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Clinical profile of eprosartan: a different angiotensin II receptor blocker.

Blankestijn PJ, Rupp H - Cardiovasc Hematol Agents Med Chem (2008)

Bottom Line: Apart from blood pressure lowering per se, also reducing the activities of the renin-angiotensin system and sympathetic nervous system appears to be important.An analysis has been made on available experimental and clinical data on eprosartan which not only is an effective and well tolerated antihypertensive agent, but also lowers the activities of the renin-angiotensin system and sympathetic nervous system.Experimental and pharmacokinetic studies on eprosartan have shown differences with the other ARBs.

View Article: PubMed Central - PubMed

Affiliation: Department of Nephrology, University Medical Center, Utrecht, The Netherlands. p.j.blankestijn@umcutrecht.nl

ABSTRACT
Rationale. The goal of antihypertensive treatment is to reduce risk of cardiovascular morbidity and mortality. Apart from blood pressure lowering per se, also reducing the activities of the renin-angiotensin system and sympathetic nervous system appears to be important. Angiotensin II receptor blocker drugs (ARBs) have provided a useful class of anti-hypertensive drugs. Eprosartan is a relatively new ARB which is chemically distinct (non-biphenyl, non-tetrazole) from all other ARBs (biphenyl tetrazoles). An analysis has been made on available experimental and clinical data on eprosartan which not only is an effective and well tolerated antihypertensive agent, but also lowers the activities of the renin-angiotensin system and sympathetic nervous system. Experimental and pharmacokinetic studies on eprosartan have shown differences with the other ARBs. The distinct properties of this non-biphenyl, non-tetrazole ARB might be relevant in the effort to reduce cardiovascular risk, also beyond its blood pressure lowering capacity.

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Related in: MedlinePlus

Schematic representation of the central nervous system (CNS) and a neuro-effector junction. Levels are indicated where angiotensin II (Ang II) can enhance (+) sympathetic activity and where angiotensin II receptor blocker (Ang II blocker) can reduce (-) sympathetic activity.Nor = noradrenaline, α = alpha-adrenoceptor, AT = angiotensin receptor
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Figure 2: Schematic representation of the central nervous system (CNS) and a neuro-effector junction. Levels are indicated where angiotensin II (Ang II) can enhance (+) sympathetic activity and where angiotensin II receptor blocker (Ang II blocker) can reduce (-) sympathetic activity.Nor = noradrenaline, α = alpha-adrenoceptor, AT = angiotensin receptor

Mentions: RAS/SNS interactions appear bi-directional and occur at different sites in the chain of events leading to angiotensin II and noradrenaline release, the two major transmitters of these two systems [1]. There is clear experimental evidence that the sympathetic outflow to the kidneys regulates renin release. Electrical stimulation of the renal nerves, as well as of certain central nervous system areas, causes an increase in renin release. There is a large body of evidence in various experimental settings indicating that angiotensin II facilitates the sympathetic nervous system on different levels. It has been shown that intra-cerebral infusion of angiotensin II causes a pressor response associated with an increase in vascular resistance. On a peripheral level, angiotensin II also elicits stimulatory action, because it stimulates neural transmission across sympathetic ganglia, potentiates at the presynaptic level noradrenaline release from sympathetic nerve terminals and amplifies the alpha-adrenoceptor mediated vasoconstrictor response to endogenous noradrenaline Fig (2). Further, angiotensin II exerts inhibitory effects on baroreflex modulation of the heart rate and sympathetic drive. The idea that AngII directly stimulates centrally originated sympathetic outflow in humans was tested in an elegant study. Intravenous infusion of AngII raised blood pressure and suppressed muscle sympathetic nerve activity. But during simultaneously infusion of nitroprusside to control blood pressure rise, MSNA increased. An identical experiment with phenylephrine infusion showed no effect on MSNA [2].


Clinical profile of eprosartan: a different angiotensin II receptor blocker.

Blankestijn PJ, Rupp H - Cardiovasc Hematol Agents Med Chem (2008)

Schematic representation of the central nervous system (CNS) and a neuro-effector junction. Levels are indicated where angiotensin II (Ang II) can enhance (+) sympathetic activity and where angiotensin II receptor blocker (Ang II blocker) can reduce (-) sympathetic activity.Nor = noradrenaline, α = alpha-adrenoceptor, AT = angiotensin receptor
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2748700&req=5

Figure 2: Schematic representation of the central nervous system (CNS) and a neuro-effector junction. Levels are indicated where angiotensin II (Ang II) can enhance (+) sympathetic activity and where angiotensin II receptor blocker (Ang II blocker) can reduce (-) sympathetic activity.Nor = noradrenaline, α = alpha-adrenoceptor, AT = angiotensin receptor
Mentions: RAS/SNS interactions appear bi-directional and occur at different sites in the chain of events leading to angiotensin II and noradrenaline release, the two major transmitters of these two systems [1]. There is clear experimental evidence that the sympathetic outflow to the kidneys regulates renin release. Electrical stimulation of the renal nerves, as well as of certain central nervous system areas, causes an increase in renin release. There is a large body of evidence in various experimental settings indicating that angiotensin II facilitates the sympathetic nervous system on different levels. It has been shown that intra-cerebral infusion of angiotensin II causes a pressor response associated with an increase in vascular resistance. On a peripheral level, angiotensin II also elicits stimulatory action, because it stimulates neural transmission across sympathetic ganglia, potentiates at the presynaptic level noradrenaline release from sympathetic nerve terminals and amplifies the alpha-adrenoceptor mediated vasoconstrictor response to endogenous noradrenaline Fig (2). Further, angiotensin II exerts inhibitory effects on baroreflex modulation of the heart rate and sympathetic drive. The idea that AngII directly stimulates centrally originated sympathetic outflow in humans was tested in an elegant study. Intravenous infusion of AngII raised blood pressure and suppressed muscle sympathetic nerve activity. But during simultaneously infusion of nitroprusside to control blood pressure rise, MSNA increased. An identical experiment with phenylephrine infusion showed no effect on MSNA [2].

Bottom Line: Apart from blood pressure lowering per se, also reducing the activities of the renin-angiotensin system and sympathetic nervous system appears to be important.An analysis has been made on available experimental and clinical data on eprosartan which not only is an effective and well tolerated antihypertensive agent, but also lowers the activities of the renin-angiotensin system and sympathetic nervous system.Experimental and pharmacokinetic studies on eprosartan have shown differences with the other ARBs.

View Article: PubMed Central - PubMed

Affiliation: Department of Nephrology, University Medical Center, Utrecht, The Netherlands. p.j.blankestijn@umcutrecht.nl

ABSTRACT
Rationale. The goal of antihypertensive treatment is to reduce risk of cardiovascular morbidity and mortality. Apart from blood pressure lowering per se, also reducing the activities of the renin-angiotensin system and sympathetic nervous system appears to be important. Angiotensin II receptor blocker drugs (ARBs) have provided a useful class of anti-hypertensive drugs. Eprosartan is a relatively new ARB which is chemically distinct (non-biphenyl, non-tetrazole) from all other ARBs (biphenyl tetrazoles). An analysis has been made on available experimental and clinical data on eprosartan which not only is an effective and well tolerated antihypertensive agent, but also lowers the activities of the renin-angiotensin system and sympathetic nervous system. Experimental and pharmacokinetic studies on eprosartan have shown differences with the other ARBs. The distinct properties of this non-biphenyl, non-tetrazole ARB might be relevant in the effort to reduce cardiovascular risk, also beyond its blood pressure lowering capacity.

Show MeSH
Related in: MedlinePlus