bluuebunny/crossref_metadata_2025 huggingface dataset:
In vivo measurement of total body magnesium and manganese in rats
Authors: Zhang R. Q. , Ellis K. J.
Published: December 2017

Mg and Mn are essential minerals in many biological processes. Thus knowledge of their absolute amounts and how those amounts may be altered is important. In the past the in vivo measurement of Mg in animals was limited by both the poor geometry of the counting system and the requirement for multiple counts of the animal over several hours. We have developed a neutron activation technique for the direct in vivo measurement of total body Mg and Mn in the rat. The counting system adapted for the technique has a response that is relatively invariant (+/- 2.5%) to differences in body size. A least-squares curve fitting technique was developed that requires only a single 5-min count of the animal. Our in vivo values for body Mg and Mn were in excellent agreement (+/- 2.0%) with the results of total carcass analysis using atomic absorption. Longitudinal changes in total body Mg and Mn were examined in vivo in two groups of animals maintained on test diets that contained different amounts of Mg.
Sodium appetite and thirst in cattle subjected to dehydration
Authors: Blair-West J. R. , Denton D. A. , McKinley M. J. , Weisinger R. S.
Published: December 2017

Cows having free access to water (hydrated) or deprived of water for 26.5 h (dehydrated) were infused for 3 h with angiotensin II or captopril solutions intravenously (iv) or intracerebroventricularly (icv) beginning 1 h before access to 0.3 M NaHCO3/NaCl solution for 2 h. The results agree with the results of the experiments with the same agents and doses in Na-deficient cows. Only iv infusion of angiotensin II stimulated Na appetite and only icv infusion of angiotensin II stimulated thirst. Therefore, barriers to the penetration of angiotensin II in the brain determined the particular site of action and elicited response. Dehydration did not stimulate Na appetite and, as shown previously, Na deficiency did not stimulate thirst, but both behaviors seem to be influenced by angiotensin-related mechanisms in the brain. The inability of iv angiotensin II to stimulate Na appetite in hydrated cows might be explained by the lack of a response caused by, and common to, Na deficiency and dehydration, e.g., upregulation of angiotensin II receptors, or reduced extracellular fluid volume.
Paraventricular nucleus modulation of glycemia and insulinemia in freely moving lean rats
Authors: Ionescu E. , Coimbra C. C. , Walker C. D. , Jeanrenaud B.
Published: December 2017

The effect of norepinephrine (NE) injection (40 nmol) into the paraventricular nucleus (PVN) on plasma insulin and glucose levels was studied in freely moving lean Zucker rats bearing chronic right jugular catheters for blood sampling and unilateral intracerebral cannulas placed just above the PVN. Already 2.5 min after NE injection, plasma glucose levels rose significantly, reaching a peak at 10 min poststimulus, whereas the insulin output was strongly inhibited. This NE-induced hyperglycemia was independent of the corticosterone levels. A ganglionic blockade performed by intravenous chlorisondamine (1 mg/kg body wt) reduced by 80% the 4.5-min NE-induced incremental glucose areas. NE-induced hyperglycemia was reduced to a large extent when the PVN alpha-adrenergic receptors were blocked with phentolamine and to a lesser extent when the beta-adrenergic receptors were blocked with propranolol. NE-induced inhibition of insulin output was not affected by these adrenergic blockers. It is concluded that, when administered locally into the PVN, NE can activate the sympathetic outflow expressed by a neurally mediated hyperglycemia through central alpha- and beta-adrenoreceptor and an inhibition of insulin output through other types of receptors and/or mechanisms.
Contribution of hepatic fibronectin synthesis to regulation of plasma fibronectin
Authors: Vincent P. A. , Saba T. M. , Lewis E. , Cho E.
Published: December 2017

Intravenous injection of gelatinized particles, which are phagocytized by the reticuloendothelial system, elicits an acute depletion of plasma fibronectin followed by restoration to normal concentrations in 6-8 h and a rebound elevation at 24 h. We determined the contribution of hepatic fibronectin synthesis to the restoration of plasma fibronectin in rats after particle infusion by measuring the net incorporation of 75selenomethionine into plasma fibronectin during the recovery period. Rats injected intravenously with gelatinized particles had a greater (P less than 0.01) incorporation of labeled 75selenomethionine into fibronectin but less (P less than 0.05) incorporation of 75selenomethionine into total plasma protein than control rats. Inhibition (86%) of hepatic fibronectin synthesis by pretreatment with cycloheximide limited the recovery of fibronectin levels by only 60%, suggesting a source(s) other than hepatic synthesis may contribute to the restoration of plasma fibronectin. Using purified human plasma fibronectin as a tracer in the plasma pool, we found that 26% of the soluble fibronectin consumed from the plasma during particle clearance was subsequently released back into the plasma over a 4-h interval. Tissue analysis indicated that 125I-labeled fibronectin, which was previously incorporated into the tissues, was not released from the tissue pool after the injection of gelatinized particles. Thus the normalization and regulation of plasma fibronectin levels after its acute depletion due to blood-borne particles is a result of 1) an increase in hepatic synthesis of fibronectin, 2) the release of fibronectin previously consumed as an opsonin during particle clearance, and 3) the release of soluble intact fibronectin from a preformed storage pool.
Endogenous cholecystokinin does not decrease food intake or gastric emptying in fasted rats
Authors: Smith G. P. , Greenberg D. , Falasco J. D. , Avilion A. A. , Gibbs J. , Liddle R. A. , Williams J. A.
Published: December 2017

