Stress: Aspects of Endocrine Hypertension

Abstract

An increase in endocrine hypertension is to be expected with a global increase in insulin-resistant obesity (few obese persons are insulin-sensitive!) (1). Some mechanisms and biomarkers for this are a deficiency of anabolic hormones (growth hormone and testosterone) and increased levels of leptin, the catabolic stress hormone cortisol, and resting heart rate (2). Concomitant obstructive sleep apnea can also have an aggravating/exacerbating effect. In some patients with androgen deficiency and sleep apnea, testosterone can be returned to normal levels by reestablishing the restorative REM sleep phase using CPAP. Primarily, however, lifestyle modifications are decisive in treatment and prevention (“First, don’t get fat”) and in individual cases growth hormone or testosterone therapy for a period limited to 3 to 6 months can be beneficial, almost as a kick-start (3, 4). Obesity-associated resting tachycardia indicates not only lack of fitness but also a burden on the cardiac atria/chambers and, under stress, long-term activation of the sympathetic nervous system. In such cases percutaneous renal denervation or baroreflex stimulation of the carotid sinus may be beneficial for selected patients, improving insulin sensitivity in a similar way to the treatment of patients with a catecholamine-secreting pheochromocytoma before and after the tumor is removed. In “typical” patients with endocrine hypertension, congenital adrenal hyperplasia (CAH) caused by 11-beta-hydroxylase or 17-alpha-hydroxylase deficiency should also be considered, although most patients with CAH present with 21-hydroxylase deficiency and may develop hypertension, or may only develop it, following overreplacement with dexamethasone or hydrocortisone (exogenous hypercortisolism/Cushing syndrome) and/or with predominant insulin resistance in connection with polycystic ovary syndrome.