Effect of parathyroidectomy on arterial hypertrophy, vascular lesions, and aortic calcium content in deoxycorticosterone-induced hypertension

Abstract

Parathyroidectomy (Px) did not prevent the development of deoxycorticosterone (DOC)-induced hypertension inasmuch as the systolic blood pressure at 4 weeks did not differ from that of parathyroid intact, DOC-treated rats. Px, however, ameliorated the percent incidence and severity index of hypertension-induced vascular lesions in the heart and kidney. There was less hyaline change in the coronary artery and renal arteriole and fewer scars in the myocardium of Px + DOC rats than in DOC-treated animals. Arterial hypertrophy in aorta, coronary artery, renal interlobular artery, and renal arteriole in hypertensive animals was not affected by Px. The aortic content of total calcium in the Px-hypertensive rats was reduced significantly as compared to parathyroid-intact hypertensive rats. The abdominal aorta in the Px + DOC group showed a greater reduction in calcium than the thoracic aorta. We conclude that calcium may not be essential in mediating hypertension-induced vascular hypertrophy. Parathyroidectomy permitted a separation of high blood pressure-hypertrophy from hyaline vascular lesions in DOC-induced hypertensive rats, likely acting upon endothelial cells to prevent movement of plasma proteins (hyaline change) from the vascular lumen into the media-subendothelial space of blood vessels.

From aldosteronism to oxidative stress: the role of excessive intracellular calcium accumulation

“…These observations collectively validated our hypothesis with regard to the pathological sequelae of events leading to this structural remodeling of myocardium in rats with chronic aldosteronism. Various co-treatments were used, which included: Spiro, an ALDO receptor antagonist, which attenuated the enhanced urinary and fecal losses of these cations to prevent hypocalcemia and hypomagnesemia and thereby ensuing SHPT; 14 a Ca 2+ -and Mg 2+ -supplemented diet, together with vitamin D 3 to enhance Ca 2+ absorption, which prevented hypocalcemia and SHPT; 82 parathyroidectomy, performed before starting ALDOST, prevented SHPT 83 and has been found to prevent vascular lesions and the rise in aortic tissue Ca 2+ content during deoxycorticosterone/salt treatment; 84 cinacalcet, a calcimimetic that resets the threshold of the parathyroid glands' Ca 2+ -sensing receptor prevents SHPT, despite hypocalcemia; 85 amlodipine, a Ca 2+ channel blocker, which prevents intracellular Ca 2+ overloading; 64 and N-acetylcysteine, an antioxidant that abrogated oxidative stress. 13 Taken together, the multitude of evidence gathered to date congruently supports that PTH-mediated intracellular Ca 2+ overloading is the most likely mechanism that leads to the induction of oxidative stress during aldosteronism, in which ROS and reactive nitrogen species, primarily derived from the mitochondria in cardiomyocytes and NADPH oxidase in vascular tissue, overwhelm cellular antioxidant defenses.…”

“…In 65,115,116 (ii) elevated [Ca 2+ ] i and total Ca 2+ concentration of PBMC in response to ALDOST and which occurs before tissue invasion, together with increased H 2 O 2 production by monocytes and lymphocytes; 65 (iii) PTH regulated T-cell activation; [117][118][119][120] (iv) parathyroidectomy prevented PBMC Ca 2+ overloading and vascular lesions; 83,84 (v) upregulated expression of antioxidant defenses in these cells; and (vi) prevention of Ca 2+ loading and oxi/nitrosative stress by cotreatment with either Spiro or an antioxidant. 13,65,116 The presence of oxi/nitrosative stress at a systemic level in these models is evidenced by increased serum levels of thiobarbituric acid-reacting substances and reduced activity of plasma a 1 -antiproteinase.…”

Effect of Parathyroidectomy on Development of Hypertension and Atrial Responsiveness in Spontaneous Hypertensive Rats

“…On the other hand, cardiac lesions characterized by accumulation of calcium have been described in the heart of uraemic rats and dogs and prevented by PTX (Lehr 1966;Kraikitpanitch et al 1978). PTX also ameliorated cardiac lesions and calcium accumulation in mineralocorticoid-induced hypertensive rats (Yang & Nickerson 1988).…”

Biomarkers in the early period of acute myocardial infarction in rat serum and protective effects of Shexiang Baoxin Pill using a metabolomic method

“…Steroid hormone biosynthesis Hypertrophy (Sheppard and Autelitano, 2002;Lister et al, 2006) 12S-HETE AA metabolism Inflammation (Funk, 2006;Wen et al, 2007) Deoxycorticosterone Steroid hormone biosynthesis Hypertrophy (Yang and Nickerson, 1988) Corticosterone…”