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W de Jong

Publications and source records attributed to W de Jong.

At least 19 recordsLinked to original sources
PubMed1995

The nigrostriatal dopamine system and the development of hypertension in the spontaneously hypertensive rat.

Several observations reported in the literature reveal a role of brain catecholaminergic systems in the development of hypertension in spontaneously hypertensive rats (SHR). As reviewed here, our results obtained with intracerebroventricular injections of 6-hydroxydopamine in your SHR point in particular to the involvement of the nigrostriatal dopamine system. The electrically stimulated release of radiolabeled dopamine in vitro from caudate nucleus slices of SHR was lower than that in slices of normotensive Wistar-Kyoto rats (WKY). Using an in vivo microdialysis method, we found that the extracellular concentration of dopamine and the metabolite DOPAC was lower in the caudate nucleus of conscious SHR than in that of WKY. We also studied the effects of lesions of the pars compacta of the substantia nigra of 4 week-old SHR and WKY, 1) on blood pressure and heart rate, 2) on the concentrations of dopamine and metabolites in the caudate nucleus and 3) on the release of radiolabeled dopamine from caudate nucleus slices using an in vitro superfusion method, 6 weeks following lesioning. Substantia nigra lesions caused a profound attenuation of the development of hypertension in SHR, with no effect on heart rate. The ratios DOPAC/dopamine and HVA/dopamine were lower in sham-treated SHR than in sham-treated WKY pointing to a lower turnover of dopamine in SHR. Six weeks after lesioning, the concentrations of dopamine were decreased in the caudate nucleus of both strains. At this time, the stimulus-evoked release of dopamine from the remaining terminals was significantly increased in caudate nucleus slices of SHR but not in slices of WKY. Thus, whereas the release of dopamine from caudata nucleus slices is lower in sham-treated SHR than in sham-treated WKY, lesioning of the substantia nigra results in a similar release of dopamine from caudate nucleus slices of lesioned SHR and sham-treated WKY. This normalization of dopaminergic activity may be the causal factor underlying the attenuation of the development of hypertension in SHR after bilateral lesioning of the pars compacta, of the substantia nigra.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1994

The nigrostriatal dopamine system: role in the development of hypertension in spontaneously hypertensive rats.

The effects of lesions in the pars compacta of the substantia nigra of 4-week-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) were studied on (a) changes in blood pressure during a period of 6 weeks following lesioning, and (b) dopamine and metabolite concentrations in the caudate nucleus and (c) the in vitro release of [3H]dopamine from caudate nucleus slices 6 weeks after the lesioning. We report here that substantia nigra lesions caused a profound attenuation of the development of hypertension in SHR. No effect on heart rate was observed. Whereas the concentrations of dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) in the caudate nucleus were not different, the amount of homovanillic acid (HVA) and the ratios DOPAC/dopamine and HVA/dopamine were lower in sham-treated SHR than in sham-treated WKY, indicating a lower turnover of dopamine in SHR. Six weeks after lesioning, the concentrations of dopamine, DOPAC and HVA were decreased in the caudate nucleus (46-66%) of both strains, whereas DOPAC/dopamine and HVA/dopamine ratios tended to be increased in both SHR and WKY. Using an in vitro superfusion method, it was found, that the electrically stimulated release of [3H]dopamine from caudate nucleus slices of sham-treated SHR was lower than from slices of sham-treated WKY at the age of 10 weeks. Six weeks after lesioning, the stimulus-evoked release of [3H]dopamine from the remaining terminals was significantly increased in caudate nucleus slices of SHR, whereas the difference did not reach statistical significance in WKY.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗
PubMed1994

Mineralocorticoid antagonist inhibits stress-induced blood pressure response after repeated daily warming.

