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W De Jong

Publications and source records attributed to W De Jong.

At least 19 recordsLinked to original sources
PubMed1992

Effect of SCH 23390 and quinpirole on novelty-induced grooming behaviour in spontaneously hypertensive rats and Wistar-Kyoto rats.

Grooming behaviour induced by exposure to a novel environment was studied in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). The dopamine D1 receptor antagonist, SCH 23390, and the dopamine D2 receptor agonist, quinpirole, were used to study brain dopamine systems in these rat strains, via their effects on grooming behaviour. The total grooming behaviour displayed in a 50-min observation period was significantly lower in SHR than in WKY. Except for the paw licking component no differences between the two strains were observed in the separate behavioural elements of grooming behaviour. SCH 23390 and quinpirole were found to suppress novelty-induced grooming behaviour of both strains. In SHR, grooming behaviour was less suppressed by SCH 23390, whereas the suppression by quinpirole was more pronounced than in WKY. These results indicate that there are alterations in central dopamine systems in SHR, probably involving changes both in dopamine D1 and D2 receptor mechanisms in the brain.

Animals↗
PubMed1992

A hybrid plant RNA virus made by transferring the noncapsid movement protein from a rod-shaped to an icosahedral virus is competent for systemic infection.

For many plant RNA viruses, multiple viral gene products, including noncapsid movement proteins and capsid proteins, contribute to the spread of infection within plants. The extent to which these factors interact to support infection spread is not known, but, for movement protein mutants of certain viruses, the inability of coinoculated "helper" viruses to complement defective movement has suggested a possible requirement for coadaptation between noncapsid movement proteins and other virus factors. To test directly for required coadaptation, the 3a movement protein gene of cowpea chlorotic mottle virus, an icosahedral bromovirus, was replaced with the nonhomologous 30-kDa movement protein gene of sunn-hemp mosaic virus, a rod-shaped, cowpea-adapted tobamovirus. The resulting hybrid virus is competent for systemic infection of cowpea, with systemic infection dependent upon expression of the 30-kDa gene. In view of the dramatic differences between cowpea chlorotic mottle virus and sunn-hemp mosaic virus in genetic organization and particle morphology, the ability of the hybrid to systemically infect cowpea implies that the tobamovirus 30-kDa movement protein functions independently of sequence-specific interactions with other viral components or sequences. Similarly, the required contribution of bromovirus capsid protein to infection movement appears to be independent of specific interaction with the natural 3a movement protein. In addition to other implications concerning movement protein and coat protein function, the results are consistent with the possibility that two or more distinguishable transfer processes may be involved in crossing different tissue barriers to achieve full systemic spread of infection.

Base Sequence↗
PubMed1992

Protective effects of an alpha-tocopherol analogue against myocardial reperfusion injury in rats.

Free radicals may cause part of the irreversible injury which occurs during myocardial infarction and reperfusion. In the present study MDL 73404, an alpha-tocopherol analogue which is a free radical scavenger has been evaluated for its effects on infarct size in an anaesthetised rat model of coronary artery ligation (60 min) and reperfusion (30 min). Intravenous infusion of the compound began 10 min before occlusion until the end of reperfusion. MDL 73404 (0.3-3 mg/kg per h) reduced infarct size, although not in a dose-related manner. Infusion of MDL 73404 (3 mg/kg per h) commencing 30 min before reperfusion until the end of reperfusion also induced a significant reduction in infarct size. In the isolated rat heart (Langendorff technique) subjected to 30 min no-flow global ischaemia, pretreatment with MDL 73404 (0.03 and 0.1 mM) in the perfusion buffer and during 30 min of reperfusion resulted in a significant increase in the maximal pressure development (+dP/dt max) and relaxation (-dP/dt max), left ventricular systolic pressure and heart rate during reperfusion, whereas left ventricular diastolic pressure was significantly reduced. In contrast, only one control heart out of five exhibited signs of recovery. Replacement, for 2 min, with a cardioplegic solution before the 30 min period of ischemia resulted in an increased heart rate and contractility during reperfusion compared to hearts that did not receive the cardioplegic solution. The presence of MDL 73404 (0.03 and 0.1 mM) in the perfusion fluid induced an additional increase in left ventricular systolic pressure to the pre-ischaemic levels. MDL 73404 may have potential for cardioprotective use in acute reperfusion of the myocardium following ischaemia.

