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S Ritter

Publications and source records attributed to S Ritter.

At least 109 records · Page 6Linked to original sources
PubMed1989

Capsaicin abolishes lipoprivic but not glucoprivic feeding in rats.

To assess the contribution of visceral sensory neurons to feeding induced by blockade of glucose and fatty acid metabolism, adult rats were anesthetized and treated systemically with capsaicin, a toxin that destroys fine-diameter unmyelinated primary sensory neurons, including many visceral sensory neurons. Rats were maintained on a fat-supplemented diet throughout experimentation. For feeding tests, intake of this diet was measured hourly for 6 h after systemic blockade of fatty acid or glucose utilization with mercaptoacetate (MA) or 2-deoxy-D-glucose (2-DG), respectively, after simultaneous administration of MA and 2-DG and after saline injection. 2-DG stimulated a dose-related feeding response that was similar in magnitude in both capsaicin and vehicle-treated rats. MA also stimulated a dose-related feeding response in vehicle-treated rats. However, capsaicin-treated rats did not eat in response to MA. In addition, 2-DG and MA were additive in their stimulation of feeding in vehicle-treated controls, but capsaicin-treated rats ate the same amount after 2-DG plus MA as they did in response to 2-DG alone. Thus glucoprivation and lipoprivation activate anatomically and chemically distinct receptors for the metabolic control of feeding.

Animals↗
PubMed1989

Capsaicin attenuates hindbrain neuron responses to circulating cholecystokinin.

Capsaicin is a neurotoxin that destroys small sensory neurons with unmyelinated axons, including a subpopulation of vagal sensory neurons. Capsaicin treatment attenuates suppression of food intake induced by systemic administration of cholecystokinin (CCK) but not by gastric distension. However, both gastric distension and intravascular CCK alter the discharge of dorsal hindbrain neurons by a vagal mechanism. Therefore, it is plausible that some hindbrain neurons receive convergent input from capsaicin-sensitive vagal neurons that are responsive to CCK and also from capsaicin-insensitive neurons that are responsive to gastric distension. To investigate this possibility we made extracellular recordings from gastric distension-responsive hindbrain neurons during intra-arterial cholecystokinin octapeptide (CCK-8) administration in anesthetized intact and capsaicin-pretreated rats. We found that capsaicin-pretreated rats exhibit attenuated neuronal discharge responses to CCK-8 but not to gastric distension. These results are consistent with the existence of convergent CCK-sensitive and gastric distension-sensitive afferent inputs to hindbrain neurons and suggest that various gastrointestinal sensory modalities may be communicated to the brain by populations of neurons that can be distinguished by their sensitivity to neurotoxins.

Animals↗
PubMed1989

Stimulation of plasma renin activity by captopril in renovascular hypertensive conscious dogs.

The increase in plasma renin activity induced by captopril is used in the clinical evaluation of renovascular hypertensive patients. This increase in plasma renin activity could result from either the concomitant fall in systemic pressure or other effects of captopril, such as the removal of an angiotensin II inhibitory effect on renin release, the increased production of bradykinin or prostaglandins, etc. To examine the effect captopril has on plasma renin activity, independent of changes in systemic pressure, captopril (5, 10 and 50 micrograms/kg iv) was administered to conscious dogs before and following the development of 1 clip-2 kidney Goldblatt hypertension. Plasma renin activity, under normal conditions remained unchanged, while during hypertension it increased 2.0, 2.8 and 3.5 fold respectively in response to the three doses of captopril. These results suggest that the development of renovascular hypertension sensitized the kidney to release renin when challenged by captopril and that the effect is independent of changes in systemic pressure.

Animals↗
PubMed1988

Cerebroventricular dilation in spontaneously hypertensive rats (SHRs) is not attenuated by reduction of blood pressure.

In previous studies, we found that spontaneously hypertensive rats (Okamoto-Aoki SHRs) suffer progressive postnatal dilation of the brain ventricles. In the present study we examined intracerebroventricular pressure and blood pressure as possible mechanisms of ventricular dilation in SHRs. We found that intracerebroventricular pressure was not elevated in SHRs. The role of blood pressure was examined in SHRs treated chronically with the antihypertensive drug, captopril, beginning in utero, and in renal hypertensive Sprague-Dawley rats (SDs). Although our experimental treatments produced significant changes in mean arterial pressures, they did not alter brain ventricular size: SDs with experimental hypertension had normal-sized brain ventricles and SHRs with pharmacologically reduced blood pressure had enlarged ventricles. These results suggest that neither increased intraventricular pressure nor high blood pressure is the sole cause of hydrocephalus in SHRs.