We report here that with a direct method for measurement of cardiovascular parameters in conscious rats, intracerebroventricular administration of the mineralocorticoid receptor (MR) antagonist RU-28318 (100 ng) reduces the blood pressure, heart rate, and the corticosterone response to a brief restraint stress, provided the rats were previously subjected to a daily 30-min exposure to 32 degrees C for 2 wk. The daily exposure to warming and restraint stress are applied identically to the training procedure required for indirect blood pressure measurement using the tail-cuff method. The basal arterial pressure is not affected by the MR antagonist. The effect of the MR antagonist on the stress-induced pressor response develops with a delay of several hours in the normotensive rats. The corticosterone response to daily warming and stress is also attenuated by the intracerebroventricular infusion of MR antagonist but with shorter onset and shorter duration. The findings suggest that conditioning to daily warming and stress imposes mineralocorticoid dependency of the pressor response, which involves MR functioning in brain.

Adrenocorticotropic Hormone↗
PubMed1994

Central effects of mineralocorticoid antagonist RU-28318 on blood pressure of DOCA-salt hypertensive rats.

The role of brain mineralocorticoid receptor (MR) sites in the pathogenesis of mineralocorticoid hypertension was studied after an intracerebroventricular injection of the MR antagonist RU-28318. Male Wistar rats received subcutaneously implanted deoxycorticosterone acetate (DOCA) pellets and were maintained on 0.9% saline as drinking solution. Under these conditions hypertension developed in approximately 5 wk as assessed in conscious rats by means of the tail-cuff technique. During the development of this hypertension (after 3 wk of DOCA-salt treatment) a single intracerebroventricular injection of the specific MR antagonist RU-28318 reduced systolic blood pressure (SBP) as measured with the tail-cuff method. A decrease in SBP was observed 2-24 h after this intracerebroventricular injection, with the lowest SBP values occurring at 8 h. In these animals (3 wk after DOCA implantation) continuous direct blood pressure recording via chronic cannulation revealed, on the day of the intracerebroventricular injection of RU-28318, a slight increase in arterial pressure during the light phase, followed by a decrease during the dark phase. In the established hypertensive rats (5 wk after DOCA RU-28318 on the arterial pressure or heart rate was detectable. It is concluded that central MR blockade during the development of the DOCA-salt hypertension reduces blood pressure within 24 h assessed with 1) the indirect method at certain time points after exposure to warming and stress and 2) the direct method during the dark phase of the diurnal cycle.

Animals↗
PubMed1994

Effect of a home exercise training program in patients with cystic fibrosis.

Physical training in patients with pulmonary diseases, including cystic fibrosis (CF), may improve exercise tolerance in these patients. Most training programs are performed in a clinical setting. Little information is available concerning the effect of home exercise training programs in CF patients. The purpose of this study was to investigate the effect of a home exercise training program in CF patients. Ten adolescent patients (seven male and three female) with CF, mean (SD) age 20.6 (6.5) years, participated in a home exercise training program for 3 months. Pretraining condition was assessed during a control period of 2 months in which patients were asked to continue their normal daily activities. Home exercise training consisted of cycle training of 15 min at a submaximal workload once a day and was supervised by a physiotherapist two times a week. A follow-up period of 1 month, in which the patients were advised to continue cycling at home without supervision, was included after the training program. Pulmonary function, bicycle exercise test performance, and the degree of limitation in activities of daily living (ADL) were measured. No significant differences were found between the two pretraining assessments. After the training period we found significant improvement in maximal exercise capacity (Wmax) (mean [SEM]: 126 [10] W before and 146 [11] W after; p = 0.004), maximal oxygen uptake (VO2max) (mean [SEM]: 31.4 [2.1] ml.kg-1.min-1 before and 36.5 [2.5] ml.kg-1.min-1 after; p = 0.008), oxygen pulse (VO2/HR) (mean [SEM]: 10.9 [0.66] ml before and 11.9 [0.74] ml after; p = 0.047), and degree of limitation in ADL (mean [SEM]: 2.4 [0.43] before and 1.5 [0.48] after; p = 0.019) as compared with the initial values. Since no significant differences were found between the posttraining values and the results at the end of the follow-up period, the patients were apparently able to maintain the training effects during the follow-up period. We conclude that in CF patients, a home exercise training program, after clinical assessment of exercise tolerance, is an effective and relatively simple treatment to improve physical performance and decrease limitation in ADL and should be included in the maintenance treatment in these patients.

