The mechanism of nitroglycerin action on the cardiac vessels

Каверина, Н. В.

doi:10.1007/bf00780367

Cited by 10 publications

(4 citation statements)

References 4 publications

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“…We have observed uptake of GTN by the brain and an increase in cGMP in brain tissue [48], and recently it was found that brain homogenates are able to metabolize GTN [49]. As early as 1960 it was proposed that the inhibition of refiex constriction of coronary vessels was mediated by increases in norepinephrine (NE) in the central nervous system (CNS) [50][51]. There are indications that GTN increases the release and synthesis of NE in brain tissues [52] and that cardiovascular effects of GTN involve a central as well as a peripheral component.…”

Section: Central Nervous Systemmentioning

confidence: 99%

Mechanisms of Action of Nitrates

Torfgård¹,

Ahlner²

1997

Nitrates Updated

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Glyceryl trlnitrate, isosorbide dinitrate, and isosorbide-o-mononitrate are organic nitrate esters commonly used in the treatment of angina pectoris, myocardial infaretion, and congestive heart failure. Organic nitrate esters have a direct relaxant effect on vascnlar smooth mnscles, and the dilation of coronary vessels improves oxygen snpply to the myocardium. The dilation of peripheral veins, and in higher doses peripheral arteries, rednces preload and afterload, and thereby lowers myocardial oxygen consumption. Inhibition of platelet aggregation is another effect that is probably of therapeutic value. Effects on the central ne"ous system and the myoeardium have been shown but not scrutinized for therapeutic importance. Both the relaxing effect on vascular smooth musele and the effect on platelets are considered to be due to a stimulation of soluble guanylate cyclase by nitric oxide derived from the organic nitrate ester molecule through metabolization catalyzed by enzymes such as glutathione 8-transferase, cytochrome P-450, and possibly esterases. The cyclic GMP produced by the guanylate cye ....... acts via cGMPdependent protein kinase. Ultimately, through various processes, the protein kinase lowers intracellular calcium; an increased uptake to and a decreased release from intracellular stores seem to be particularly important.Keg Words. organic nitrate esters, glyceryl trlnitrate, nitroglycerin, isosorbide dinitrate, isosorbide-o-mononitrate, cyclic GMP Nitroglycerin was introduced as a therapeutic agent for the treatment of angina pectoris more than a century ago [1], and since then several other nitro compounds with similar chemical properties have been introduced, for example, isosorbide dinitrate (ISDN), isosorbide-5-mononitrate (IS-5-MN), and pentaerythritol tetranitrate. An essential feature of all these compounds is a nitrate ester bond (R-O-N02). The nitrate ester group distinguishes the or-21 U. Thadani et al. (eds.), Nitrates Updated

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Section: Central Nervous Systemmentioning

confidence: 99%

Mechanisms of Action of Nitrates

Torfgård¹,

Ahlner²

1997

Nitrates Updated

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“…NTG inhibits reflex vasoconstriction of coronary vessels and the effect is reported to be mediated by increases in release of NE in the central nervous system. 11,12 NTG increases the release and enhances the synthesis of NE at noradrenergic terminals in the heart and brain. [13][14][15] Increasing central noradrenergic activation and sympathomimetic activity correlates with the complex pharmacological effects of the drug.…”

Section: Discussionmentioning

confidence: 99%

“…9,10 Systemically administered NTG inhibits reflex vasoconstriction of coronary vessels, and the effect is reported to be mediated by increases in the release of norepinephrine (NE) in the central nervous system. 11,12 Ma and Long have demonstrated that nitroglycerin increases the release and synthesis of NE in the brain, and it has been suggested that central…”

mentioning

confidence: 99%

Effects of Nitric Oxide and Noradrenergic Activation in the Posterior Hypothalamus on Arterial Pressure Tolerance to Nitroglycerin in Rats

Guettler

2008

J Cardiovasc Pharmacol Ther

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The effects of nitric oxide (NO) and noradrenergic activation in the posterior hypothalamus on arterial pressure tolerance induced by subcutaneous injection of nitroglycerin (NTG) was investigated in anesthetized Sprague-Dawley rats. Intravenous injections of NTG (3, 10, and 30 microg/kg) and sodium nitroprusside (1, 3, and 10 microg/kg) produced dose-dependant decreases in arterial blood pressure. Tolerance to NTG was produced by subcutaneous administration of 4.0 mg of NTG as 4 separate hourly injections of 1.0 mg each, affecting the dose-dependent response of NTG IV injection. The 4 high-dose NTG pulse injections produced a marked shift in the dose-response curves for arterial pressure depression induced by intravenous injection of the challenge doses of NTG, but did not alter hypotensive responses to sodium nitroprusside. The tolerance responses to arterial pressure depression were enhanced by a bilateral microinjection of NTG (1 nmol) and by diethylamine NONOate (1 nmol), an NO donor, into the posterior hypothalamus. Bilateral microinjection of guanethidine (1.5 nmol), a noradrenergic blocker, into the posterior hypothalamus inhibits NTG tolerance in a period of time within 2 hours. We conclude that exogenous NO and noradrenergic activation in the posterior hypothalamus play an important role in arterial pressure tolerance to systemically administered NTG.

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“…It is therefore no surprise that glyceryl trinitrate, apart from its potent vasomotor effects, seems to exert other cardiovascular responses. Early investigators demonstrated that glyceryl trinitrate inhibits reflex coronary vasoconstriction, and the effect was found to be mediated by significant release of norepinephrine in the central nervous system 28 , 29 …”

Section: The Presumed Vasovagal Effect Of Nitratesmentioning

confidence: 99%

The ‘Vasovagal Effect’ of Nitrates: An Under‐recognised Complication of Nitrate Use

Lydakis

Ay²,

1998

Int J Clinical Practice

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SUMMARY Nitrates are useful drugs in cardiovascular medicine. They have a presumed vasovagal effect, which is a rare but often under‐recognised complication that is partly caused by central inhibition of the sympathetic nervous system. However, no consistent variable associated with the presumed vasovagal effects following nitrate administration can be identified, and there are only limited reports of the phenomenon in the literature. In fact, the true prevalence of such a complication is unknown, because no data from observational studies exist, although it would seem likely to be a rare event. A greater awareness and recognition of this unusual effect of nitrate use is necessary in view of the increasing use of nitrates. Fortunately, recovery is generally the rule with supportive management.

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The mechanism of nitroglycerin action on the cardiac vessels

Cited by 10 publications

References 4 publications

Mechanisms of Action of Nitrates

Mechanisms of Action of Nitrates

Effects of Nitric Oxide and Noradrenergic Activation in the Posterior Hypothalamus on Arterial Pressure Tolerance to Nitroglycerin in Rats

The ‘Vasovagal Effect’ of Nitrates: An Under‐recognised Complication of Nitrate Use

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