There was a dose-dependent decrease in blood pressure for aliskiren 75 mg , 150 mg and 300 mg .
Aliskiren had no effect on blood pressure variability .
Due to very limited information available regarding change in heart rate and pulse pressure , it was not possible to meta-analyze these outcomes .Mortality and non-fatal serious adverse events were not increased .
AUTHORS ' CONCLUSIONS Compared to placebo , aliskiren lowered BP and this effect is dose-dependent .
This magnitude of BP lowering effect is similar to that for angiotensin-converting enzyme ( ACE ) inhibitors and angiotensin receptor blockers ( ARBs ) .
There is no difference in mortality , nonfatal serious adverse events or withdrawal due to adverse effects with short term aliskiren monotherapy .
BACKGROUND Hypertension is a chronic condition associated with an increased risk of mortality and morbidity .
Renin is the enzyme responsible for converting angiotensinogen to angiotensin I , which is then converted to angiotensin II .
Renin inhibitors are a new class of drugs that decrease blood pressure ( BP ) by preventing the formation of both angiotensin I and angiotensin II .
OBJECTIVES To quantify the dose-related BP lowering efficacy of renin inhibitors compared to placebo in the treatment of primary hypertension .
To determine the change in BP variability , pulse pressure , and heart rate and to evaluate adverse events ( mortality , non-fatal serious adverse events , total adverse events , withdrawal due to adverse effects and specific adverse events such as dry cough , diarrhoea and angioedema ) .
Plasma renin and the antihypertensive effect of the orally active renin inhibitor aliskiren in clinical hypertension.
BACKGROUND Aliskiren is the first in a new class of orally effective renin inhibitors for the treatment of hypertension . METHODS In 569 patients with mild-to-moderate hypertension , blood pressure ( BP ) , plasma renin activity ( PRA ) and plasma renin concentration ( PRC ) were measured before and after 8 weeks of double-blind treatment with once-daily oral doses of aliskiren ( 150 , 300 or 600 mg ) , irbesartan 150 mg or placebo . RESULTS Aliskiren 150 , 300 and 600 mg and irbesartan 150 mg significantly reduced mean cuff sitting systolic BP ( SBP ) from baseline ( p < 0.001 vs. placebo ) . Aliskiren 150 , 300 and 600 mg significantly reduced geometric mean PRA by 69 % , 71 % and 75 % from baseline respectively ( p < 0.05 vs. placebo ) . Irbesartan 150 mg significantly increased PRA by 109 % ( p < 0.05 vs. placebo ) . Aliskiren dose-dependently increased PRC from baseline by 157 % , 246 % and 497 % , at 150 , 300 and 600 mg respectively , compared with a 9 % decrease with placebo ( p < 0.05 ) . PRC increased significantly more with aliskiren 300 and 600 mg compared with irbesartan 150 mg ( 105 % ; p < 0.05 ) . Regression analysis showed no significant correlations between baseline PRA and changes in SBP in any of the treatment groups , but interestingly , the slopes of the regression lines between changes in SBP and log-transformed baseline PRA were + 2.0 for placebo and -1.5 , -1.8 and -2.3 for aliskiren 150 , 300 and 600 mg respectively . The slope for irbesartan 150 mg ( -1.4 ) was similar to that for aliskiren 150 mg . CONCLUSIONS Aliskiren reduces SBP and PRA and increases PRC dose-dependently . In contrast , irbesartan reduces SBP but increases both PRC and PRA . As PRA is a measurement of angiotensin I-generating capacity , PRA can be used for measuring the ability of an antihypertensive agent to prevent the generation or action of Ang II , either directly ( renin inhibitors , beta-blockers , central alpha(2)-agonists ) or indirectly ( AT(1)-receptor blockers , ACE inhibitors )
There was a dose-dependent decrease in blood pressure for aliskiren 75 mg , 150 mg and 300 mg .
Aliskiren had no effect on blood pressure variability .
Due to very limited information available regarding change in heart rate and pulse pressure , it was not possible to meta-analyze these outcomes .Mortality and non-fatal serious adverse events were not increased .
AUTHORS ' CONCLUSIONS Compared to placebo , aliskiren lowered BP and this effect is dose-dependent .
This magnitude of BP lowering effect is similar to that for angiotensin-converting enzyme ( ACE ) inhibitors and angiotensin receptor blockers ( ARBs ) .
There is no difference in mortality , nonfatal serious adverse events or withdrawal due to adverse effects with short term aliskiren monotherapy .
BACKGROUND Hypertension is a chronic condition associated with an increased risk of mortality and morbidity .
Renin is the enzyme responsible for converting angiotensinogen to angiotensin I , which is then converted to angiotensin II .
Renin inhibitors are a new class of drugs that decrease blood pressure ( BP ) by preventing the formation of both angiotensin I and angiotensin II .
OBJECTIVES To quantify the dose-related BP lowering efficacy of renin inhibitors compared to placebo in the treatment of primary hypertension .
To determine the change in BP variability , pulse pressure , and heart rate and to evaluate adverse events ( mortality , non-fatal serious adverse events , total adverse events , withdrawal due to adverse effects and specific adverse events such as dry cough , diarrhoea and angioedema ) .