Animals↗
PubMed1991

Effect of the dopamine D2 receptor agonist quinpirole on the in vivo release of dopamine in the caudate nucleus of hypertensive rats.

Using an in vivo microdialysis method, we found that the extracellular concentrations of dopamine and its main metabolite dihydroxyphenylacetic acid (DOPAC) were lower in the caudate nucleus of 8-week-old spontaneously hypertensive rats (SHR) than in the same area of age-matched normotensive Wistar-Kyoto rats (WKY). No differences in the extracellular concentrations of dopamine and DOPAC were found between renal and deoxycorticosterone acetate (DOCA)-salt hypertensive rats when compared to their respective controls. After subcutaneous administration of the dopamine D2 receptor agonist quinpirole (10, 33 and 100 micrograms/kg), the amount of dopamine and DOPAC in the dialysates was diminished dose dependently. The quinpirole-mediated inhibition of dopamine release was more pronounced in SHR than in WKY, whereas inhibition of the extracellular DOPAC concentration was not different. Compared to WKY, the dose-response curve for the inhibition of dopamine release by quinpirole was shifted to the left in SHR and the maximal inhibition in response to the highest dose was significantly greater. Renal and DOCA-salt hypertensive rats showed no differences in the quinpirole-induced inhibition of the extracellular concentrations of striatal dopamine and DOPAC compared to their controls. The present findings on changes in dopaminergic neurotransmission and D2 autoreceptor-mediated modulation of dopamine release in genetically hypertensive rats but not in rats with experimentally induced hypertension provide further evidence for the hypothesis that alterations in the nigrostriatal dopamine system may be involved in the initiation of the development of spontaneous hypertension.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1991

The electrically stimulated release of [3H]noradrenaline from nucleus tractus solitarii slices in vitro is modulated via mu-opioid receptors.

The electrically stimulated release of [3H]noradrenaline ([3H]NA) from slices of the nucleus tractus solitarii (NTS) from the rat in vitro was inhibited by the alpha 2-adrenoceptor agonist, clonidine, in a concentration-dependent manner and enhanced by the alpha 2-adrenoceptor antagonist, yohimbine. Phenylephrine, isoprenaline, carbachol, quinpirole and SKF 38393, all at 10(-6) M, did not affect the stimulus-evoked release of [3H]NA. The opioid peptides, alpha- and gamma-endorphin, did not have a significant effect on the stimulus-evoked release of [3H]NA; however, beta-endorphin reduced it in a concentration-dependent manner. [Leu5]Enkephalin also reduced [3H]NA release, but higher concentrations were necessary. The selective delta opioid receptor agonists, [D-Pen2,D-Pen5]enkephalin (DPDPE) and [D-Ser2(O-tert-butyl),Leu5]enkephalyl-Thr6 (DSTBULET), as well as the selective kappa opioid receptor agonist, U-69593, were not effective. The selective mu opioid receptor agonist, [D-Ala2,NMePhe4,Gly-ol5]enkephalin (DAGO), concentration dependently reduced the stimulus-evoked release of [3H]NA to the same extent as beta-endorphin did. Naloxone, while having no effect on stimulus-evoked [3H]NA release, antagonized the effect of DAGO. These results corroborate that the release of NA from noradrenergic terminals in the NTS region of the medulla oblongata of the rat is modulated via alpha 2-adrenoceptors and suggest that the release of NA in the NTS in rats is also modulated via mu opioid receptors.

Adrenergic alpha-Agonists↗
PubMed1979

An opposing role for the adrenals in the hypotensive effects of propranolol in the spontaneously hypertensive rat.

d,l-Propranolol (1 and 5 mg/kg s.c.) did not cause a fall in blood pressure and induced only a limited decrease in heart rate in conscious spontaneously) hypertensive rats (SHR). In contrast, after bilateral adrenalectomy, d,l-propranolol induced a rapid and profound decrease in blood pressure and heart rate. Decreases in heart rate and blood pressure in the individual animals were not correlated. The effects were mainly caused by l-propranolol but an additional effect of d-propranolol cannot be excluded. The decrease in blood pressure was not observed after removal of the adrenal medulla. Heart rate decreased only slightly in these animals. After treatment of adrenalectomized SHR with corticosterone (1 mg/kg b.w./h) the decrease in blood pressure due to d,l-propranolol was completely abolished. The fall in heart rate was diminished. Central injection of d,l-propranolol into the lateral brain ventricle of adrenalectomized SHR caused cardiovascular changes which were less pronounced than those following peripheral injection of comparable doses. The inhibitory effects of d,l-propranolol also occurred in adrenalectomized normotensive Wistar Kyoto rats. However, no significant changes in blood pressure and only a limited fall in heart rate were observed in adrenalectomized normotensive and renal hypertensive Wistar rats. It is concluded that the presence of the adrenal cortex, but not of the adrenal medulla prevents acute hypotension and bradycardia after propranolol in the conscious SHR.