To investigate the hypothesized inhibitory effect of cholecystokinin (CCK) released from the small intestine on food intake and gastric emptying, we infused soybean trypsin inhibitor (STI) into the stomach or duodenum of male rats deprived of food for 17 h. Intraduodenal infusions of STI (100-200 mg) before real or sham feeding, or during sham feeding, had no effect on food intake. Intragastric infusions of STI (100-200 mg) also had no effect on gastric emptying. Identical infusions of STI, however, increased bioassayable plasma CCK six to ninefold. The failure of endogenous, small intestinal CCK released by STI to decrease food intake or to decrease gastric emptying is evidence against the hypothesis that the inhibitions of food intake and of gastric emptying are physiological functions of small intestinal CCK in food-deprived rats. In contrast to the negative results with STI, administration of exogenous CCK-8 (2-4 micrograms/kg ip) significantly inhibited food intake and gastric emptying despite producing smaller increases of plasma CCK than STI produced. The reason for the differential effects of exogenous and endogenous CCK is not clear and requires further investigation.
Urinary bladder and hindlimb stimuli inhibit T1-T6 spinal and spinoreticular cells
Authors: Hobbs S. F. , Oh U. T. , Brennan T. J. , Chandler M. J. , Kim K. S. , Foreman R. D.
Published: December 2017

Upper thoracic spinal neurons are primarily excited by cardiopulmonary spinal afferent input but are excited and inhibited by splanchnic afferent input. These data suggest that the greater the number of segments between a spinal neuron and spinal afferent input the greater the probability that the afferent input will inhibit the spinal neuron. Based on this idea we hypothesized that visceral (urinary bladder) and somatic (hindlimb) afferent input would inhibit upper thoracic spinal neurons. To test this hypothesis the activities of 69 spinal and 27 spinoreticular tract neurons in 45 alpha-chloralose-anesthetized cats were studied. Only neurons excited by both visceral and somatic thoracic afferent input were studied. Urinary bladder distension (UBD) inhibited 48 (50%), excited 6 (6%), and did not affect 41 (43%) of these neurons. Also, UBD inhibited the excitatory responses of these cells to noxious visceral and somatic stimuli. Hindlimb pinch also inhibited greater than 50% of the neurons. These data indicate that visceral and somatic afferent input to the lumbosacral spinal cord inhibits the activity of upper thoracic neurons. This inhibitory effect may play a role in localization of sensory and motor responses to noxious stimuli.
Regulation of lung liquid secretion by arginine vasopressin in fetal sheep
Authors: Wallace M. J. , Hooper S. B. , Harding R.
Published: December 2017

We have investigated the influence of gestational age on the inhibition of fetal lung liquid secretion by arginine vasopressin (AVP). In eight fetal sheep, lung liquid secretion rates were measured before and during infusion of AVP (300 mu.kg-1.h-1) at gestational ages between 110 and 148 days. During infusions, the concentration of AVP in fetal plasma increased from less than 8.7 +/- 0.2 pg/ml to 848.7 +/- 75.1 pg/ml. Fetal plasma epinephrine concentrations were not altered during AVP infusion. Infusions of AVP had no effect on fetal lung secretion before 135 days of gestation; they caused a 40.8% inhibition between 136 and 140 days, and at ages greater than 140 days induced an inhibition of 78.4%. In two ewes during labor, AVP infusion caused either a complete inhibition of secretion or reabsorption of lung liquid. The inhibitory effect of AVP increased in an exponential-like fashion with increasing gestational age and appeared to parallel the preparturient rise in fetal plasma cortisol concentrations. Our results indicate that AVP may be involved in the clearance of lung liquid at term and that AVP is unlikely to mediate the inhibitory effect of fetal asphyxia on lung liquid secretion, at least until after 135 days of gestation.
Hypertonic and hypovolemic stimulation of thirst in pigs
Authors: Anderson C. R. , Houpt T. R.
Published: December 2017

Young female pigs weighing from 15 to 45 kg were used. Plasma osmolality was slowly raised by an intravenous infusion of 15% NaCl. The behavioral threshold was when the pigs began to drink water, and the rise of osmolality was the stimulus. In 23 measurements on 8 pigs the rise of osmolality to initiate drinking was 10.4 +/- 1.4 mosmol/kg (mean +/- SE). There was also an estimated 3.8 +/- 1.4% rise of blood volume. Control infusions of 0.9% NaCl for 1 h usually resulted in no drinking, and plasma osmolality fell by 6.7 +/- 2.1 mosmol/kg, while blood volume did not change. Hypovolemia was effected using furosemide (1 mg/kg body wt) to cause excretion of nearly isotonic urine. Blood volume changes were estimated from plasma protein and packed cell volume data. In 28 measurements on 6 pigs, drinking occurred when blood volume had decreased by 6.7 +/- 1.8%. During 2-h control periods, blood volume did not change appreciably. Plasma osmolality decreased during both the furosemide treatment (by 3.5 +/- 0.7 mosmol/kg) and the controls (by 4.1 +/- 0.8 mosmol/kg).
In vitro osmosensitive hypothalamic neurons from hypertensive and normotensive rats
Authors: Travis K. A. , Boulant J. A.
Published: December 2017