Animals↗
PubMed1988

Capsaicin-induced neuronal degeneration: silver impregnation of cell bodies, axons, and terminals in the central nervous system of the adult rat.

Capsaicin is a neurotoxic substance valued in neurobiological research because of its ability to selectively damage small unmyelinated primary sensory neurons. Previous work has indicated that systemic capsaicin administration causes permanent neuronal degeneration in neonatal rats, but evidence that capsaicin has a similar effect in adults is equivocal and incomplete. Therefore, we used silver impregnation, a method that labels degenerating neurons, to examine the central nervous system of adult rats after systemic capsaicin treatment. Adult rats were injected with a single intraperitoneal dose of capsaicin (50 or 90 mg/kg) or vehicle solution and killed 6, 12, 18, 24, 48, 96, or 240 hours later. Sections of brain and spinal cord were stained with the Carlsen-de Olmos cupric silver method. As reported previously, stained sections revealed degeneration in areas known to be innervated by small-diameter primary sensory fibers: the substantia gelatinosa of the spinal cord dorsal horn and spinal trigeminal nucleus, the solitary nucleus and tract, and the lateral borders of the area postrema. In addition, axon and terminal degeneration was observed in several discrete forebrain and hindbrain areas not previously associated with capsaicin-induced degeneration in either adult or neonatal rats: the inferior olive, the olivary pretectal nucleus, the interpeduncular nucleus, the suprachiasmatic nucleus, and the lateral septum/medial accumbens region. Furthermore, degenerating cell bodies were observed in the intrafascicular nucleus of the ventromedial midbrain tegmentum, in the supramammillary nucleus, and in the posterior hypothalamic area. Unilateral nodose ganglionectomy produced terminal staining on the denervated side very similar to that induced bilaterally by capsaicin. In addition, unilateral nodose ganglionectomy 1 month prior to capsaicin injection greatly attenuated staining in the ipsilateral nucleus of the solitary tract, confirming the hypothesis that capsaicin damages vagal sensory neurons innervating this nucleus. Capsaicin-induced damage in adult rats was long-lasting, since the second of two capsaicin treatments spaced 4.5 months apart produced no additional degeneration.

Animals↗
PubMed1988

Lesion of vagal afferent terminals impairs glucagon-induced suppression of food intake.

Selective hepatic branch vagotomy impairs glucagon-induced inhibition of food intake. However, the relative importance of afferent and efferent neurons in glucagon satiety has not been directly investigated. In this experiment, lesions were placed in the area postrema (AP) and immediately subjacent nucleus of the solitary tract (NTS) where hepatic vagal afferents have been reported to terminate. We found that these lesions impaired glucagon-induced satiety under testing conditions similar to those that reveal a glucagon satiety deficit in rats with selective hepatic branch vagotomies. Since these lesions did not damage the underlying dorsal motor nucleus of the vagus, our results suggest that our AP/NTS lesions impaired glucagon satiety by damaging terminal fields of vagal afferent neurons. Finally, our lesions did not impair satiety induced by cholecystokinin (CCK), a response mediated by gastric vagal afferent neurons. This latter result suggests that the vagal afferent terminal fields required for glucagon- and CCK-induced satiety are not coextensive.

Afferent Pathways↗
PubMed1988

Effect of pteridines on normal and neoplastic cell lines of Xiphophorus.

The effect of three pteridines namely biopterin, isoxanthopterin and xanthopterin on cell growth, viability and morphology of three embryo and one melanoma derived cell lines was studied. Pteridines were assayed in the range of 10(-6) M to 10(-4) M. Biopterin exerted no influence on all cell lines tested, whereas isoxanthopterin and xanthopterin caused a decrease in growth rate with increasing concentrations. The strongest decrease of cell growth was exerted by 10(-4) M xanthopterin. Furthermore at this concentration xanthopterin reduced the viability of normal cells and influenced the morphology of both normal and neoplastic cells. In general, normal cells were more sensitive to pteridines than neoplastic cells.

Animals↗
PubMed1987

Reduction of 125I-angiotensin II binding sites in rat brain following monosodium glutamate treatment.

Adult Sprague-Dawley rats were pretreated with 6 g/kg of monosodium glutamate (MSG). After one month, specific binding of 125I-angiotensin II was measured in membrane preparations from the brain. A 40-45% decrease in the number of 125I-angiotensin II binding sites was observed in brain tissues containing circumventricular organs. No decrease in binding sites was observed in the thalamus/hypothalamus brain region, which resides totally within the blood-brain barrier. The results suggest that MSG can destroy angiotensin-sensitive neurons in circumventricular structures, which are located primarily outside the blood-brain barrier.

