Sleep during Ramadan intermittent fasting.

During the month of Ramadan intermittent fasting, Muslims eat exclusively between sunset and sunrise, which may affect nocturnal sleep. The effects of Ramadan on sleep and rectal temperature (Tre) were examined in eight healthy young male subjects who reported at the laboratory on four occasions: (i) baseline 15 days before Ramadan (BL); (ii) on the eleventh day of Ramadan (beginning of Ramadan, BR); (iii) on the twenty-fifth day of Ramadan (end of Ramadan, ER); and (iv) 2 weeks after Ramadan (AR). Although each session was preceded by an adaptation night, data from the first night were discarded. Polysomnography was taken on ambulatory 8-channel Oxford Medilog MR-9000 II recorders. Standard electroencephalogram (EEG), electro-oculogram (EOG) and electromyogram (EMG) recordings were scored visually with the PhiTools ERA. The main finding of the study was that during Ramadan sleep latency is increased and sleep architecture modified. Sleep period time and total sleep time decreased in BR and ER. The proportion of non-rapid eye movement (NREM) sleep increased during Ramadan and its structure changed, with an increase in stage 2 proportion and a decrease in slow wave sleep (SWS) duration. Rapid eye movement (REM) sleep duration and proportion decreased during Ramadan. These changes in sleep parameters were associated with a delay in the occurrence of the acrophase of Tre and an increase in nocturnal Tre during Ramadan. However, the 24-h mean value (mesor) of Tre did not vary. The nocturnal elevation of Tre was related to a 2-3-h delay in the acrophase of the circadian rhythm. The amplitude of the circadian rhythm of Tre was decreased during Ramadan. The effects of Ramadan fasting on nocturnal sleep, with an increase in sleep latency and a decrease in SWS and REM sleep, and changes in Tre, were attributed to the inversion of drinking and meal schedule, rather than to an altered energy intake which was preserved in this study.

Effect of neuropeptide Y on bradykinin-induced release of prostacyclin and thromboxane from guinea pig perfused lung.

We have previously reported that neuropeptide Y (NPY) inhibits responses induced by various agonists (noradrenaline, vasoactive intestinal peptide, substance P,5-hydroxytryptamine) in isolated guinea pig trachea. Although the underlying mechanisms have not been fully characterized, it was found that the NPY-evoked inhibition was specifically expressed with agents for which locally released prostaglandins (PGs) are important determinants for their myotropic activity. In the present study, we have extended these findings by examining whether NPY was capable of regulating the release of prostacyclin and thromboxane A2 induced by bradykinin (BK) from naive and ovalbumin-sensitized guinea pig perfused lungs. Our results showed that infusion of NPY (0.24 microM) through the lung significantly inhibited the release of 6-keto-PGF1 alpha (> 30%) and thromboxane B2 (50%) induced by intraarterial administration of BK (3 micrograms) from untreated and ovalbumin-sensitized guinea pig perfused lung. However, the inhibitory effect of NPY was lost in the immunological production of prostaglandins. These results suggest that NPY may act as a regulatory agent of the release of cyclooxygenase-derived products by possibly acting on events preceding phospholipase A2 activation.

Modulation of Ca2+ and Na+ transport by taurine in heart and vascular smooth muscle.

Using the whole-cell voltage clamp technique, taurine was found to affect different types of various ionic currents including T and L-type Ca2+ currents, slow Na+ and fast Na+ currents as well as the delayed outward K+ current. Also, in normal situations, taurine had no effect on the Na(+)-Ca2+ exchange current. The effect of taurine on the different types of ionic currents appears to depend on [Ca2+]o and [Ca2+]i and may also vary according to the tissue or cell type studied. Using standard Ca2+ imaging techniques, short-term exposure (10 to 20 min) of single heart cells and aortic vascular smooth muscle cells was found to increase total intracellular free Ca2+ in a dose-dependent manner. However, using 3-dimensional Ca2+ and Na+ imaging techniques, long-term exposure of heart and vascular smooth muscle cells to taurine was found to decrease both nuclear and cytosolic Ca2+ without significantly changing either nuclear or cytosolic Na+ levels. Long-term exposure to taurine was found to prevent cytosolic and nuclear increases of Ca2+ induced by permanent depolarization of heart cells with high [K+]o. This preventive effect of taurine on nuclear Ca2+ overload was associated with an increase of both cytosolic and nuclear free Na+. Thus, the effect of long-term exposure to taurine on intranuclear Ca2+ overload in heart cells seems to be mediated via stimulation of sarcolemma and nuclear Ca2+ outflow through the Na(+)-Ca2+ exchanger.

R-type calcium channel involved in endothelin-1-induced contraction of rabbit aorta.

The mechanism of Ca2+ mobilization induced by endothelin-1 (ET-1) and the receptor subtype responsible for this effect were examined in the rabbit aorta. We have used preparations with intact and denuded endothelium. Experiments were designed to measure both Fura-2-[Ca]i fluorescence and contractile tension simultaneously. In both preparations, ET-1 (10(-10) to 10(-7) M) induced contractions and increases of the fluorescence ratio in a concentration-dependent manner. ET-1-induced contractions and elevations of [Ca]i were blocked by the dual L- and R-type calcium-channel blocker (-)PN200 110 (10(-6) M), whereas nifedipine (10(-6) M) affected only the latter parameter. BQ-123, a selective ET(A) receptor antagonist, almost totally blocked the ET-1-induced contraction and elevation of [Ca]i. Our results illustrate the activation of the R-type calcium channel by ET-1 on the smooth muscle and on the endothelium rabbit aorta. This effect of ET-1 on the R-type calcium channel is mediated by ET(A) and ETB receptor stimulation.

The rabbit saphenous vein: a tissue preparation specifically enriched in NPY-Y1 receptor subtype.

Neuropeptide Y (NPY), a co-transmitter in noradrenergic sympathetic nerves of the cardiovascular system, was tested on isolated segments of rabbit saphenous vein. NPY caused strong, long lasting and concentration dependent contraction resistant to adrenergic blockade. PYY, a NPY related peptide, shared this property. As pressor agents, both peptides were about 100-fold more potent than norepinephrine and at their highest concentrations caused a contraction of a similar magnitude as NE. Gradual shortening of N-terminal end of the NPY molecule caused major loss of potency and reduction of intrinsic activity; which suggests that the entire molecule is required to produce full biological activity in this vascular preparation. Addition of [Leu31,Pro34]pNPY, a NPY analog with specific agonist properties at Y1 receptors, mimicked the effect of NPY whereas NPY (13-36), a selective agonist at Y2 receptors, caused a 2 log unit shift to the right of the concentration response curve. These results suggest that the vasoconstrictor effect of NPY in rabbit saphenous vein results from a direct effect on smooth muscle cells and that the receptors involved are of the Y1 subtype.

Bronchoconstrictor action of neuropeptide Y (NPY) in isolated guinea pig airways.

Responses of various preparations of guinea pig and rat airways to synthetic porcine neuropeptide Y were analysed in vitro. NPY in doses up to 10(-6) M, induced a dose dependent contraction in trachea, bronchi and lung parenchymal strips of the guinea pig but did not have any effect in similar preparations obtained from the rat. In guinea pig airways the contractile responses to NPY were small in size and characterized by a slow onset and a long duration. This effect of the peptide was not dependent on pre-junctional nerve stimulation but rather mediated through the secondary generation of cyclooxygenase products. It is concluded that NPY may contribute per se to regulating the resting tone of guinea pig airways.