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)

In rabbits the topical administration of sodium azide (NaNs) or sodium nitroprusside (SNP) increased intraocular pressure in a dose-response manner. These agents, which activate guanylate cyclase, elevated cyclic GMP in the aqueous humor. Systemic blood pressure and pulse were not altered. Tonographic outflow facility was unchanged, suggesting an increase in aqueous humor flow as the mechanism for the elevation of intraocular pressure. Posterior chamber aqueous humor ascorbate concentration was decreased in the eye receiving the NaN3 or SNP. Systemic pretreatment with phenoxybenzamine, an alpha-adrenergic blocking agent, prevented the elevation of intraocular pressure observed following NaN3 and SNP. Pretreatment with systemic indomethacin, propranolol, or acetazolamide or the topical application of atropine or epinephrine failed to alter the elevation of intraocular pressure by either NaN3 or SNP.
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PMID:Increased intraocular pressure following topical azide or nitroprusside. 19 56

This study was performed to investigate the putative relationship between nitric oxide (NO) and adenosine A(2) receptors on central cardiovascular regulation in the posterior hypothalamus of rats. Posterior hypothalamic injection of drugs was performed in anesthetized, artificially ventilated male Sprague-Dawley rats. Injection of adenosine A(2) receptor agonist 5'-(N-cyclopropyl)-carboxamidoadenosine (CPCA; 1, 2 and 5 nmol) produced a dose-dependent decrease of blood pressure and heart rate. Pretreatment with adenosine A(2) receptor antagonist 3,7-dimethyl-1-propargylxanthine (10 nmol) blocked the depressor and bradycardiac effects of CPCA (5 nmol). Pretreatment with soluble guanylate cyclase inhibitor LY-83,583 (5 nmol) attenuated the depressor and bradycardiac effects of CPCA (5 nmol). In addition, pretreatment with NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (40 nmol) attenuated the depressor and bradycardiac responses of CPCA (5 nmol). These results suggest that adenosine A(2) receptor in the posterior hypothalamus plays an inhibitory role in central cardiovascular regulation and that NO participates in the inhibitory response induced by adenosine A(2) receptor stimulation in the posterior hypothalamus.
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PMID:The involvement of nitric oxide on the adenosine A(2) receptor-induced cardiovascular inhibitory responses in the posterior hypothalamus of rats. 1205 34

Cardiovascular inhibitory effects induced by posterior hypothalamic adenosine A(2) receptors and their modulation by nitric oxide were suggested by our previous report. In this experiment, we examined the modulation of cardiovascular effects of adenosine A(2) receptor stimulation by adenylate cyclase, guanylate cyclase and ATP-sensitive K(+) channel in the posterior hypothalamus. Posterior hypothalamic injection of drugs was performed in anesthetized, artificially ventilated male Sprague-Dawley rats. Injection of adenosine A(2) receptor agonist 5'-(N-cyclopropyl)-carboxamidoadenosine (CPCA; 1, 2 and 5 nmol) produced a dose-dependent decrease of blood pressure and heart rate. Pretreatment with adenosine A(2) receptor antagonist 3,7-dimethyl-1-propargylxanthine (10 nmol) blocked the depressor and bradycardiac effects of CPCA (5 nmol). Pretreatments with adenylate cyclase inhibitor MDL-12330 (10 nmol) and guanylate cyclase inhibitor LY-83583 (5 nmol) attenuated the depressor and bradycardiac effects of CPCA (5 nmol). In addition, pretreatment with ATP-sensitive K(+) channel blocker glipizide (20 nmol) attenuated the depressor and bradycardiac responses of CPCA (5 nmol). These results suggest that posterior hypothalamic adenosine A(2) receptors play an inhibitory role in the central cardiovascular regulation and that both adenylate cyclase and guanylate cyclase mediate the depressor and bradycardiac actions of adenosine A(2) receptors. Also, ATP-sensitive K(+) channel mediates the posterior hypothalamic cardiovascular regulations of adenosine A(2) receptors.
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PMID:Modification of cardiovascular response of posterior hypothalamic adenosine A(2) receptor stimulation by adenylate cylase, guanylate cyclase and by K(ATP) channel blockade in anesthetized rats. 1278 21

