Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.6.1.2 (guanylate cyclase)
 8,497 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two phenomena may lead to an increase in intracellular calcium concentration of vascular smooth muscle cells: an increase in the permeability of the cell membrane to Ca2+ ions; liberation of Ca2+ ions from the intracellular reservoirs. The calcium channels of smooth muscle are varied. There are two types of voltage operated calcium channels: the fast (T) and the slow (L) channels. The calcium channels activated by extracellular membrane receptors are not voltage dependent. Only the L calcium channels are sensitive to dihydropyridines. The liberation of Ca2+ from the sarcoplasmic reticulum which is the intracellular reservoir of calcium can be controlled by two different mechanisms: a direct mechanism by the influx of Ca2+ into the cell through the voltage-operated channels; by the intermediary of a second intracellular messenger. High conductance calcium channels controlled by cytosolic Ca2+ and by IP2 have been demonstrated on the membrane of the sarcoplasmic reticulum. The contraction of smooth muscle may therefore be regulated directly through control of the phosphorylation of the contractile proteins by the intermediary of the systems of adenylate and guanylate cyclase.
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PMID:[The excitation-contraction coupling of the vascular smooth muscle cells]. 164 54

The ability of ANP to inhibit the hydrolysis of phosphoinositides was examined in [3H] myoinositol-labeled intact murine Leydig tumor (MA-10) cells. Arginine vasopressin (AVP) stimulated the formation of inositol monophosphate (IP1), inositol bisphosphate (IP2), and inositol trisphosphate (IP3) both in a time-and dose-dependent manner in MA-10 cells. ANP inhibited the AVP-induced formation of IP1, IP2, and IP3 in these cells. The inhibitory effect of ANP on the AVP-stimulated formation of IP1, IP2, and IP3 accounted for 30%, 38% and 42%, respectively, which was observed at the varying concentrations of AVP. ANP caused a dose-dependent attenuation in AVP-stimulated production of IP1, IP2 and IP3 with maximum inhibition at 100 nM concentration of ANP. The production of inositol phosphates was inhibited in the presence of 8-bromo cGMP in a dose-dependent manner, whereas dibutyryl-cAMP had no effect on the generation of these metabolites. The LY 83583, an inhibitor of guanylyl cyclase and cGMP production, abolished the inhibitory effect of ANP on the AVP-stimulated production of inositol phosphates. Furthermore, 10 microM LY 83583 also inhibited the ANP-stimulated guanylyl cyclase activity and the intracellular accumulation of cGMP by more than 65-70%. The inhibition of cGMP-dependent protein kinase by H-8, significantly restored the levels of AVP-stimulated inositol phosphates in the presence of either ANP or exogenous 8-bromo cGMP. The results of this study suggest that ANP exerts an inhibitory effect on the production of inositol phosphates in murine Leydig tumor (MA-10) cells by mechanisms involving cGMP and cGMP-dependent protein kinase.
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PMID:Atrial natriuretic peptide inhibits the phosphoinositide hydrolysis in murine Leydig tumor cells. 881 70