Activities of Daily Living↗
PubMed1994

Effects of positive expiratory pressure breathing during exercise in patients with COPD.

The effect of breathing with a positive expiratory pressure of 5 cm H2O was investigated in eight patients with COPD (mean [SD]FEV1 = 54 [13] percent predicted). Specific work of breathing (Wsp) and myoelectrical activity of the following respiratory muscles were measured at rest: scalene muscle, parasternal muscle, and abdominal muscles. Minute ventilation (VE), end-tidal CO2 (FETCO2), physiologic dead space ventilation (VD/VT), oxygen uptake (VO2), and carbon dioxide output (VCO2) were measured at rest and during an incremental bicycle exercise test. Dyspnea sensation during exercise was quantified using the CR10 Borg-scale. All measurements were performed with and without positive expiratory pressure (PEP). During PEP breathing at rest mean (SEM) Wsp increased from 0.54 (0.13) J/L to 1.08 (0.10) J/L. The SEM VE decreased from 12.4 (1.0) L/min to 10.5 (1.1) L/min, and SEM VD/VT decreased from 0.39 (0.03) to 0.34 (0.03). There was a tendency for an increased phasic respiratory muscle activity during PEP breathing of all three muscles as compared with undisturbed breathing, but the changes were not statistically significant. During the exercise test with PEP, VE, VD/VT, VO2, and VCO2 were significantly lower, and FETCO2 was significantly higher as compared with the values obtained during the exercise test with undisturbed breathing. Dyspnea sensation during the exercise test with PEP, however, was higher than during the test with undisturbed breathing. The PEP breathing at rest may be useful in patients with COPD as it increases the efficiency of ventilation by reducing dead space ventilation. This beneficial effect also occurs during exercise, but here it is accompanied by increased dyspnea sensation.

Dyspnea↗
PubMed1993

Complete saturation of protamine sulphate by dsDNA is necessary in order to obtain a highly sensitive and specific anti-dsDNA ELISA.

A protamine sulphate (PS) pretreated solid phase coated with different amounts of dsDNA has been used to develop a sensitive, specific and reproducible anti-dsDNA ELISA. Using low concentrations of a dsDNA coat 50% of SLE sera were found to be positive and false positive reactivity due to anti-PS reactivity was found in 3/40 patients with other auto-immune diseases (OAID). In contrast, when PS was saturated with higher concentrations of dsDNA 80% of SLE sera were detected, the reproducibility of the results was better and anti-PS reactivity of OAID patients with an anti-PS reactivity disappeared. The sera of three other OAID patients contained low avidity anti-dsDNA, measured after a salt elution step in the ELISA procedure, and 2/60 patients with non-auto-immune disease exhibited a false positive anti-dsDNA reactivity since they reacted with the solid phase even in the absence of PS and dsDNA. Thus an ELISA procedure using a PS pretreated solid phase permits the sensitive, specific and reproducible measurement of anti-dsDNA antibodies only if a high concentration of dsDNA is coated on the PS and appropriate controls are performed.

Adult↗
PubMed1993

Effect of positive expiratory pressure on breathing pattern in healthy subjects.

