British journal of pharmacology
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1. The opioid type of swim-stress induced antinociception (SIA) is mediated via mu-sites in preweanling rats and predominantly by delta-sites in postweanling animals. We have studied the effect of delay of weaning on the receptor transition of this behaviour in the developing rat. 2. ⋯ In 30 day old non-weaned rats, naltrindole (5 mg kg-1) abolished the swim SIA. 6. In conclusion, transition from mu to delta-receptor control of swim SIA in rat pups can be delayed by between 5 and 10 days by delay of weaning. The environmental stimulus of weaning can activate opioid receptor subtype operation of biological responses in the developing animal.
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1. Ischaemia-reperfusion injury in the kidney is associated with a loss of autoregulation, an increase in renal vascular resistance (RVR), a decrease of renal blood flow (RBF) and ultimately acute renal failure. The aim of this study was to investigate the role of the release of endogenous nitric oxide (NO) in the recovery of RBF after ischaemic injury of the renal vascular bed. 2. ⋯ Moreover, dexamethasone(3 mg kg-1, i.v., 60 min prior to I/R, n = 6), an inhibitor of the induction of NO synthase,had no effect on either RBF or RVR in rats subjected to I/R. In contrast to I/R, lipopolysaccaride(LPS, endotoxin; 5 mg kg-1, i.p., n = 3) caused a significant induction of a calcium-independent NO synthase activity in the kidney.6. These results confirm the importance of the release of vasodilator cyclo-oxygenase metabolites in the compromised renal circulation and indicate that the formation of NO derived from the constitutive, but not the inducible NO synthase, is also important for the maintenance of RBF after I/R injury of the renal vascular bed.
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1. The vascular actions of N omega-nitro-L-arginine methyl ester (L-NAME), sodium nitroprusside and noradrenaline were investigated in cats under chloralose anaesthesia with controlled vascular tone and ventilation. Cardiac output, heart rate, vascular pressures and mean circulatory filling pressure (MCFP) were measured. ⋯ The depression of cardiac output by L-NAME is attributed to the increase in Rvr, partly compensated by the rise in MCFP. For a given rise in MCFP, the increase in R, was seven times greater after L-NAME than after noradrenaline, and the difference in the relative actions of the two drugs on resistance and capacitance vessels largely accounts for their contrasting effects on venous return. A procedure is suggested for replacement of vascular nitric oxide by nitroprusside infusion and blood volume expansion.
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1. The effects of intrathecal (i.t.) administration of beta-endorphin and two shorter fragments, human and ovine beta-endorphin1-27, were examined for antinociceptive activity in the tail-flick and paw-pressure tests in the rat. Additionally, the ability of ovine beta-endorphin1-27 to influence the action of i.t. beta-endorphin, morphine and [D-Pen2-D-Pen5]enkephalin (DPDPE) was also examined in these tests. 2. ⋯ Administration of ovine beta-endorphin1-27 (1.44 nmol, i.t.) significantly attenuated the antinociceptive effect of morphine (14.9 nmol, i.t.) in both tests and the effect of DPDPE (38.7 nmol) in the tail-flick test. 6. The results show that beta-endorphin1-27 acts as an opioid antagonist at the spinal level in the rat. Its ability to inhibit the action of morphine and DPDPE suggests that it may attenuate beta-endorphin action by an interaction with mu- and/or delta-opioid receptors.
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1. We have investigated whether porcine endocardial cells in culture express the inducible, Ca(2+)-independent form of nitric oxide (NO) synthase. 2. NO synthase activity in cytosolic extracts of endocardial cells was measured by estimation of the rate of formation of L-[14C]-citrulline from L-[14C]-arginine. 3. ⋯ Simultaneous addition of dexamethasone (0.01-1 microM) or cycloheximide (0.03-3 microM) inhibited in a concentration-dependent manner TNF alpha- and IL-1 beta-induced expression of Ca(2+)-independent NO synthase activity. Neither dexamethasone (1 microM) nor cycloheximide (3 microM) had any effect on the activity of the constitutive NO synthase. 6. The possible pathophysiological consequences of endocardial expression of the inducible NO synthase are discussed.