Altered mitochondrial function, calcium signaling, and catecholamine release in chromaffin cells of diabetic and SHR rats
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2017
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Musial, Diego C. 
Bomfim, Guilherme H.
Miranda-Ferreira, Regiane
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Comorbidity of diabetes and hypertension is frequent. Here, we have performed a comparative study in three animal models namely, normotensive Wistar Kyoto (WKY) rats, streptozotocin-induced diabetic rats (STZ), and spontaneously hypertensive rats (SHR). With respect WKY rats, we have found the following alterations in adrenal chromaffin cells from STZ and SHR rats: (1) diminished Ca2+ currents; (2) augmented [Ca2+](c) elevations and catecholamine release in cells stimulated with angiotensin II or high K+; (3) unchanged expression of angiotensin II receptors AT(1) and AT(2); (4) higher density of secretory vesicles at subplasmalemmal sites; (5) mitochondria with lower cristae density that were partially depolarized; and (6) lower whole cell ATP content. These alterations may have their origin in (i) an augmented capacity of the endoplasmic reticulum Ca2+ store likely due to (ii) impaired mitochondrial Ca2+ uptake; (iii) augmented high-[Ca2+](c) microdomains at subplasmalemmal sites secondary to augmented calcium-induce calcium release and to inositol tris-phosphate receptor mediated enhanced Ca2+ mobilization from the endoplasmic reticulum; and (iv) augmented vesicle pool. These alterations seem to be common to the two models of human hypertension here explored, STZ diabetic rats and SHR hypertensive rats.
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European Journal Of Pharmacology. Amsterdam, v. 815, p. 416-426, 2017.