Acute effects of hydrocortisone on plasma nitrate/nitrite activity and forearm vasodilator responsiveness in normal human subjects

Abstract

1. The aim of the present study was to examine the acute effects of cortisol infusion on plasma nitrate/nitrite (NO) activity and forearm vascular responsiveness to acetylcholine. 2. We performed two randomized, placebo-controlled, cross-over studies. Study A examined the effects of intravenous hydrocortisone (200 mg over a 3 h period) on blood pressure (BP) and plasma NO activity in six healthy male volunteers. Study B examined the effects of intra-arterial hydrocortisone on cholinergic vasodilator responsiveness in six healthy male volunteers. Vasodilator responsiveness was measured by bilateral strain gauge plethysmography. 3. In study A, there was no significant change in BP during the hydrocortisone infusion. Comparing values obtained following 180 min infusion of hydrocortisone and control, there were significant increases in plasma cortisol (3441 +/- 342 vs 209 +/- 29 nmol/L, respectively; P < 0.001) and glucose (5.7 +/- 0.2 vs 4.6 +/- 0.2 mmol/L, respectively; P < 0.05) and a reduction in plasma renin concentration (PRC) (8.1 +/- 1.2 vs 11.0 +/- 1.8 pg/mL, respectively; P < 0.05) following hydrocortisone infusion. However, there were no significant changes in either plasma NO or in the endogenous NO synthase inhibitors asymmetrical and symmetrical dimethylarginine. 4. In study B, there was no significant change in BP or in cholinergic vasodilator responsiveness during the hydrocortisone infusion. 5. Short-term cortisol infusions do not alter biochemical or physiological markers of NO activity. If cortisol-induced hypertension is mediated by suppression of NO activity in humans, it seems likely that these changes take more than 3 h to become detectable.

Influence of aerobic exercise training on cardiovascular and endocrine-inflammatory biomarkers in hypertensive postmenopausal women

“…Additionally, it has been reported that cortisol impairs NO production measured by NOx − levels attributing thus, the cortisol-induced hypertension to the NO deficiency in both human and experimental model [53] , [54] . However, most of the studies have examined the interaction between cortisol and arterial hypertension in male subjects [55] and no one examined the effects of exercise training on endocrine-inflammatory mediators in hypertensive postmenopausal women. In our study, we found no effects of the exercise training in the cortisol concentration in hypertensive postmenopausal women.…”

Heart Rate Variability and Sympathetic Skin Response in Male Patients Suffering From Acute Alcohol Withdrawal Syndrome

“…However, it remains unclear which of these mechanisms are causal rather than epiphenomena or amplifiers and modulators of the sympathetic system. Current interest is focused on vascular effects of cortisol and the role of the nitric oxide (NO) system (Whitworth et al, 2000;Williamson et al, 2005), which transmits biological information in both the central nervous and the cardiovascular system under physiological and pathophysiological conditions (Moncada, 1992). There is evidence that isosorbide dinitrate (ISDN) given to rats undergoing withdrawal worsens withdrawal signs, suggesting NO to be involved in AWS (Adams et al, 1995) and to modulate cardiovascular effects (Kahkonen and Zvartau, 2003).…”