Vargas F, Garcia del Rio C, Luna J D, Haro J M, Osorio C
Department of Biochemistry, Faculty of Medicine, University of Granada, Spain.
Acta Endocrinol (Copenh). 1988 May;118(1):22-30. doi: 10.1530/acta.0.1180022.
In this paper we studied the role of thyroid gland function in two experimental hypertension models with different pathophysiological mechanisms: deoxycorticosterone-salt (DOCA-salt, volume dependent) and Goldblatt 2-kidney, 1-clip (2K1C, renin dependent). DOCA-salt hypertensive rats showed lower T3 and T4 serum levels by the third week of induced hypertension. Goldblatt 2K1C hypertensive rats, however, exhibited normal values for both hormones. Treatment with thyroxine accelerated the evolution of hypertension and did not affect the PRA of DOCA-salt rats. Radiothyroidectomy inhibited DOCA-salt and Goldblatt 2K1C hypertension, and prevented the suppression of PRA in DOCA-salt rats, without altering PRA or serum aldosterone in Goldblatt 2K1C rats. These results suggest that: a) a thyroid depressing factor is not activated in Goldblatt 2K1C rats; b) thyroidectomy interferes with the suppressor effect of mineralocorticoid on renin secretion; and c) normal thyroid activity is required for the hypertensive effect of the renin-angiotensin-aldosterone system in Goldblatt 2K1C rats.
在本文中，我们研究了甲状腺功能在两种具有不同病理生理机制的实验性高血压模型中的作用：脱氧皮质酮-盐（DOCA-盐，容量依赖性）和戈德布拉特二肾一夹（2K1C，肾素依赖性）。DOCA-盐高血压大鼠在诱导高血压的第三周时血清T3和T4水平降低。然而，戈德布拉特2K1C高血压大鼠这两种激素的值均正常。甲状腺素治疗加速了高血压的进展，且不影响DOCA-盐大鼠的血浆肾素活性（PRA）。甲状腺切除抑制了DOCA-盐和戈德布拉特2K1C高血压，并防止了DOCA-盐大鼠PRA的抑制，而不改变戈德布拉特2K1C大鼠的PRA或血清醛固酮。这些结果表明：a）戈德布拉特2K1C大鼠中未激活甲状腺抑制因子；b）甲状腺切除干扰了盐皮质激素对肾素分泌的抑制作用；c）戈德布拉特2K1C大鼠中肾素-血管紧张素-醛固酮系统的高血压作用需要正常的甲状腺活性。