Angiotensin II↗
PubMed1987

Area postrema lesions block feeding induced by systemic injections of monosodium glutamate.

Glutamate is an amino acid neurotransmitter capable of producing widespread receptor-mediated neuronal excitation. Recently we reported that high doses of monosodium glutamate (MSG) given systemically stimulate food intake in a dose-related fashion. Since glutamate does not cross the blood-brain barrier, it seems possible that feeding was stimulated by an action of glutamate on neurons within circumventricular organs (CVOs), areas of the brain in which the blood-brain barrier is deficient. In this experiment, we tested the hypothesis that systemic MSG stimulates feeding by an action on the area postrema (AP), a CVO in the caudal hindbrain. AP-lesioned rats (APLs) and sham-operated controls (shams) were injected with saline or MSG (2 and 6 g/kg, SC, one dose per week). Food intake was measured for 3 hr immediately following the injection. Shams increased their food intake significantly in response to both doses of MSG, but APLs did not. This result suggests that systemic glutamate may stimulate feeding by an action on the AP.

Animals↗
PubMed1986

Progressive postnatal dilation of brain ventricles in spontaneously hypertensive rats.

Cross-sectional areas of the forebrain ventricles were measured from coronal sections in spontaneously hypertensive rats (SHRs) 4, 8, 12, 16, 21 and 56 weeks of age and in age-matched Wistar--Kyoto (WKY) and Sprague--Dawley (SD) normotensive rats. Progressive ventricular dilation and associated attrition of brain tissue was observed in SHRs of both sexes after 4 weeks of age, and was present in animals obtained from two different suppliers. In some SHRs, ventricle size was increased to 270% of control. Hence, it seems likely that some systemic and behavioral signs which are concomitant with hypertension in the SHR may be attributable to hydrocephalus and its neuropathological correlates.

Aging↗
PubMed1986

Dose-related stimulation of feeding by systemic injections of monosodium glutamate.

Monosodium glutamate (MSG) is an excitotoxin capable of both stimulating and lesioning neurons in circumventricular organs (CVOs) after systemic administration. In this study, MSG and equiosmotic concentrations of NaCl were administered subcutaneously to adult rats in order to observe the effects on food and water intake. MSG (0.5, 1, 2 and 6 g/kg), but not NaCl, stimulated feeding. The magnitude of the feeding was dose-related. After the highest dose, rats consumed 4.4 g of pelleted food. Since MSG does not cross the blood-brain barrier, we conclude that feeding was stimulated by an action of glutamate on CVOs. Doses of MSG that stimulated feeding did not alter blood glucose concentration. Neonatal MSG treatment, which is known to be more damaging to circumventricular neurons than adult treatment, greatly reduced or abolished subsequent MSG-induced stimulation of feeding in adults. Both MSG and NaCl stimulated drinking. Since the magnitude of the drinking response was similar for both solutes and was directly related to the osmotic strength of the solutions, we conclude that the drinking response after MSG was mediated by cellular dehydration.

Animals↗
PubMed1986

Stimulation of insulin release and suppression of feeding by hepatic portal glucagon infusion in rats.

Plasma insulin and glucose concentrations were measured in rats by remote blood sampling techniques 5 and 25 min after the start of a continuous intraportal glucagon infusion (0.33, 1.0, 3.3, 10 and 33 micrograms/kg/min). Plasma insulin levels were elevated in a dose-related fashion by glucagon, with the highest dose producing a 23-fold increase above control levels. In contrast, the glycemic effect of glucagon was not dose-related. Glucagon-induced hyperglycemia was similar for all glucagon doses, despite the fact that a glucagon dose range spanning two orders of magnitude was used. In a second experiment, plasma glucose and insulin were measured as described above at two glucagon infusion rates (1 and 10 micrograms/kg/min), but the animals were allowed to eat during the infusion. Results showed that the effects of glucagon infusions on plasma insulin and glucose were additive with the normal prandial changes in these substances. Finally, food intake was inversely related to insulin level and dissociated from the hyperglycemia during glucagon infusion. These results show that exogenous glucagon provides a potent stimulus for insulin release in the rat both in the presence and in the absence of food. Furthermore, these results in combination with other data suggest that glucagon-induced hyperinsulinemia merits further investigation as one possible determinant of glucagon satiety in the rat.

Animals↗
PubMed1986

Glucagon satiety: diurnal variation after hepatic branch vagotomy or intraportal alloxan.