The purpose of this study was to register breathing patterns, in healthy subjects, during breathing with a positive expiratory pressure. Integrated electromyographic (IEMG) activity of the following muscles was assessed: scalene muscle, parasternal muscle and abdominal muscles, using surface electrodes. Inspiration time, expiration time, total breathing cycle time, tidal volume and breathing frequency were measured using a water-sealed spirometer. Functional residual capacity was measured using a body plethysmograph. Oxygen uptake and carbon dioxide output were measured using an automatized ergometry set-up. All measurements were performed during undisturbed breathing and during breathing with positive expiratory pressures of 5 and 15 cmH2O. Phasic activity, but not tonic activity, of the scalene muscles and the abdominal muscles increased significantly during breathing with the expiratory pressures. No significant change was observed in phasic or tonic activity of the parasternal muscle. Mean (SD) tidal volume increased significantly from 0.8(0.2) l during undisturbed breathing to 1.1(0.3) l and 1.5(0.7) l during breathing with the expiratory pressures of 5 cmH2O and of 15 cmH2O, respectively. Respiration times, breathing frequency, oxygen uptake, carbon dioxide output and functional residual capacity remained unchanged. It can be concluded that, in healthy subjects, positive expiratory pressure increases tidal volume by activity of both expiratory and inspiratory muscles, while functional residual capacity remains unchanged. The changes appeared to be pressure dependent.

Adult↗
PubMed1992

Differential effects of ACTH4-10, DG-AVP, and DG-OXT on heart rate and passive avoidance behavior in rats.

A computerized telemetry system was used to monitor heart rate (HR), core temperature (CT), and gross locomotor activity in rats treated with saline or neuropeptides during a passive avoidance behavior task. Rats were exposed to a single mild footshock (0.15 mA, for 3 s). Retention tests were conducted at 24 and 48 h after the learning trial. One h prior to the 24-h retention test, each rat received one of the following treatments (SC): saline (SAL), desglycinamide [Arg8]-vasopressin (DG-AVP), ACTH4-10, or desglycinamide-oxytocin (DG-OXT), at a dose of 3 micrograms/rat for DG-AVP and DG-OXT, and 50 micrograms/rat for ACTH4-10. Rats treated with SAL showed a modest increase in avoidance latency accompanied by bradycardia at both retention tests. Rats receiving DG-AVP retained the highest avoidance latency among the experimental groups at both the 24- and 48-h retention test. These rats showed a decrease in HR of the same magnitude as the SAL-treated animals at both retention tests. Rats treated with ACTH4-10 showed an increase in avoidance latency during the 24-h but not during the 48-h retention test. In addition, following ACTH4-10 treatment, a tachycardiac response was found during the 24-h retention test. DG-OXT induced both behavioral and cardiac responses opposite to those found in rats given DG-AVP. CT gradually increased while the rats remained on the platform, irrespective of the treatment. Changes in HR and CT were not influenced by somatomotor activity, as no difference in gross locomotor activity was found among the groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1991

Hypothalamic blood flow autoregulation remains unaltered following surgical and pharmacological blockade of central vasopressin.

Experiments were carried out in urethane anaesthetized, ventilated rats to determine if brain arginine-vasopressin (AVP) plays a physiological role in cerebral blood flow autoregulation. Autoregulation was tested by determining local hypothalamic blood flow in the mediobasal hypothalamic area (HBF; H2-gas clearance technique) during consecutive stepwise lowering of systemic mean arterial pressure to 80, 60 and 40 mm Hg, by hemorrhage. Endogenous AVP was blocked by transecting the rostral, lateral and dorsal neuronal connections of the hypothalamus (including the median eminence) from all major brain areas, by bilateral transection of the vasopressin-containing fibres in the hypothalamo-hypophyseal tract to the median eminence at the level of the lateral retrochiasmatic area (RCAL), and finally by intracerebroventricular (i.c.v.) administration of an AVP antagonist, d(CH2)5Tyr(Me)AVP (AAVP). Significant increases of daily water intake indicated impaired vasopressin release following both types of surgical transection. Resting HBF was significantly elevated both after surgical isolation of the hypothalamus and after 10 ng AAVP administration compared to controls. Blood flow autoregulation in the hypothalamic region was seriously impaired following surgical isolation of the hypothalamus. However, HBF autoregulation remained just as effective as that of the control rats following either selective bilateral transection of the vasopressin pathways or following AAVP treatment. The present data indicate that AVP may play a role in the control of resting hypothalamic blood flow, but does not support a role of AVP in HBF autoregulatory mechanisms.

Animals↗
PubMed1991

Effect of anaesthetics on the release of beta-endorphin-immunoreactivity in rat plasma.

