原发性醛固酮增多症(原醛症)是继发性高血压的常见病因之一,部分患者亦可伴有低血钾,醛固酮瘤及特发性醛固酮增多症是其主要的病理亚型.原醛症的诊断包括筛查、确诊及分型诊断3个步骤,传统影像学结合体位刺激的方法进行分型诊断,假阳性及假阴性率均较高,肾上腺静脉插管采血可作为影像学检查的补充.醛固酮瘤及原发性肾上腺增生患者应予手术治疗,特发性醛固酮增多症患者多采用药物治疗,螺内酯是其首选药物。

Primary aldosteronism

Several forms of the polypeptide atrial natriuretic factor (ANF) have been isolated recently from rat and human atria and identified1–3; they are probably associated with the secretory granules of atrial tissue4 The potent ability of ANFs to increase urine sodium content is mediated by their direct action on the kidney5,6 We report here the high intrinsic activity of a synthetic replicate of one form of this molecule, ANF(8-33) (ref 7), to inhibit directly basal aldosterone secretion and its ability to antagonize the stimulatory effects of adrenocorticotropin (ACTH) and angiotensin II (AN-II) on the secretion of aldosterone by rat adrenoglomerulosa cells in vitro Our results suggest that ANF is of clinical importance in the management of aldosterone-dependent hypertension by modifying the adrenocortical response to endogenous ACTH and AN-II

Inhibition of aldosterone production in the adrenal glomerulosa by atrial natriuretic factor

Regulation of Aldosterone Biosynthesis

Publisher Summary This chapter discusses the organization, characteristics, release, and modulation of hypophyseal and other endocrinologically relevant pools of opioid peptides and their possible target sites and functions. The nature and role of opioid mechanisms in the control of the endocrine secretion of various tissues are considered in the chapter. Many conditions—for example, stress, nutritional status, degree of hydration, and phase of circadian or estrus cyclicity—have biochemically been shown to be (1) associated with alterations in the activity of endocrine-like opioid systems and (2) related to opioid-mediated changes in behavioral, physiological, and endocrinological measures. It is the unification of these complementary sources of information and the assignation of particular functions to particular endocrine-like pools of opioids that are of importance. The chapter also discusses a particular aspect of the function of opioid mechanisms, including endocrine-like opioid peptide systems—that is, of their modulation of the secretion of hormones into the systemic circulation. The ability of opioids to modify these endocrine parameters is among their most striking properties and, especially in the case of antagonists, no less impressive than their role in antinociceptive processes. There are multifarious sites of attack and mechanisms of action by which opioid mechanisms may modulate endocrine secretion. Similarly, a diversity of opioid ligands and receptor types is implicated in particular cases. An elucidation of the roles of individual ligands and receptor types at specific loci and their relationships to other control systems under specific conditions has not been achieved.

The endocrinology of the opioids.

Co-localization of vasoactive intestinal peptide (VIP) and enkephalins in chromaffin cells of the adrenal gland of amphibia. Stimulation of corticosteroid production by VIP

In vitro application of the morphinomimetic met-enkephalin resulted in inhibition of mineralocorticoid production by aldosterone-producing adenomas. Aldosterone, deoxycorticosterone, and corticosterone production by adrenocortical cells isolated from aldosteronomas has been studied under basal conditions and after stimulation with ACTH-(1-24). The blocking effect of met-enkephalin on the rate of aldosterone, deoxycorticosterone, and corticosterone release was significant at a concentration as low as 10(-11) M (P less than 0.001, P less than 0.01, and P less than 0.001, respectively). Dose-dependent inhibition of steroid biosynthesis became more apparent with increasing amounts of met-enkephalin in the incubation medium (10(-11)-10(-5) M); at a concentration of 10(-5) M, met-enkephalin decreased the production of aldosterone by 45%, that of deoxycorticosterone by 51%, and that of corticosterone by 44%. Increased steroid biosynthesis stimulated by ACTH-(1-24) was also significantly blocked by met-enkephalin. In a concentration of 10(-5) M, met-enkephalin produced significant decreases in aldosterone (P less than 0.001), deoxycorticosterone (P less than 0.05), and corticosterone (P less than 0.001) production compared to the peak values obtained after stimulation with 0.85 X 10(-10) M ACTH-(1-24). These data allow us to conclude that the inhibitory effect of met-enkephalin on mineralocorticoid production exerted at the level of the adrenals might be complementary to the factor(s) thought to be involved in the regulation of adrenal steroid production, playing a role similar to that of the biogenic amines originating in the adrenal medulla and regulating the adrenal cortex by a peripheral neurohumoral paracrine mechanism.

Sandor Vida

Papers

Met-Enkephalin Inhibits Mineralocorticoid Production in Isolated Human Aldosteronoma Cells