Single-unit activity was recorded in hypothalamic tissue slices from spontaneously hypertensive (SH) and normotensive Wistar-Kyoto (WKY) rats to identify differences in neuronal osmosensitivity between these two strains. Neurons were characterized according to location, firing rate, temperature sensitivity, and response to hyposmotic (280 mosmol/kgH2O) and hyperosmotic (320 mosmol/kgH2O) media. More than half of the thermosensitive neurons were also osmosensitive. Three groups of osmosensitive neurons were identified: 1) low-firing neurons excited by hyposmolality and inhibited by hyperosmolality, 2) high-firing neurons excited by hyposmolality, and 3) high-firing neurons excited by hyperosmolality. There were no differences between strains in terms of the proportions of osmosensitive neurons. Compared with WKY neurons, however, SH osmosensitive neurons displayed reduced sensitivity to hyperosmotic media. Also, SH osmotically insensitive neurons displayed lower spontaneous firing rates. These differences in osmosensitivity and spontaneous activity may provide a neuronal basis to explain some of the differences in water and sodium regulation observed in hypertensive rats.
Metabolic effects of aminophylline in weanling rats
Authors: Vonlanthen M. G. , McCarter R. J. , Casto D. T.
Published: December 2017

Methylxanthines are commonly used to treat asthma and apnea in infants and children. A physiological effect of these compounds is an elevation of the metabolic rate, but the mechanism of this increase is unclear. We have investigated the hypothesis that this elevation of metabolic rate in young animals is in part due to increased physical activity. Metabolic rate and spontaneous physical activity of weanling Fischer 344 rats were measured before and during 2 days of aminophylline administration. Our results show increased metabolic rate measured over 23 h, concomitant with increased activity during treatment. Resting metabolic rate was not elevated. The results suggest that increased physical activity plays a major role in increasing metabolic rate during aminophylline treatment. Metabolic rate returned to control levels on the 2nd day of treatment despite a smaller but still significant elevation in physical activity. This suggests development of tolerance to the effects of aminophylline on activity together with adaptation to the metabolic effects of this drug.
Dexfenfluramine: action with estradiol on food intake and body weight in ovariectomized rats
Authors: Souquet A. M. , Rowland N. E.
Published: December 2017

Previous work from this laboratory has shown that chronic administration of dexfenfluramine (DF) caused substantial weight loss in rats that were overweight 3-4 mo after ovariectomy (OVX), but not in OVX rats that were of normal weight, as a result of estrogen replacement. The present study was conducted to determine whether the enhanced weight loss in the former group is because of either overweight per se or an inhibitory effect of estrogen on DF. Starting either 0, 6, or 14 wk after OVX, when weight gain was zero, moderate, or near maximal, respectively, rats received a 12-day regimen of either estradiol or the oil vehicle and either DF (3 mg.kg-1.day-1 by osmotic minipump) or no drug. DF had no effect on either food intake or weight gain of groups treated during 0-2 wk after OVX but had significant anorectic and weight loss actions in groups treated 6-8 and 14-16 wk after OVX. Estrogen had a similar effect at all three times and in the 14-wk group produced an effect that was additive with that of DF. Measures of plasma glucose and triglycerides and adipose tissue lipoprotein lipase activity did not correlate with the effectiveness of the drug to promote weight loss.
Involvement of proteins in light resetting ocular circadian oscillators of Aplysia
Authors: Raju U. , Yeung S. J. , Eskin A.
Published: December 2017

The effect of inhibitors of protein synthesis on the phase shifting action of light was investigated. Anisomycin and cycloheximide appeared to block advance phase shifts produced by light. This result suggested that light might phase shift by changing the synthesis of some proteins. Examining proteins separated by two-dimensional gel electrophoresis, we found that incorporation of amino acids into 11 proteins was changed during a 6-h light pulse. Nine of these 11 proteins were affected by light in a phase-dependent manner. Elevated extracellular potassium and 8-bromo-guanosine 3',5'-cyclic monophosphate (cGMP), two treatments that mimic effects of light on the rhythm, also changed amino acid incorporation into a number of proteins. All of the five proteins affected by 8-bromo-cGMP were also affected in the same manner by light. Three proteins were affected similarly by elevated potassium, light, and 8-bromo-cGMP. Exposure of eyes to label at different times after light treatment showed that the effects of light on some proteins were long lasting. In addition, some proteins were not affected during light but were affected only several hours after light. Some of the eye proteins affected by light were also altered by serotonin (5-HT), another phase-shifting agent. The proteins affected by light, elevated potassium, 8-bromo-cGMP, and 5-HT are candidates for components of the circadian system either as an element of the entrainment pathway or the oscillator mechanism.
Effects of ileal transposition on food intake, dietary preference, and weight gain in Zucker obese rats
Authors: Chen D. C. , Stern J. S. , Atkinson R. L.
Published: December 2017

