Inspra is indicated for the treatment of hypertension (high blood pressure) and may be used alone or in combination with other anti-hypertensive agents. Inspra is also being studied for use in heart failure; as a selective aldosterone receptor antagonist, Inspra may offer advantages over currently available non-selective aldosterone antagonists.
Inspra for oral administration contains 25 mg, 50 mg, or 100 mg of eplerenone. The recommended starting dose of Inspra is 50 mg administered once daily. The full therapeutic effect of Inspra is apparent within 4 weeks.
Inspra was demonstrated to be effective in lowering high blood pressure in over 3,000 patients and was generally well tolerated. Patients treated with Inspra 50 to 200 mg daily experienced significant decreases in sitting systolic and diastolic blood pressure at trough with differences from placebo of 6-13 mm Hg (systolic) and 3-7mm Hg (diastolic). These effects were confirmed by assessments with 24-hour ambulatory blood pressure monitoring (ABPM).
Blood pressure lowering was apparent within 2 weeks from the start of therapy with Inspra, with maximal antihypertensive effects achieved within 4 weeks. Stopping Inspra following treatment for 8-24 weeks in six studies did not lead to adverse event rates in the week following INSPRA withdrawal greater than following placebo or active control withdrawal. Blood pressures in patients not taking other antihypertensives rose 1 week after Inspra withdrawal by about 6/3 mm Hg, suggesting that Inspra antihypertensive effect was maintained through 8-24 weeks.
Adverse events associated with the use of Inspra may include (but are not limited to) the following:
The hormone aldosterone is a key component within the RAAS (renin angiotensin aldosterone system) and plays a significant role in the body’s regulation of the cardiovascular system. Inspra works with relative selectivity to block aldosterone receptors.Aldosterone synthesis, which occurs in the adrenal gland, is modulated by multiple factors, including angiotensin II and non-RAAS mediators such as adrenocorticotropic hormone (ACTH) and potassium. Aldosterone binds to mineralocorticoid receptors in both epithelial (e.g., kidney) and nonepithelial (e.g., heart, blood vessels, and brain) tissues and increases blood pressure through induction of sodium reabsorption and possibly other mechanisms.
Eplerenone has been shown to produce sustained increases in plasma renin and serum aldosterone, consistent with inhibition of the negative regulatory feedback of aldosterone on renin secretion. The resulting increased plasma renin activity and aldosterone-circulating levels do not overcome the effect of eplerenone on blood pressure.
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