Hepatic vagotomized and hepatic portal alloxan-injected rats and their controls were tested for glucagon satiety at three time points during the circadian photoperiod: 6 hr into the light cycle with no food deprivation using a palatable liquid food; at the onset of the dark cycle after 6 hr food deprivation using pelleted rat chow; and 3 hr into the dark cycle after 9 hr food deprivation using pelleted chow. Glucagon failed to suppress intake in hepatic vagotomized and alloxan-treated rats when tests were conducted during the light cycle or at the onset of the dark cycle. In contrast, in tests conducted 3 hr into the dark cycle, glucagon suppressed food intake significantly in both hepatic vagotomized and alloxan-treated rats. Glucagon suppressed food intake significantly in controls in all tests. These results indicate that the hepatic vagus is not the sole mediator or glucagon satiety. Moreover, the fact that alloxan-treated rats and hepatic vagotomized rats responded in a similar manner to glucagon at all testing times suggests that hepatic portal alloxan treatment damages hepatic vagal fibers.

Alloxan↗
PubMed1986

Dose-related suppression of feeding by intraportal glucagon infusion in the rat.

Continuous intraportal infusion of pancreatic glucagon during a feeding test conducted in the dark phase of the circadian photoperiod produced a dose-related suppression of feeding in rats. At the end of the 30 min of infusion, food intake was suppressed 10% at the infusion rate of 0.33 micrograms X kg-1 X min-1 and 45% at the highest infusion rate studied (100 micrograms X kg-1 X min-1). At infusion rates of 33 and 100 micrograms X kg-1 X min-1, the suppression of cumulative intake persisted for 30 min after the termination of the infusion, but no effect on 24-h intake was observed. Glucagon's glycemic effects were measured for two glucagon doses (1 and 10 micrograms X kg-1 X min-1) in the absence of food using a paradigm similar to that used for the feeding tests. In contrast to the suppression of food intake, the hyperglycemic effects of glucagon were not dose related for the two doses tested. The hyperglycemia was similar in magnitude 5 min after the start of the infusion at both infusion rates. Subsequently, plasma glucose concentrations declined more rapidly at the higher than at the lower glucagon dose. This difference in the effect of glucagon on glucose disposal may be important for glucagon's satiating effect.

Animals↗
PubMed1986

Glucagon-induced inhibition of feeding is impaired by hepatic portal alloxan injection.

Subdiabetogenic doses of alloxan injected into the hepatic portal vein of rats abolished glucagon-induced inhibition of feeding (glucagon satiety) both in daytime tests using a palatable food and in nighttime tests using their standard pelleted diet. In contrast, inhibition of food intake by cholecystokinin and epinephrine and stimulation of feeding by 2-deoxy-D-glucose were not impaired by alloxan. Alloxan-induced deficits in glucagon satiety did not appear to result from generalized hepatocellular necrosis, because satiety deficits outlasted histological signs of toxicity and because furosemide, which produced a similar degree of hepatotoxicity, did not impair glucagon satiety. In addition, alloxan's effects were not associated with impaired glycogen storage or mobilization. Recovery of glucagon satiety occurred in some animals but not until 3-6 mo after alloxan. The degree of recovery was inversely related to alloxan dose. Our results indicate that, when administered into the hepatic portal vein, alloxan may be a relatively specific toxin for cells involved in the mediation of glucagon satiety. The specificity of the deficit and the time course of recovery suggest that the alloxan-sensitive cells may be hepatic vagal neurons.

Alanine Transaminase↗
PubMed1986

Extended aortic arch anastomosis for repair of coarctation in infancy.

Surgical repair of coarctation of the aorta was performed in 17 infants, median age 14 days, median weight 3.5 kg. Extended end-to-end aortic arch anastomosis was used. A long incision was made in the inferior aspect of the aortic isthmus and arch, which was then anastomosed to the obliquely trimmed distal aorta. The aortic arch was hypoplastic in eight patients. Mean cross-clamp time was 17.1 min. Pulmonary artery bands were placed in five patients. Follow-up two-dimensional echocardiographic and Doppler studies on 13 patients 1 to 56 months after surgery demonstrated normal distal aortic flow in 10, slightly decreased flow in two, and diminished flow in one. Patients with abnormal Doppler flow showed no gradient in one case and a 30 mm Hg gradient in two. Extended aortic arch anastomosis is safe in infancy, leaves no native coarctation shelf tissue in the repaired segment, does not sacrifice the subclavian artery, is useful in hypoplastic isthmus, and is at low risk to develop aneurysm or recoarctation.

Aorta, Thoracic↗