This study evaluated the effects of ileal transposition (IT) surgery on food intake, body weight, and dietary preferences in Zucker obese rats. Eight rats had a 10-cm segment of terminal ileum transposed to the upper jejunum. Eight rats underwent sham IT (SIT) and six rats had no surgery (CON). During weeks 1-10 and 21-24, rats were fed a selection diet of protein (casein), carbohydrate (corn starch), and fat (lard) in three separate dishes. Rat chow was fed from weeks 11 to 20. IT rats had a lower weight and a lower change in weight from base line throughout most of the study. Energy intake was less in IT vs. SIT rats during the selection periods (weeks 1-10 and 21-24), but did not differ on the chow diet (weeks 11-20). Digestible energy, measured at weeks 10, 20, and 24, was lower in IT rats only at week 10. IT rats had no malabsorption by fecal calorie measurements. IT rats ate fewer fat calories at both selection periods. We conclude that IT causes long-term reduction in body weight, no malabsorption or long-term changes in digestible energy, and a persistent decrease in preference for dietary fat. Further studies are needed to determine whether increased energy expenditure is a mechanism for the long-term difference in body weight after IT.
Computer-assisted long-term measurements of urinary output and other biological data
Authors: Reinhardt H. W. , Palm U. , Mohnhaupt R. , Dannenberg K. , Boemke W.
Published: December 2017

A computerized system is described, combining automatic collection of urine in short intervals (minutes) over long periods (days) and recordings of body temperature, MABP, and heart rate in chronically instrumented conscious dogs. During the studies the dogs are housed in metabolic cages. Indwelling catheters and electrical wires are connected to a specially designed swivel and directed out of the cage to the next room. Infusions, blood sampling, and monitoring can be performed from this room without disturbance to the dogs. Three examples of recordings are given. In one of these examples the sodium excretion patterns on 5 consecutive days under continuous saline infusion in one dog is evaluated. Urine was collected every 20 min. Sodium excretion showed cyclic variations. Fourier analysis exhibited 18-h periods and 4- to 8-h periods. The described system renders, e.g., coherent time series analysis possible for a variety of simultaneously recorded physiological variables and may thus acquire considerable importance for integrative physiology.
Cortisol inhibition of vasopressin and ACTH responses to arterial hypotension in conscious dogs
Authors: Raff H. , Skelton M. M. , Cowley A. W.
Published: December 2017

We evaluated the role of cortisol as a feedback inhibitor of the vasopressin response to arterial hypotension. Conscious dogs (n = 5) were each studied on 10 different days. There were five different pretreatments: 1) isotonic saline (control), 2) 5.5 or 3) 11 nmol cortisol.kg-1.min-1 iv for 30 min, 4) 6.8 pmol ACTH-(1-24).kg-1.min-1 iv for 30 min, or 5) 1.5 mg dexamethasone im given the night before experimentation. These pretreatments were followed by a stimulus period (30 min) during which mean arterial pressure was decreased a moderate (-19 +/- 1 mmHg) or severe (-29 +/- 1 mmHg) degree with a controlled infusion of intravenous sodium nitroprusside. The vasopressin response to moderate hypotension was not consistently inhibited by any of the pretreatments. In contrast, the large vasopressin response to severe hypotension in the control experiments (from 3.1 +/- 0.3 to 270 +/- 113 pg/ml) was significantly attenuated by cortisol infusion in a dose-dependent manner. Adrenocorticotropin infusion was more effective than dexamethasone as an inhibitor of the vasopressin response to severe hypotension. The data suggest that physiological increases in cortisol inhibit the large increase in vasopressin in response to severe arterial hypotension.
Mechanism of prostaglandin E2-induced increase of proximal sodium reabsorption in the rat
Authors: Kinoshita Y. , Knox F. G.
Published: December 2017

Prostaglandin E2, when infused directly into the renal interstitium, enhances sodium reabsorption by the superficial proximal convoluted tubules of anesthetized Sprague-Dawley rats. The present study was designed to investigate the role of angiotensin II in the prostaglandin E2-induced stimulation of proximal sodium reabsorption. Micropuncture at the superficial late proximal tubule demonstrated a significant increase in the fractional reabsorption of sodium from 39.9 +/- 2.3% in control conditions to 51.8 +/- 3.0% (n = 9, P less than 0.01) during the renal interstitial infusion of prostaglandin E2. The stimulatory effect of prostaglandin E2 on proximal sodium reabsorption was markedly attenuated by pretreatment with saralasin. During intravenous saralasin infusion, prostaglandin E2 did not significantly change the fractional reabsorption of sodium from 42.2 +/- 5.8 to 45.4 +/- 6.0% (n = 7, NS). In summary, the stimulatory effect of renal interstitial infusion of prostaglandin E2 on proximal sodium reabsorption was attenuated by pretreatment with saralasin. Therefore renal interstitial infusion of prostaglandin E2 may enhance proximal sodium reabsorption, at least in part, through stimulation of angiotensin II production in the rat kidney.
Angiotensin II mediates drinking elicited by eating in the rat
Authors: Kraly F. S. , Corneilson R.
Published: December 2017

