Vitamin D deficiency causes inward hypertrophic remodeling and alters vascular reactivity of rat cerebral arterioles

Figures

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  Fig 1. Cerebral artery geometry and nucleus count of the smooth muscle layer. (A) VDD significantly increased the wall thickness (* p<0.05, n = 10–11) as well as (B) the wall thickness / lumen diameter ratio (** p<0.01, n = 10–11). (C) The cross-sectional area of the vessel walls increased significantly in VDD as compared to the Control group (* p<0.05, n = 9–9) at 50 mmHg intraluminal pressure. All these parameters were measured under passive conditions. (D) Significantly more nuclei were detected in the smooth muscle layer of anterior cerebral arteries of VDD animals as compared to controls (*** p<0.0001, n = 4–6). (E) The thickness of the tunica media was increased in the VDD group as compared to the control animals (* p<0.05, n = 4–4). (F) In addition, VDD significantly decreased the intima / media ratio of cerebral arteries (* p<0.05, n = 4–4).

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  Fig 2. The tangential wall stress of the cerebral arteries in relaxed condition. VDD caused a decrease in the tangential stress of the vessel wall throughout the entire pressure range under passive conditions (* p<0.05, n = 10–11).

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  Fig 3. Alterations of vascular reactivity in VDD. VDD caused alterations in the smooth muscle tone and endothelium-dependent relaxation capacity of arterioles. (A) Anterior cerebral arteries possessed myogenic tone and this tone was greater in the VDD group measured at 50 mmHg intraluminal pressure (** p<0.01, n = 8–8). (B) In addition, UTP-induced contraction also increased in the VDD group at 50 mmHg intraluminal pressure (* p<0.05, n = 10–9). (C) Bradykinin induced endothelium-dependent relaxation after precontraction in the Control group, but did not relax the arterioles in the VDD group at 50 mmHg intraluminal pressure (* p<0.05, n = 9–9).

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  Fig 4. Elastic components of the vessel wall. (A) Representative images of cerebral arterioles stained with Weigert’s resorcin-fuchsin. (B) Elastic fiber density did not differ between the groups according to measurement of green color intensity as a function of distance from the luminal surface measured on resorcin-fuchsin-stained segments.

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  Fig 5. Evaluation of immunohistochemical staining of arterioles. (A) Representative immunohistochemical images of cerebral arterioles stained for eNOS. (B) VDD caused a decrease in the expression of eNOS in the endothelium of arterioles (* p<0.05, n = 4–6). (C) Representative immunohistochemical images of cerebral arterioles stained for COX-2. (D) The expression of COX-2 in the endothelial layer increased in VDD as compared to Control (* p<0.05, n = 4–4).