Cardiovascular inhibitory effects induced by the posterior hypothalamic adenosine A(2) receptors were suggested by our previous reports. In this experiment, we examined the influence of the posterior hypothalamic adenosine A(2B) receptors on central cardiovascular regulation of blood pressure (BP) and heart rate (HR). Posterior hypothalamic injection of drugs was performed in anesthetized, artificially ventilated male Sprague-Dawley rats. Injection of 5'-(N-cyclopropyl)-carboxamidoadenosine (CPCA; 2 nmol), an adenosine A(2) receptor agonist, showed the decrease of arterial blood pressure and heart rate, and the alloxazine, an adenosine A(2B) receptor antagonist, partially blocked the depressor and bradycardiac effects of CPCA (2 nmol). To examine the role of adenosine A(2B) receptors among the adenosine A(2) subtypes, we applied the 5'-N-Ethylcarboxamidoadenosine (NECA), an adenosine A(2B) receptor agonist, to the posterior hypothalamus. Injection of NECA (1, 4 and 8 nmol) produced a dose-dependent decrease of arterial blood pressure and HR. Pretreatment with alloxazine (5 nmol) partially blocked the depressor and bradycardiac effects of NECA (4 nmol). Also, pretreatment with LY-83,583 (5 nmol), a soluble guanylate cyclase inhibitor, attenuated the depressor and bradycardiac effects of NECA (4 nmol). However, pretreatment with MDL-12,330 (10 nmol), an adenylate cyclase inhibitor, did not affect these effects of NECA (4 nmol). These results suggest that adenosine A(2B) receptor in the posterior hypothalamus plays an inhibitory role in central cardiovascular regulation, and that guanylate cyclase mediates the depressor and bradycardiac actions of adenosine A(2B) receptors.
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PMID:Involvement of guanylate cyclase in the cardiovascular response induced by adenosine A2B receptor stimulation in the posterior hypothalamus of the anesthetized rats. 1736 36

In this experiment, we examined the influence of the posterior hypothalamic adenosine A(2A) receptors on the central cardiovascular regulation of blood pressure (BP) and heart rate (HR). Posterior hypothalamic injection of drugs was performed in anesthetized, artificially ventilated male Sprague-Dawley rats. Injection of CGS-21680HCl (CGS; 20 nmol), an adenosine A(2A) receptor agonist, elicited a decrease of arterial BP and HR, while injection of 8-(3-Chlorostyryl)caffeine (CSC; 10 nmol), an adenosine A(2A) receptor antagonist, blocked the depressor and bradycardiac effects of CGS (20 nmol). To examine the mechanisms of cardiovascular regulation of adenosine A(2A) receptors in the posterior hypothalamus, we applied the adenylate cyclase and guanylate cyclase inhibitors, to the posterior hypothalamus. Pretreatment with MDL-12,330 (MDL; 10 nmol), an adenylate cylase inhibitor, attenuated the depressor and bradycardiac effects of CGS. However, pretreatment with, LY-83,583 (LY; 5 nmol), a soluble guanylate cyclase inhibitor, did not alter the effects of CGS. Additionally, we examined the modification of the cardiovascular effects of adenosine A(2A) receptors through the ATP-sensitive K+ channel in the posterior hypothalamus. Posterior hypothalamic administration of glipizide (20 nmol) significantly attenuated the cardiovascular depressor actions elicited by CGS. These results suggest that adenosine A(2A) receptors in the posterior hypothalamus play an inhibitory role in central cardiovascular regulation, and that adenylate cyclase, but not guanylate cyclase, mediates the depressor and bradycardiac actions of adenosine A(2A) receptors. Furthermore, ATP-sensitive K+ channels mediate the posterior hypothalamic cardiovascular regulation of adenosine A(2A) receptors.
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PMID:Modification of the cardiovascular response of posterior hypothalamic adenosine A(2A) receptor stimulation by adenylate cyclase and KATP channel blockade in anesthetized rats. 1913 85