Captopril (CA) was used to block synthesis of endogenous angiotensin II (ANG II) in periphery and/or brain of adult male Sprague-Dawley rats in tests for drinking elicited by eating pelleted chow. Blockade of ANG II-converting enzyme (ACE) in periphery alone (using 0.5 mg/kg CA) increased drinking elicited by eating, whereas simultaneous blockade of ACE in periphery and brain (using subcutaneous 100 mg/kg CA or subcutaneous 0.5 mg/kg plus third ventricular 25 micrograms CA) decreased such drinking. The inhibitory effect of 100 mg/kg CA on water-to-food ratio was prevented by a dipsogenically subthreshold subcutaneous dose (5 micrograms/kg) of ANG II. Blockade of ACE in brain alone (third ventricular 25 micrograms CA) had no effect on food-related drinking. Pharmacological antagonism of ANG II (100 mg/kg CA) together with antagonism of histamine H1 and H2 receptors (using intraperitoneal dexbrompheniramine and cimetidine) were not additive in their inhibitory effects on drinking elicited by eating. Blockade of ACE (100 mg/kg CA) inhibited drinking elicited by subcutaneous histamine, but blockade of histamine receptors failed to inhibit drinking elicited by subcutaneous ANG II. These results support a role for endogenous ANG II under what appear to be physiological conditions for drinking behavior, i.e., when drinking is elicited by eating, and they suggest the working hypothesis of ANG II mediation of a histaminergic mechanism for food-related drinking in the rat.
Effect of Ca2(+)-channel agonists and antagonists on skeletal muscle sugar transport
Authors: Westfall M. V. , Sayeed M. M.
Published: December 2017

The purpose of this study was to determine whether changes in cellular Ca2+ caused by Ca2(+)-channel modifiers affect skeletal muscle sugar transport. Rat soleus muscles were isolated, and sugar transport was measured monitoring efflux of 3-O-methylglucose (3-MG). Muscles were "loaded" with 3-O-[methyl-14C]methyl-D-glucose in Krebs-Ringer-bicarbonate (KRB) media and then sequentially washed in radioisotope-free KRB. Cellular Ca2+ was modified by adding a Ca2+ agonist (BAY K 8644) and/or Ca2+ antagonists (nifedipine, nitrendipine, diltiazem) to the "load" and "wash" media. Alterations in cellular Ca2+ were determined from soleus muscle 45Ca2+ uptake measurements. Addition of 0.25 microM BAY K 8644 enhanced insulin-mediated 3-MG transport and 1 microM nifedipine prevented the agonist effect. A high concentration of BAY K 8644 (6 microM) led to increased basal but attenuated insulin-mediated 3-MG transport. Nifedipine (4 microM) and diltiazem (20 microM) blocked the BAY K 8644-induced changes in basal and insulin-mediated 3-MG transport. Nifedipine (4 microM) also attenuated the stimulation of cellular Ca2+ uptake by 6 microM BAY K 8644. Nitrendipine was unable to reverse the changes in basal or insulin-mediated 3-MG transport caused by BAY K 8644. These results indicate that a low concentration of BAY K 8644 enhanced insulin-stimulated skeletal muscle sugar transport, whereas a high concentration of the agonist led to a diminished ability of insulin to stimulate sugar transport. The effects of the Ca2+ agonist were presumably mediated through modulation of cellular Ca2+ as these effects were blunted by the Ca2+ antagonists.
Enzymes of the kallikrein-kinin system in rainbow trout
Authors: Lipke D. W. , Olson K. R.
Published: December 2017

Evidence for a kallikrein-kinin system (KKS) in fish is incomplete. In the present study, components of the KKS were identified in rainbow trout. Tissues were assayed for kallikrein-like esterolytic activity using three synthetic kallikrein substrates (TAME, VGAN, and PPAN), and the presence of kallikrein substrate (kininogen) in trout plasma was estimated by bradykinin (BK) radioimmunoassay of plasma activated with trypsin (T). Formation of pressor-depressor substances in vivo by porcine glandular kallikrein (GK) and T was measured after intra-arterial injection into unanesthetized trout. Gill and kidney contained kallikrein activity (TAME and VGAN assays); little activity was observed with PPAN. Aprotinin inhibited gill activity (TAME assay). T liberated 42 +/- 3 (SE) ng (n = 10) of immunoreactive BK per milliliter of plasma. Injection of GK in vivo reduced plasma kininogen levels for over 24 h. GK produced pressor responses only in fish pretreated with the angiotensin-converting enzyme (ACE) inhibitor captopril. This effect was mediated partly through stimulation of alpha-adrenergic receptors. T produced slight pressor responses that were captopril insensitive. These results show that trout possess elements of the KKS system including kallikrein-like enzymatic activity, kininogen, receptor-mediated vascular sensitivity to kallikrein products, and kininolytic activity consistent with ACE (kininase II).
Identification of vagal preganglionics that mediate cephalic phase insulin response
Authors: Berthoud H. R. , Powley T. L.
Published: December 2017

