vascular smooth muscle cells.

Since recent studies demonstrate that vascular smooth muscle cells synthesize two distinct guanylate cyclase-stimulatory gases, NO and CO, we examined possible regulatory interactions between these two signaling molecules. Treatment of rat aortic smooth muscle cells with the NO donors, sodium nitroprusside, S-nitroso-N-acetyl-penicillamine, or 3-morpholinosydnonimine, increased heme oxygenase-I (HO-1) mRNA and protein levels in a concentration and time-dependent manner. Both actinomycin D and cycloheximide blocked NO-stimulated HO-1 mRNA and protein expression. Nuclear run-on experiments demonstrated that NO donors increased HO-1 gene transcription between 3- and 6-fold. In contrast, NO donors had no effect on the stability of HO-1 mRNA. Incubation of vascular smooth muscle cells with the membrane-permeable cGMP analogues, dibutyryl cGMP and 8-bromo-cGMP, failed to induce HO-1 gene expression. Treatment of vascular smooth muscle cells with NO donors also stimulated the production and release of CO, as demonstrated by the CO-dependent increase in intracellular cGMP levels in coincubated platelets. Finally, incubating vascular smooth muscle cells with interleukin-1 beta and tumor necrosis factor-alpha induced NO synthesis and also significantly increased the level of HO-1 protein. The cytokine-stimulated production of both NO and HO-1 protein in smooth muscle cells was blocked by the NO synthase inhibitor methyl-L-arginine. These results demonstrate that exogenously administered or endogenously released NO stimulates HO-1 gene expression and CO production in vascular smooth muscle cells. The ability of NO to induce HO-catalyzed CO release from vascular smooth muscle cells provides a novel mechanism by which NO might modulate soluble guanylate cyclase and, thereby, vascular smooth muscle cell and platelet function.

Animals↗
PubMed1990

[Expression of oncogenes by smooth muscle cells in atherosclerotic lesions].

Smooth muscle cells in the thickened intima of the aorta also expressed sis, mye, and c-fos, in addition to collagen types I, III, IV and type V. In the cultures of smooth muscle cells isolated from human aorta, collagen I, III and gelatinase were produced without any other special conditions for the culture. In the presence of PDGF, collagen type V and collagenase production was detected in the culture. Oncogene expression was not detected in the cultured cells when tested by the indirect immunofluorescence technique. Immortalized smooth muscle cells with SV 40 expressed myc, SV 40 large T antigen, and p53 without inhibition of collagen and collagenolytic enzymes production.

Arteriosclerosis↗
PubMed1981

Effects of unsymmetrical ester substituted 1,4-dihydropyridine derivatives and their optical isomers on contraction of smooth muscle.

The optical isomers of two nifedipine-like 1,4-dihydropyridine derivates have been synthesised and tested in vitro. The (-)-isomer (S-configuration of both compounds) was more potent than the racemate, which in turn was more potent than the (+)-isomer (R-configuration). The S-configuration isomers are approximately ten times more potent that nifedipine, and may represent the optimal structure and configuration for binding to and inhibiting calcium channels.

Animals↗
PubMed1988

Angiotensin converting enzyme inhibitors (captopril, CGS14831 and CGS14824A) antagonise in vitro smooth muscle prostanoid synthesis: evidence for calcium channel blockade.

The present study investigated the effect of the angiotensin-converting enzyme (ACE) inhibitors, captopril, CGS14824A and CGS14831 on in vitro rat aortic and urinary bladder prostacyclin (PGI2; measured as 6-oxo-PGF1 alpha by radioimmunoassay) synthesis. PGI2 synthesis was stimulated with adrenaline (aorta), carbachol (bladder), calcium ionophore A23187, arachidonate and trauma. The ACE inhibitors antagonised adrenaline-, carbachol- and A23187-stimulated PGI2 synthesis in the aorta and bladder (CGS14824A greater than captopril greater than CGS14831) but were without effect on trauma- or arachidonate-stimulated PGI2 synthesis. The patterns of inhibition of these ACE inhibitors, using the same stimulatory regimes, was very similar to those previously observed by us with known calcium channel blockers (nifedipine, verapamil). These data suggest that: (i) ACE inhibitors possess calcium channel blocking properties, which may be of relevance to the antihypertensive action of these drugs; and (ii) ACE inhibitors did not stimulate vascular PGI2 synthesis as has been previously suggested.

Angiotensin-Converting Enzyme Inhibitors↗