Analgesia and anaesthesia produced by fentanyl, urethane and ether, but not pentobarbital, occurred concomitantly with an increase in the concentration of plasma beta-endorphin like immunoreactivity (BEIR), probably of pituitary origin. This increase was not associated with significant changes in pituitary or brainstem beta-endorphin content. Pretreatment with naloxone caused a reduction in plasma BEIR increase following Hypnorm, ether and urethane; and in the analgesia following Hypnorm and urethane. Pentobarbital, alone or in combination with naloxone, did not increase the concentration of plasma beta-endorphin. These results may indicate participation of endogenous opioids in the mechanism of action of urethane.

Analgesics↗
PubMed1991

Effects of dynorphin A(1-13) and of fragments of beta-endorphin on blood pressure and heart rate of anesthetized rats.

The effect on blood pressure and heart rate of central administration of dynorphin A(1-13) and of beta-, gamma-, and alpha-endorphin related peptides was studied in urethane-anesthetized rats. Intracerebroventricular (i.c.v., 0.1-10 micrograms) administration of beta-endorphin resulted in a dose-dependent, naltrexone-reversible hypotension and bradycardia. N-terminally modified fragments of beta-endorphin did not reduce blood pressure and heart rate. On the other hand, a dose of 10 micrograms of beta-endorphin(1-27), which lacks the four C-terminal amino acid residues of beta-endorphin, induced a fall in blood pressure and had a biphasic effect on heart rate. These responses, however, were resistant to pretreatment with naltrexone. None of the fragments of beta-endorphin smaller than beta-endorphin(1-27) affected blood pressure when administered i.c.v. in a dose of 10 micrograms. A small transient bradycardia was observed after i.c.v. administration of 10 micrograms of beta-endorphin(1-26), alpha, and gamma-endorphin. The naltrexone-reversible bradycardic response of alpha- and gamma-endorphin was not present in des-tyrosine- and des-enkephalin-alpha- and gamma-endorphin and also not in alpha-endorphin(10-16) and gamma-endorphin(10-17). Upon i.c.v. administration (0.1-50 micrograms) a dose-dependent, naltrexone-reversible decrease in blood pressure and heart rate was induced by dynorphin A(1-13). The present data indicate a hypotensive influence of beta-endorphin, beta-endorphin(1-27), and dynorphin A(1-13), whereas other fragments of beta-endorphin had little or no effect on the cardiovascular parameters investigated.

Anesthesia↗
PubMed1991

Role of brain dopamine systems in the development of hypertension in the spontaneously hypertensive rat.

We studied the role of central dopamine in the development of hypertension. Earlier work had shown that depletion of brain dopamine can inhibit the age-related rise in blood pressure in spontaneously hypertensive rats (SHR). In an open-field test, locomotor activity of Wistar-Kyoto controls was inhibited by haloperidol, apomorphine and sulpiride, but these drugs had less effect in SHR. The stimulation-evoked release of [3H]-dopamine from slices of the striatum of SHR was smaller than that from slices of WKY. The inhibition of the stimulation-evoked release of [3H]-dopamine by quinpirole was greater in SHR than in WKY. The results from the lesion experiments and from the behavioural activity studies would suggest an enhanced release of central dopamine in SHR, which might contribute to the development of hypertension in these animals. However, the in vitro release experiments (and subsequent in vivo microdialysis experiments) do not support such an enhanced release but rather showed decreased release of striatal dopamine in SHR.

Animals↗
PubMed1991

Endogenous opioid peptides and blood pressure regulation during controlled, stepwise hemorrhagic hypotension.