To define the vagal circuitry mediating the cephalic phase insulin response (CPIR), this reflex was measured in conscious, freely moving rats that had previously undergone selective abdominal vagotomies that spared different columnar subpopulations of dorsal motor nucleus of the vagus (dmnX) neurons. The CPIR was defined as an increase of plasma insulin from basal at 2 min after the start of ingestion. The CPIR measured in peripheral blood after chow ingestion was reliable and significant (P less than 0.05) in rats with all branches intact, +24.9 +/- 5.1 microU/ml (+130% increase from basal); rats with only the two gastric branches and the hepatic branch intact, +27.0 +/- 3.5 microU/ml (+153%); and rats with only the hepatic branch intact, +13.5 +/- 4.8 microU/ml (+188%). No significant response occurred in animals with only the two celiac branches intact, +1.8 +/- 1.8 microU/ml (+15%) or in those with none of the branches intact, +3.9 +/- 3.3 microU/ml (+21%). The CPIRs measured in portal vein blood were generally larger but showed the same pattern across groups. Plasma glucose measurements of portal vein blood indicated that with chow ingestion no significant absorption had occurred by 2 min, whereas with either milk or glucose intake absorption did occur. Subsequent bilateral electrical cervical vagal stimulation-induced insulin and glucagon responses in the same animals under anesthesia showed the same branch dependency. It is concluded that the CPIR is mediated by the two gastric and the hepatic branches but not the two celiac vagal branches. The perikarya of the preganglionics innervating the pancreatic B-cells are contained within a large pool occupying the two medial columns of the dmnX.
Modulation of baroreflex by varying insulin and glucose in conscious dogs
Authors: Fitzovich D. E. , Randall D. C.
Published: December 2017

We developed a conscious, chronically instrumented canine preparation (n = 5 dogs) in which insulin concentration was precisely controlled to study the effects of controlled variations of plasma insulin and glucose concentrations on cardiac responses to bilateral carotid occlusion and dobutamine. Endogenous insulin secretion was reduced to negligible levels using alloxan and then replaced by continuous, constant intravenous insulin infusion at a rate (0.625 +/- 0.115 U/h) sufficient to maintain fasting normoglycemia (85 +/- 9 mg/100 ml); plasma immunoreactive insulin (IRI) in this basal "normal insulin, normal glucose" (NI,NG) condition was 0.362 +/- 0.45 ng/ml (NS vs. prealloxan fasting concentration). A fivefold increase of IRI from NI,NG levels with normoglycemia maintained (5 x NI,NG) reduced (P less than 0.05) the maximal first time derivative of left ventricular pressure (LV dP/dtmax) from 3,010 +/- 62 to 2,398 +/- 91 (SE) mmHg/s but had no effect on LV dP/dtmax when plasma glucose was elevated to 298 +/- 25 mg/100 ml (5 x NI,HG). The LV dP/dtmax increase during bilateral carotid occlusion (BCO) in the NI,NG state of 124 +/- 17 mmHg/s was significantly reduced (P less than 0.05) in the 5 x NI,HG state to 58 +/- 18 mmHg/s but was not altered in the 5 x NI,NG state. Reduction of plasma insulin to one-fifth of the normal fasting level had no effect on basal cardiac function or the responses to BCO. There were no other statistically significant effects of insulin or glucose concentration on cardiovascular responses to BCO or to infusion of dobutamine. Our data indicate that physiologically realistic variations in plasma IRI and glucose concentrations interact and may modulate cardiovascular responses to changes in autonomic nervous activity, even though previously reported effects of pharmacological doses of insulin were not observed.
In vivo myocyte sodium activity and concentration during hemorrhagic shock
Authors: Chiao J. J. , Minei J. P. , Shires G. T. , Shires G. T.
Published: December 2017