Adrenal Glands↗
PubMed1979

Effect of catecholamine-receptor stimulating agents on blood pressure after local application in the nucleus tractus solitarii of the medulla oblongata.

The effect of various catecholamines and alpha-mimetics, given by microinjection in the A2-region of the nucleus tractus solitarii (NTS), on blood pressure was investigated in anesthetized male rats. A dose-dependent decrease of blood pressure and heart rate was induced by adrenaline as the most effective drug, followed by noradrenaline, dopamine, alpha-methylnoradrenaline and octopamine. Ablation of the rostral or caudal part of the NTS, or removal of the area postrema did not diminish the effect of alpha-methylnoradrenaline. Higher doses of noradrenaline and alpha-methylnoradrenaline caused an initial rise of blood pressure, while the blood pressure lowering effect of noradrenaline was diminished, and that of alpha-methylnoradrenaline and dopamine delayed. Isoprenaline and the (+)-stereoisomers of noradrenaline and alpha-methylnoradrenaline were ineffective. The hypotensive effect of dopamine was not prevented by systemic injection of the dopamine beta-hydroxylase inhibitor FLA 63. Prior application of haloperidol, yohimbine and phentolamine antagonized the hypotensive response to dopamine and alpha-methylnoradrenaline. Application of peripherally effective alpha-mimetics into the A2-region had no or little effect, while high doses increased blood pressure. Tyramine and clonidine caused some decrease of blood pressure. Clonidine also decreased blood pressure when it was applied in the area of the locus coeruleus. Application of isoprenaline in the locus coeruleus also decreased blood pressure while in contrast adrenaline, noradrenaline, dopamine and alpha-methylnoradrenaline increased blood pressure. The present data suggest that the catecholaminergic receptors in the A2-region of the NTS differ from the classic vascular alpha-receptor and that the NTS also may contain structures which can antagonize the decrease in blood pressure.

Animals↗
PubMed1979

Transformation and T antigen induction by linearized BK virus DNA.

Linearized unit length DNA obtained after cleavage of the supercoiled DNA of the human papovavirus BKV by PstI (.031) induced transformation and T antigen less efficiently than DNA cleaved by EcoRI (0.0), BamHI (0.98), KpnI (0.90) or HhaI (0.73). BKV DNA cleaved by XbaI (0.27 and 0.95) did not induce T antigen.

Animals↗
PubMed1978

Differential development of renal, DOCA-salt, and spontaneous hypertension in the rat after neonatal sympathectomy.

The development of hypertension was studied in rats after neonatal sympathectomy by s.c. injection of 6-hydroxydopamine HCl. Three different types of hypertension were investigated: renal hypertension in the two-kidney Goldblatt model, steroid hypertension produced by deoxycorticosterone (DOCA) implantation and saline as drinking fluid, and genetic hypertension in the spontaneous hypertensive rat (SHR). Blood pressure was measured directly in conscious animals via the iliac artery. Mean blood pressure of conscious sympathectomized (SX) normotensive rats was not significantly different from that of normotensive controls. Renal hypertension reached the same level in controls and SX rats four weeks after application of a renal artery clip. DOCA-salt hypertension developed faster and to a higher level in SX rats than in control rats. The hypertension in SX DOCA-salt hypertensive rats was accompanied by a marked tachycardia. In contrast hypertension did not develop in SX SHR. Up to 12 months of age mean blood pressure was markedly lower than that of control SHR, but slightly higher than that of SX normotensive Wistar Kyoto rats. These differential effects of neonatal sympathectomy on the development of hypertension in the rat may point to differences in the pathophysiological mechanisms. It is concluded that an intact sympathetic nervous system is essential for the development of hypertension in SHR. In DOCA-salt hypertension the intact sympathetic nervous system appears to protect against a rapid rise in blood pressure.

Animals↗