These findings indicate that room light exerts a profound suppressive effect on melatonin levels and shortens the body's internal representation of night duration. Hence, chronically exposing oneself to electrical lighting in the late evening disrupts melatonin signaling and could therefore potentially impact sleep, thermoregulation, blood pressure, and glucose homeostasis.
The human circadian pacemaker controls the timing of the release of the pineal hormone melatonin, which promotes sleep, decreases body temperature, and diminishes cognitive performance. Abnormal melatonin secretion has been observed in psychiatric and circadian disorders. Although melatonin secretion is directly suppressed by exposure to light in a nonlinear intensity-dependent fashion, little research has focused on the effect of prior photic history on this response. We examined eight subjects in controlled laboratory conditions using a within-subjects design. Baseline melatonin secretion was monitored under constant routine conditions and compared with two additional constant routines with a fixed light stimulus for 6.5 h of 200 lux (50 microW/cm(2)) after approximately 3 d of photic exposure during the subjective day of either about 200 lux (50 microW/cm(2)) or about 0.5 lux (0.15 microW/cm(2)). We found a significant increase in melatonin suppression during the stimulus after a prior photic history of approximately 0.5 lux compared with approximately 200 lux, revealing that humans exhibit adaptation of circadian photoreception. Such adaptation indicates that translation of a photic stimulus into drive on the human circadian pacemaker involves more complex temporal dynamics than previously recognized. Further elucidation of these properties could prove useful in potentiating light therapies for circadian and affective disorders.
Patients with normal-or high-renin non-modulating essential hypertension fail to shift their adrenal sensitivity on a low sodium diet in response to an infusion of angiotensin II (Ang II). In a prior study, 72 hours of converting enzyme inhibition (CEI) partially corrected this subnormal aldosterone response to Ang II hi patients with non-modulating hypertension. Since it was uncertain whether the failure to restore normal adrenal responsiveness reflected a continued abnormality or an insufficient duration of CEI, the present study was performed wherein subjects were studied before CEI and then 72 hours and 6 weeks after CEI. Adrenal and renovascular responses were assessed in 13 subjects with normal-or high-renin hypertension in response to an infusion of Ang II (0.3, 1.0, and 3.0 ng/kg/min) in balance on a 10 meq Na + /100 meq K + diet. Eight of 13 had a normal plasma aldosterone increment above control levels (215 ng/dl) and were classified as modulators; the remaining subjects (five of 13) were classified as non-modulators. Enalapril was then administered for 72 hours and 6 weeks, and the assessment of the Ang II dose-response relations was repeated. In the modulators, there was no change compared with levels before CEI in the aldosterone dose-response curve or threshold sensitivity to infused Ang II at either 3 days or 6 weeks after CEI administration. In the non-modulators, CEI for 72 hours partially restored aldosterone responsiveness, but more prolonged CEI for 6 weeks completely corrected the defect, restoring aldosterone responsiveness on a sodiumrestricted diet to that seen hi modulators and in normotensive control subjects. The threshold dose for a significant increase hi plasma aldosterone above control levels progressively shifted from 3 ng/kg/min (72 hours of CEI) to 1 ng/kg/min (6 weeks of CEI). After CEI, basal p-aminohippurate clearance progressively increased in both groups, but a significant increment above control levels was only observed in non-modulators at 6 weeks; CEI enhanced renovascular responsiveness to infused Ang II equally hi the two hypertensive subgroups. Complete correction of the renal abnormality in a previous study and the adrenal defect in the present study by CEI without demonstrable changes in circulating Ang II levels provide support for a tissue defect in the renin-angiotensin system in non-modulating hypertensive subjects. (Hypertension 1989;13:371-377)
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