The increase in intracellular Na+ concentration ([ Na+]i) and H2O content and decrease in K+ concentration during hemorrhagic shock have been observed. However, the state of the increased [Na+]i has never been defined. In this investigation double-barreled Na(+)-selective microelectrodes were used to directly measure in vivo intracellular Na+ activity (alpha Na) in skeletal muscle cells during prolonged hemorrhagic shock. Resting membrane potential, [Na+]i, and H2O content were also studied concomitantly. Sustained hemorrhagic shock with metabolic acidosis was produced in 12 rabbits after removal of approximately 40% of estimated blood volume under light anesthesia. During prolonged shock, resting membrane potentials of skeletal muscle cells depolarized to -74.7 +/- 1.7 mV from a base-line value of -92.6 +/- 0.4 mV. [Na+]i increased to 14.22 +/- 0.45 mmol/l from a base-line value of 11.50 +/- 0.32 mmol/l. Intracellular H2O content also had a 2.2% increase, whereas levels of [K+]i and extracellular H2O content decreased significantly. However, alpha i(Na) remained unchanged (4.07 +/- 0.19 mmol/l in base line and 4.04 +/- 0.20 mmol/l during shock). This makes the intracellular apparent activity coefficient for Na+ fall significantly from 0.356 in base line to 0.286 during shock. This result indicates that the extra Na+ that diffused into cell because of membrane dysfunction was bound to the fixed charges and/or compartmentalized into subcellular organelles. The unchanged alpha i(Na) also indicates that the depolarization of resting membrane potentials during sustained severe hypovolemia was not caused by the increased [Na+]i. The increase in extracellular [K+] during shock could account for the fall of the resting membrane potentials.(ABSTRACT TRUNCATED AT 250 WORDS)
Release of ANP and its physiological role in pulmonary injury due to HCl
Authors: Wakabayashi G. , Ueda M. , Aikawa N. , Naruse M. , Abe O.
Published: December 2017

The effect of pulmonary injury induced by aspiration of HCl on plasma atrial natriuretic polypeptide (ANP) level was examined in rats given a constant infusion of water and electrolytes. In addition, using specific antiserum against ANP, we investigated the physiological role of ANP in rats after HCl aspiration. Rats were housed individually in metabolic cages and were given a constant infusion of sodium solution via catheters chronically inserted into the jugular vein. Plasma ANP levels were elevated at 3 and 24 h after tracheal injection of 0.2 ml of 0.1 N HCl via the cricothyroid membrane. Urine volume and urinary sodium excretion increased during the first 24 h after acid aspiration. However, this increase was reduced by the injection of anti-ANP serum. Furthermore, the injection of anti-ANP serum resulted in a significant (P less than 0.05) increase in wet lung weight from a value of 0.74 +/- 0.06 (HCl aspiration with normal rabbit serum injection) to 0.83 +/- 0.07% of body weight. These results indicate that ANP plays a physiological role in the regulation of urinary water and sodium excretion after pulmonary acid injury and suggest that ANP elevated in plasma after pulmonary injury may prevent pulmonary edema with its diuretic action and/or some direct action on water movement in the lung.
Hematocrit modulates response of ANP to volume expansion in immature rats
Authors: Chevalier R. L. , Thornhill B. A. , Peach M. J. , Carey R. M.
Published: December 2017

Compared with the adult, the immature kidney responds to acute volume expansion (VE) with reduced diuresis and natriuresis. The underlying mechanisms are poorly understood. Diuresis and natriuresis are blunted despite a lower hematocrit (Hct) in the immature rat, which should enhance the response to VE. The present study was designed to evaluate the role of atrial natriuretic peptide (ANP), its second messenger, guanosine 3',5'-cyclic monophosphate (cGMP), and Hct in the regulation of the renal response to acute saline VE (3% body wt) during postnatal development in rats. Anesthetized Sprague-Dawley rats were studied in the preweaning (group P) or postweaning period (group W). In additional groups, Hct was increased in preweaned rats (group PI) and decreased in postweaned rats (group WD) by isovolemic exchange transfusion before VE. Although control plasma ANP concentration [( ANP]) was not different among the four groups, the increased diuretic and natriuretic response to VE in group W was associated with a greater increase in [ANP] and urinary cGMP excretion (UcGMPV) than in group P (P less than 0.05). Experimental increases in Hct in group PI resulted in greater [ANP] after VE but a reduction in UcGMPV and diuresis (P less than 0.05), whereas decrease in Hct in group WD increased UcGMPV without a significant effect on [ANP], diuresis, or natriuresis. We conclude that ANP may contribute to the increasing renal response to VE with maturation and that Hct modulates ANP release, UcGMPV, and the renal response to VE in postnatal maturation.
Cerebrospinal fluid pressure in conscious rats during prostaglandin E1 fever
Authors: Malkinson T. J. , Cooper K. E. , Veale W. L.
Published: December 2017

Intraperitoneal body temperature was monitored from groups of 10 conscious adult male Wistar rats. The daily body temperature rhythm was determined, and an intraperitoneal body temperature dose response relationship was established for prostaglandin E1 (PGE1) delivered into a lateral cerebral ventricle (LCV). Cerebrospinal fluid pressure was measured by direct cannulation of a LCV. Heart rate, arterial and central venous blood pressure, and blood gases were also measured in groups of 10 animals. It was found that there was a daily rhythm in intraperitoneal body temperature that was higher at night than during the day but stable between 0800 and 1600 h. A significant temperature dose (20-2,000 ng)-response relationship was established for administration of PGE1 into the LCV. Cerebrospinal fluid pressure when measured from the LCV increased significantly during the "chill" phase of the PGE1-induced fever. Carotid arterial blood pressure also significantly increased at this time as did central venous pressure, particularly so with vigorous shivering. There was a significant fall in arterial CO2 partial pressure, a slight rise in pH, and no change in arterial O2 partial pressure. These data support the hypothesis that a significant increase in cerebrospinal fluid pressure occurs during the chill phase of a PGE1-induced fever in the conscious rat.
Somatostatin and innervation of the heart of the snake Elaphe obsoleta
Authors: Donald J. A. , O'Shea J. E. , Lillywhite H. B.
Published: December 2017

