Hydralazine tablet clinical pharmacology: Difference between revisions
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==CLINICAL PHARMACOLOGY== | |||
Although the precise mechanism of action of hydralazine is not fully understood, the major effects are on the cardiovascular system. Hydralazine apparently lowers blood pressure by exerting a peripheral vasodilating effect through a direct relaxation of vascular smooth muscle. Hydralazine, by altering cellular calcium metabolism, interferes with the calcium movements within the vascular smooth muscle that are responsible for initiating or maintaining the contractile state. | |||
The peripheral vasodilating effect of hydralazine results in decreased arterial blood pressure ([[diastolic ]]more than [[systolic]]); decreased peripheral vascular resistance; and an increased heart rate, stroke volume, and cardiac output. The preferential dilatation of arterioles, as compared to veins, minimizes [[postural hypotension]] and promotes the increase in cardiac output. Hydralazine usually increases [[renin ]]activity in plasma, presumably as a result of increased secretion of renin by the renal juxtaglomerular cells in response to reflex sympathetic discharge. This increase in renin activity leads to the production of [[angiotensin II]], which then causes stimulation of [[aldosterone ]]and consequent sodium reabsorption. Hydralazine also maintains or increases renal and cerebral blood flow. | |||
Hydralazine is rapidly absorbed after oral administration, and peak plasma levels are reached at 1 to 2 hours. Plasma levels of apparent hydralazine decline with a half-life of 3 to 7 hours. Binding to human plasma protein is 87%. Plasma levels of hydralazine vary widely among individuals. Hydralazine is subject to polymorphic acetylation; slow acetylators generally have higher plasma levels of hydralazine and require lower doses to maintain control of blood pressure. Hydralazine undergoes extensive hepatic metabolism; it is excreted mainly in the form of metabolites in the urine. | |||
<ref name="dailymed.nlm.nih.gov">{{Cite web | last = | first = | title = HYDRALAZINE HYDROCHLORIDE TABLET [PLIVA INC.] | url = http://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=ddbbdb09-3202-42d7-bbb0-08331dde2f54 | publisher = | date = | accessdate = 10 March 2014 }}</ref> | <ref name="dailymed.nlm.nih.gov">{{Cite web | last = | first = | title = HYDRALAZINE HYDROCHLORIDE TABLET [PLIVA INC.] | url = http://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=ddbbdb09-3202-42d7-bbb0-08331dde2f54 | publisher = | date = | accessdate = 10 March 2014 }}</ref> | ||
Revision as of 19:34, 10 March 2014
| Hydralazine |
|---|
| HYDRALAZINE tablet® FDA Package Insert |
| Indications and Usage |
| Dosage and Administration |
| Contraindications |
| Warnings |
| Precautions |
| Adverse Reactions |
| Drug Interactions |
| Use in Specific Populations |
| Overdosage |
| Description |
| Clinical Pharmacology |
| Nonclinical Toxicology |
| How Supplied/Storage and Handling |
| Labels and Packages |
| HYDRALAZINE injection® FDA Package Insert |
| Indications and Usage |
| Dosage and Administration |
| Contraindications |
| Warnings |
| Precautions |
| Adverse Reactions |
| Drug Interactions |
| Use in Specific Populations |
| Overdosage |
| Description |
| Clinical Pharmacology |
| Nonclinical Toxicology |
| How Supplied/Storage and Handling |
| Labels and Packages |
| Clinical Trials on Hydralazine |
| ClinicalTrials.gov |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Abdurahman Khalil, M.D. [2]
CLINICAL PHARMACOLOGY
Although the precise mechanism of action of hydralazine is not fully understood, the major effects are on the cardiovascular system. Hydralazine apparently lowers blood pressure by exerting a peripheral vasodilating effect through a direct relaxation of vascular smooth muscle. Hydralazine, by altering cellular calcium metabolism, interferes with the calcium movements within the vascular smooth muscle that are responsible for initiating or maintaining the contractile state.
The peripheral vasodilating effect of hydralazine results in decreased arterial blood pressure (diastolic more than systolic); decreased peripheral vascular resistance; and an increased heart rate, stroke volume, and cardiac output. The preferential dilatation of arterioles, as compared to veins, minimizes postural hypotension and promotes the increase in cardiac output. Hydralazine usually increases renin activity in plasma, presumably as a result of increased secretion of renin by the renal juxtaglomerular cells in response to reflex sympathetic discharge. This increase in renin activity leads to the production of angiotensin II, which then causes stimulation of aldosterone and consequent sodium reabsorption. Hydralazine also maintains or increases renal and cerebral blood flow.
Hydralazine is rapidly absorbed after oral administration, and peak plasma levels are reached at 1 to 2 hours. Plasma levels of apparent hydralazine decline with a half-life of 3 to 7 hours. Binding to human plasma protein is 87%. Plasma levels of hydralazine vary widely among individuals. Hydralazine is subject to polymorphic acetylation; slow acetylators generally have higher plasma levels of hydralazine and require lower doses to maintain control of blood pressure. Hydralazine undergoes extensive hepatic metabolism; it is excreted mainly in the form of metabolites in the urine.
References
- ↑ "HYDRALAZINE HYDROCHLORIDE TABLET [PLIVA INC.]". Retrieved 10 March 2014.