Detail of "66575-29-9"

Reference

A dose-response study of forskolin, stimulatory hormone, and guanosine triphosphate analog on adenylate cyclase from several sources

A dose-response study of forskolin, stimulatory hormone, and guanosine triphosphate analog on adenylate cyclase from several sources. Ruiz, Juan; Shi, Qi Huang; Ho, Ren Jye (Sch. Med., Univ. Miami, Miami, FL 33101, USA). Arch. Biochem. Biophys., 251(1), 139-47 (English) 1986. CODEN: ABBIA4. ISSN: 0003-9861. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Section cross-reference(s): 13 Relationships involving forskolin [66575-29-9] stimulation of adenylate cyclase (AC) [9012-42-4] from a variety of sources and the potentiation of forskolin effects by stimulatory hormones (glucagon [9007-92-5], ACTH [9002-60-2], and epinephrine [51-43-4]) and b,g-imidoguanosine 5'-triphosphate [Gpp(NH)p] [34273-04-6] were examd. The effects on AC were examd. using membrane prepns. of rabbit adipocytes, rat adipocytes, rat erythrocytes, and rat liver. Also examd. was the AC of liver membranes of rat pretreated with pertussis toxin as well as that solubilized from rat liver membranes. Maximal forskolin stimulation of AC in all prepns. studied revealed a consistent 10-fold increase in AC activity. The EC50 for forskolin was 10 mM for rat liver, 15 mM for rabbit and rat adipocytes, and 17 mM for rat erythrocyte AC stimulation. In all cases, the AC activity attained by forskolin stimulation was further enhanced by stimulatory hormones in a dose-dependent manner. Furthermore, a combination of all 3 activators [forskolin, stimulatory hormone, and Gpp(NH)p] resulted in an even greater overall stimulation to levels ranging from 25-30-fold over unstimulated activity levels. In the presence of satg. levels of each stimulatory hormone and Gpp(NH)p, the EC50 for forskolin diminished markedly to the range 0.5-4.0 mM. In the absence of any apparent tissue specificity for forskolin stimulation, the general pattern of these results further implicates the catalytic site of the AC complex as the site of forskolin activation. 9007-92-5 and 60-92-4 are just another two chemicals used in this study. Furthermore, activation of addnl. components of the complex by Gpp(NH)p and tissue specific hormones may further influence the AC activity and thereby potentiate the stimulation by forskolin. .

Vasodilating agents and platelet function: intracellular free calcium concentration, cyclic nucleotides, and shape-change response

Vasodilating agents and platelet function: intracellular free calcium concentration, cyclic nucleotides, and shape-change response. Erne, P.; Mittelholzer, E.; Rogg, H.; Resink, T. J.; Buehler, F. R. (Dep. Res., Univ. Hosp., Basel CH-4031, Switz.). J. Cardiovasc. 7261-97-4 and 364-98-7 which are cas registry numbers are also used here. Pharmacol., 8(Suppl. 8), 102-6 (English) 1986. CODEN: JCPCDT. ISSN: 0160-2446. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The adenylate-cyclase activator forskolin [66575-29-9], the guanylate-cyclase stimulator nitroprusside [15078-28-1], the phosphodiesterase inhibitor Ro 15-2041 [77448-87-4], different Ca-entry blockers, as well as various vasodilators, and an atrial natriuretic peptide were tested for antiplatelet activity. Thrombin, vasopressin, ADP, arachidonic acid, and the dihydropyridine Ca agonist CGP 28392 were used as platelet activators. The physiol. and biochem. parameters of platelet function studied included shape-change reaction, intracellular free-Ca modulation, and cyclic nucleotide formation. When inhibition of the shape-change response occurred, it was accompanied by inhibition of the increase in intracellular free Ca. The results suggest a possible intracellular site of action of Ca entry blockers in platelets, and confirm the importance of modulation of cyclic nucleotides in the regulation of platelet function , regardless of the mechanism of platelet activation. Addnl. antiplatelet activity of antihypertensive agents may have a beneficial effect in reducing the assocd. risk of thromboembolic complications in essential hypertension. .