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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

Relationship between cerebral arteriolar diameter and aldosterone level. Relationship between aldosterone (ALD) plasma level and cerebral arteriolar internal diameter in WKY-solvent (open square), WKY-ALD (full square), SHR-solvent (open triangle), SHR-ARB (open circle), SHR-ARB + ALD (full circle), SHR-ACEI (open lozenge), and SHR-ACEI + ALD (full lozenge). Pooled n = 78. Linear regression equation: Y = −0.29X + 59; r2 = 0.161; degrees of freedom = 76 (P < 0.05).
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Figure 3: Relationship between cerebral arteriolar diameter and aldosterone level. Relationship between aldosterone (ALD) plasma level and cerebral arteriolar internal diameter in WKY-solvent (open square), WKY-ALD (full square), SHR-solvent (open triangle), SHR-ARB (open circle), SHR-ARB + ALD (full circle), SHR-ACEI (open lozenge), and SHR-ACEI + ALD (full lozenge). Pooled n = 78. Linear regression equation: Y = −0.29X + 59; r2 = 0.161; degrees of freedom = 76 (P < 0.05).

Mentions: On the basis of the argument it has been postulated that aldosterone acts strictly as a mineralocorticoid hormone on renal and other epithelia, to maintain electrolytic homeostasis (Delyani et al., 2001). However, already in the 1970s it was suggested that aldosterone may play a negative role in vascular diseases such as stroke (Brunner et al., 1972). More recently evidence has revealed that aldosterone acts also on non-epithelial vascular sites; other results have shown that blocking the effects of aldosterone with antagonists such as spironolactone diminishes cerebrovascular lesions in the rat model of stroke (the SHR-SP; Rocha et al., 1998). Recently our group has detected an inverse linear relationship between plasma aldosterone levels and the diameter of the cerebral arteriole in SHR (Figure 3). Arguments are emerging therefore, that suggest the mineralocorticoid receptor as a potential therapeutic target for stroke prevention (Osmond et al., 2008).


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

Atkinson J - Front Pharmacol (2011)

Relationship between cerebral arteriolar diameter and aldosterone level. Relationship between aldosterone (ALD) plasma level and cerebral arteriolar internal diameter in WKY-solvent (open square), WKY-ALD (full square), SHR-solvent (open triangle), SHR-ARB (open circle), SHR-ARB + ALD (full circle), SHR-ACEI (open lozenge), and SHR-ACEI + ALD (full lozenge). Pooled n = 78. Linear regression equation: Y = −0.29X + 59; r2 = 0.161; degrees of freedom = 76 (P < 0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 3: Relationship between cerebral arteriolar diameter and aldosterone level. Relationship between aldosterone (ALD) plasma level and cerebral arteriolar internal diameter in WKY-solvent (open square), WKY-ALD (full square), SHR-solvent (open triangle), SHR-ARB (open circle), SHR-ARB + ALD (full circle), SHR-ACEI (open lozenge), and SHR-ACEI + ALD (full lozenge). Pooled n = 78. Linear regression equation: Y = −0.29X + 59; r2 = 0.161; degrees of freedom = 76 (P < 0.05).
Mentions: On the basis of the argument it has been postulated that aldosterone acts strictly as a mineralocorticoid hormone on renal and other epithelia, to maintain electrolytic homeostasis (Delyani et al., 2001). However, already in the 1970s it was suggested that aldosterone may play a negative role in vascular diseases such as stroke (Brunner et al., 1972). More recently evidence has revealed that aldosterone acts also on non-epithelial vascular sites; other results have shown that blocking the effects of aldosterone with antagonists such as spironolactone diminishes cerebrovascular lesions in the rat model of stroke (the SHR-SP; Rocha et al., 1998). Recently our group has detected an inverse linear relationship between plasma aldosterone levels and the diameter of the cerebral arteriole in SHR (Figure 3). Arguments are emerging therefore, that suggest the mineralocorticoid receptor as a potential therapeutic target for stroke prevention (Osmond et al., 2008).

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