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Stroke, high blood pressure and the Renin-Angiotensin-aldosterone system - new developments.

Atkinson J - Front Pharmacol (2011)

Bottom Line: This review considers whether a case can be made for a protective effect of inhibitors and blockers of the renin-angiotensin-aldosterone system (RAAS) on the cerebral circulation.It first looks at whether there exists a preferential effect on the cerebral circulation during a drug-induced lowering of high arterial blood pressure and cardiovascular morbi-mortality.This is followed by exploration of possible new directions in the inhibition of the RAAS and its effect on stroke.

View Article: PubMed Central - PubMed

Affiliation: Pharmacology Laboratory, Pharmacy Faculty, Nancy University Villers, France.

ABSTRACT
This review considers whether a case can be made for a protective effect of inhibitors and blockers of the renin-angiotensin-aldosterone system (RAAS) on the cerebral circulation. It first looks at whether there exists a preferential effect on the cerebral circulation during a drug-induced lowering of high arterial blood pressure and cardiovascular morbi-mortality. It then goes on to consider background studies on the relationship between inhibition of the RAAS and stroke. This is followed by exploration of possible new directions in the inhibition of the RAAS and its effect on stroke.

No MeSH data available.


Related in: MedlinePlus

Effects of angiotensins on cerebral arteriolar diameter (from Vincent et al., 2005). Cumulative concentration–response curve for arteriolar vasoconstriction evoked by angiotensin II [(A), n = 7], and effects of the ACEI, captopril (10−5 M, solid bar), on vasoconstriction induced by angiotensin I, angiotensin II, and 5HT [(B), n = 4]. Results are expressed as % fall in diameter. Values are mean ± SEM. *P ≤ 0.05 vs. baseline; †P ≤ 0.05 vs. responses induced by angiotensin I. (C) Cumulative concentration–response curve for the arteriolar vasomotor response to angiotensin II in presence of the angiotensin AT1 receptor antagonist, telmisartan (10−5 M). Results are expressed as % change in diameter. Values are mean ± SEM; n = 5. *P ≤ 0.05 vs. baseline; †P ≤ 0.05 vs. responses induced by angiotensin II alone.
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Figure 2: Effects of angiotensins on cerebral arteriolar diameter (from Vincent et al., 2005). Cumulative concentration–response curve for arteriolar vasoconstriction evoked by angiotensin II [(A), n = 7], and effects of the ACEI, captopril (10−5 M, solid bar), on vasoconstriction induced by angiotensin I, angiotensin II, and 5HT [(B), n = 4]. Results are expressed as % fall in diameter. Values are mean ± SEM. *P ≤ 0.05 vs. baseline; †P ≤ 0.05 vs. responses induced by angiotensin I. (C) Cumulative concentration–response curve for the arteriolar vasomotor response to angiotensin II in presence of the angiotensin AT1 receptor antagonist, telmisartan (10−5 M). Results are expressed as % change in diameter. Values are mean ± SEM; n = 5. *P ≤ 0.05 vs. baseline; †P ≤ 0.05 vs. responses induced by angiotensin II alone.

Mentions: Debate continues over whether a certain mechanism of action (in this case blockade of the RAAS) confers additional beneficial impact on cardiovascular morbi-mortality over and above the reduction in blood pressure (Figure 1). Potential mechanisms involved – especially for ARBs – have been discussed in several reviews (Chrysant, 2005; Thöne-Reineke et al., 2006). These include the possibility that blockade of the angiotensin II type 1 receptor (vasoconstrictor) by ARB treatment, “uncovers” angiotensin II stimulation of the vasodilator angiotensin II type 2 receptor. Our group has shown that in the presence of the ARB, telmisartan, angiotensin II produces dilatation of cerebral arterioles in an animal model of hypertension, the spontaneously hypertensive rats (SHR; Vincent et al., 2005; Figure 2).


Stroke, high blood pressure and the Renin-Angiotensin-aldosterone system - new developments.

Atkinson J - Front Pharmacol (2011)

Effects of angiotensins on cerebral arteriolar diameter (from Vincent et al., 2005). Cumulative concentration–response curve for arteriolar vasoconstriction evoked by angiotensin II [(A), n = 7], and effects of the ACEI, captopril (10−5 M, solid bar), on vasoconstriction induced by angiotensin I, angiotensin II, and 5HT [(B), n = 4]. Results are expressed as % fall in diameter. Values are mean ± SEM. *P ≤ 0.05 vs. baseline; †P ≤ 0.05 vs. responses induced by angiotensin I. (C) Cumulative concentration–response curve for the arteriolar vasomotor response to angiotensin II in presence of the angiotensin AT1 receptor antagonist, telmisartan (10−5 M). Results are expressed as % change in diameter. Values are mean ± SEM; n = 5. *P ≤ 0.05 vs. baseline; †P ≤ 0.05 vs. responses induced by angiotensin II alone.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3108479&req=5

Figure 2: Effects of angiotensins on cerebral arteriolar diameter (from Vincent et al., 2005). Cumulative concentration–response curve for arteriolar vasoconstriction evoked by angiotensin II [(A), n = 7], and effects of the ACEI, captopril (10−5 M, solid bar), on vasoconstriction induced by angiotensin I, angiotensin II, and 5HT [(B), n = 4]. Results are expressed as % fall in diameter. Values are mean ± SEM. *P ≤ 0.05 vs. baseline; †P ≤ 0.05 vs. responses induced by angiotensin I. (C) Cumulative concentration–response curve for the arteriolar vasomotor response to angiotensin II in presence of the angiotensin AT1 receptor antagonist, telmisartan (10−5 M). Results are expressed as % change in diameter. Values are mean ± SEM; n = 5. *P ≤ 0.05 vs. baseline; †P ≤ 0.05 vs. responses induced by angiotensin II alone.
Mentions: Debate continues over whether a certain mechanism of action (in this case blockade of the RAAS) confers additional beneficial impact on cardiovascular morbi-mortality over and above the reduction in blood pressure (Figure 1). Potential mechanisms involved – especially for ARBs – have been discussed in several reviews (Chrysant, 2005; Thöne-Reineke et al., 2006). These include the possibility that blockade of the angiotensin II type 1 receptor (vasoconstrictor) by ARB treatment, “uncovers” angiotensin II stimulation of the vasodilator angiotensin II type 2 receptor. Our group has shown that in the presence of the ARB, telmisartan, angiotensin II produces dilatation of cerebral arterioles in an animal model of hypertension, the spontaneously hypertensive rats (SHR; Vincent et al., 2005; Figure 2).

Bottom Line: This review considers whether a case can be made for a protective effect of inhibitors and blockers of the renin-angiotensin-aldosterone system (RAAS) on the cerebral circulation.It first looks at whether there exists a preferential effect on the cerebral circulation during a drug-induced lowering of high arterial blood pressure and cardiovascular morbi-mortality.This is followed by exploration of possible new directions in the inhibition of the RAAS and its effect on stroke.

View Article: PubMed Central - PubMed

Affiliation: Pharmacology Laboratory, Pharmacy Faculty, Nancy University Villers, France.

ABSTRACT
This review considers whether a case can be made for a protective effect of inhibitors and blockers of the renin-angiotensin-aldosterone system (RAAS) on the cerebral circulation. It first looks at whether there exists a preferential effect on the cerebral circulation during a drug-induced lowering of high arterial blood pressure and cardiovascular morbi-mortality. It then goes on to consider background studies on the relationship between inhibition of the RAAS and stroke. This is followed by exploration of possible new directions in the inhibition of the RAAS and its effect on stroke.

No MeSH data available.


Related in: MedlinePlus