In the present study, the role of the endogenous opioid peptide systems in the regulation of blood pressure during standardized, stepwise hemorrhagic hypotension was investigated in anesthetized rats. Central as well as peripheral administration of naloxone resulted in an increase in the bleeding volumes required to reduce blood pressure. Bleeding volumes also increased after the peripheral injection of naloxone methobromide, an analog of naloxone that does not readily cross the blood-brain barrier. Following central administration of antisera against beta- and alpha-endorphin and dynorphin A(1-13), the amount of blood that had to be withdrawn to induce hypotension was elevated. In rats treated with an antiserum against [Met5] enkephalin or gamma-endorphin, bleeding volumes did not differ from those of rats treated with control serum. These data indicate that activation of central and possibly also of peripheral opiate receptors plays a role in the control of blood pressure during blood loss. Dynorphin A(1-13), beta- and alpha-endorphin, or closely related peptides might be the endogenous ligands for the receptors that are blocked by naloxone.

Animals↗
PubMed1990

Disturbed hypothalamic blood flow autoregulation in the rat following hypophysectomy: a role of pituitary beta-endorphin?

The effect of hypophysectomy on hypothalamic blood flow autoregulation was studied in anesthetized, artificially ventilated rats. Local hypothalamic blood flow (HBF, H2-gas clearance method) was measured. Efficiency of autoregulation was tested by determining HBF during standardized hemorrhagic hypotension when systemic arterial pressure was lowered to 80, 60 and 40 mm Hg by consecutive, step-wise bleeding. HBF autoregulation was well maintained until 80 mmHg, but not completely at 60 and 40 mmHg arterial pressure in the sham-operated control group. In contrast, autoregulation was abolished at all levels in the hypophysectomized rats: HBF followed the changes in arterial pressure in these animals. Following hypophysectomy, the concentration of immunoreactive beta-endorphin (beta-EP) decreased drastically in plasma but remained unchanged in cerebrospinal fluid. Administration of beta-EP (200 pg/100 g b. wt.) to hypophysectomized rats by the intravenous route had no effect on autoregulation, while intracerebroventricular administration of the same dose restored autoregulation. The present findings suggest that the pituitary plays a role in hypothalamic blood flow autoregulation.

Animals↗
PubMed1990

Analysis of the cardiovascular changes evoked by microinjection of NaCl into the nucleus tractus solitarii of rats: evidence for a Na+/Ca2+ relationship.

The effect of various ionic solutions microinjected into the nucleus tractus solitarii (NTS) on blood pressure, heart rate and respiration rate was investigated in urethane-anesthetized rats. Unilateral microinjection of solutions containing NaCl (154 mM), NaCl (154 mM) and KCl (2.8 mM) or NaNO3 (154 mM) into a restricted area of the NTS evoked acute decreases in blood pressure, heart rate and respiration rate. However, calcium chloride (0.36-3.3 mM), present in the microinjection solutions, reduced the decrease in all 3 recorded parameters in a concentration-dependent manner. A disturbance in the Na+/Ca2+ ionic ratio may account for the changes evoked by the administered solutions. These results indicate the presence of a restricted area in the NTS which is sensitive to changes in some vegetative functions.

Animals↗
PubMed1990

Central vasopressin impairs the baroreceptor heart rate reflex in conscious rats.

In conscious, unrestrained rats, the resting values of mean arterial blood pressure (BP) and heart rate (HR) as well as the baroreceptor heart rate reflex (BHR) were measured before and after intracerebroventricular (i.c.v.) application of arginine vasopressin (AVP). The BHR was induced by intravenous (i.v.) injection of different doses of phenylephrine. Basal values of BP and HR were 114 +/- 2.4 mm Hg and 376 +/- 13 beats/min (mean +/- SE). These values were not altered by i.c.v. application of vehicle or 5, 10, 30, 300, 3,000 pg AVP or 1 pg AVP antagonist [(D(CH2)5Tyr(Me)-AVP)]. Ten and 30 pg AVP administered i.c.v. attenuated the phenylephrine-induced decrease in HR. Lower or higher doses of AVP were not effective. Administration of the AVP antagonist i.c.v. sensitized the BHR. When the BHR was rechecked 24 h after treatment, the influence of the i.c.v.-administered peptides had disappeared. We conclude that AVP through the cerebrospinal fluid impairs the baroreflex regulation.

Animals↗