Cardiovascular effects of valsartan and amlodipine in salt-loaded spontaneously hypertensive rats
Journal
International Journal of Recent Research in Arts and Sciences
Date Issued
2022-10
Author(s)
Bogoeva Kostovska, Ksenija
DOI
ISSN: 1857-8128
Abstract
Salt sensitivity defined as increase in blood pressure in response to high dietary salt
intake, is an independent risk factor for cardiovascular disease and mortality [1]. Even in the
absence of prominent elevations of blood pressure after salt-loading, salt sensitivity may be
revealed by structural and functional injury to target organs such as vasculature, heart and
kidneys [2-4]. Available data strongly suggest that salt overload exerts these adverse effects
through pressure independent mechanisms [5, 6]. Moreover, recent results also suggest that the
renin– angiotensin system (RAS) is involved in mediating the adverse effects of salt, since RAS
blockade prevented or ameliorated salt-induced cardiovascular and renal injury [5, 7].
Treatment strategies give advantage to hypertension therapies that can provide benefits
beyond blood pressure lowering. Angiotensin receptor blockers (ARBs) are often supplemented
with calcium channel blockers (CCBs) for treatment of hypertension [8]. Valsartan blocks the
vasoconstrictor and aldosterone-secreting effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT1 receptor in the vascular smooth muscle. Amlodipine inhibits
calcium ion influx across cell membranes, with a greater effect on vascular smooth muscle cells.
This causes vasodilation and a reduction in peripheral vascular resistance, thus lowering
blood pressure.
The objective of this study was to evaluate protective effects of 12-week treatment with
valsartan and amlodipine given as monotherapy and as a combination on the heart and large
blood vessels histopathology in salt loaded SHR rats.
intake, is an independent risk factor for cardiovascular disease and mortality [1]. Even in the
absence of prominent elevations of blood pressure after salt-loading, salt sensitivity may be
revealed by structural and functional injury to target organs such as vasculature, heart and
kidneys [2-4]. Available data strongly suggest that salt overload exerts these adverse effects
through pressure independent mechanisms [5, 6]. Moreover, recent results also suggest that the
renin– angiotensin system (RAS) is involved in mediating the adverse effects of salt, since RAS
blockade prevented or ameliorated salt-induced cardiovascular and renal injury [5, 7].
Treatment strategies give advantage to hypertension therapies that can provide benefits
beyond blood pressure lowering. Angiotensin receptor blockers (ARBs) are often supplemented
with calcium channel blockers (CCBs) for treatment of hypertension [8]. Valsartan blocks the
vasoconstrictor and aldosterone-secreting effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT1 receptor in the vascular smooth muscle. Amlodipine inhibits
calcium ion influx across cell membranes, with a greater effect on vascular smooth muscle cells.
This causes vasodilation and a reduction in peripheral vascular resistance, thus lowering
blood pressure.
The objective of this study was to evaluate protective effects of 12-week treatment with
valsartan and amlodipine given as monotherapy and as a combination on the heart and large
blood vessels histopathology in salt loaded SHR rats.
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