The innervation of the heart of the snake Elaphe obsoleta was examined with peptide immunohistochemistry, glyoxylic acid-induced catecholamine fluorescence, and in vitro physiological preparations. Snakes were anesthetized with Nembutal. Many somatostatin (SOM)-like immunoreactive (LI) axons were observed in the sinus venosus, atria, and ventricle. Cell bodies with SOM-LI were found in the intracardiac nerve trunks of the sinus venosus, the interatrial septum, and the atrioventricular region. The SOM-LI axons and cell bodies were not affected by 6-hydroxy-dopamine and capsaicin. They are probably intrinsic parasympathetic neurons. Adrenergic, neuropeptide Y-LI, substance P-LI, and calcitonin gene-related peptide-LI axons were found in the sinus venosus, atria, and ventricle. In spontaneously beating sinoatrial or electrically driven atrial preparations, applied SOM (6 x 10(-9) M and 6 x 10(-8) M) decreased the force of atrial contraction and/or the rate of beating. The effects of SOM were tachyphylactic. SOM had no effect on the force of contraction of the driven ventricle. Stimulation of the left and right vagus nerves elicited negative chronotropic and inotropic responses followed by poststimulus positive inotropic and chronotropic responses. Atropine abolished the inhibition, and bretylium abolished the excitation. After cholinergic and adrenergic blockade, high-frequency vagal nerve stimulation had no effect on heart rate and the force of contraction. Thus, although there is an extensive distribution of intrinsic SOM-LI neurons in the heart and although applied SOM is a potent inhibitor of rate and force, SOM in the vagal neurons does not appear to act as a direct inhibitory transmitter to the cardiac muscle or pacemaker cells.
Possible role of basolateral cell membrane in proximal renal tubule osmoregulation
Authors: Terreros D. , Kanli H. , Coombs J.
Published: December 2017

The cellular response to hypotonic stimulation was studied with videometric methods in 266 proximal renal tubules dissected from Carassius auratus (goldfish). In hypotonic solutions (low NaCl), cells underwent rapid swelling followed by gradual shrinking toward isotonic volume (volume-regulatory decrease phase, VRD). Hypothermia (8 degrees C), increased extracellular potassium (15, 25, and 40 mM), quinine (0.1 mM), barium (0.5 mM), 4,4'-diisothio-cyanostilbene-2,2'-disulfonic acid (DIDS; 0.02 mM), acetazolamide (0.1 mM), decrements in extracellular bicarbonate, and increases in extracellular chloride impaired VRD. Ouabain (1.0 mM), furosemide (0.1 mM), and the chloride channel blocker 5-nitro-2-(3-phenylpropylalanine) benzoate (NPPB; 0.001 mM) had no effect. While VRD occurred in the absence of extracellular calcium influx, addition of the calcium ionophore A23187 (0.01 mM) in the presence of ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA; 2.0 mM) impaired this process both in acidic and alkaline media. Trifluoroperazine (0.01 mM) reversibly inhibited VRD. The effect of this calmodulin inhibitor could not be overridden with the cationic ionophore gramicidin (0.5 microM). The data suggest that Carassius proximal renal tubular cells volume regulate in hypotonic solutions by the loss of KCl and osmotically obligated water. We postulate that the main efflux of potassium is through a calcium-gated potassium channel with its counter ion extruded through a calmodulin-regulated Cl(-)-HCO3- exchanger.
Distribution of atrial natriuretic peptide receptor subtypes in rat brain
Authors: Brown J. , Czarnecki A.
Published: December 2017

The presence and distribution of atrial natriuretic peptide (ANP) clearance receptors in rat brain were investigated by use of des[Gln18,Ser19,Gly20,Leu21,Gly22]ANP-(4-2 3) (C-ANP), a specific ligand of this receptor, to displace bound alpha-125I-labeled ANP. alpha-125I-ANP (200 pM) bound significantly to arachnoid mater, subfornical organ, choroid plexus, area postrema, median preoptic nucleus, and supraoptic and paraventricular nuclei. Binding was reversible at all sites with unlabeled alpha-ANP. Binding dissociation constants for alpha-ANP were measured for the first three sites and were all in the nanomolar range. C-ANP competed with alpha-125I-ANP only for binding sites on arachnoid mater, 1 microM C-ANP displacing radioligand from at least 60% of these sites. No alpha-125I-ANP was displaced by completely unrelated peptides. The reversible binding of 125I-Tyr0-ANP-(5-25), another relatively selective ligand of the clearance receptor, was also concentrated on arachnoid mater. Therefore, high-affinity binding sites for alpha-ANP on arachnoid mater may be clearance receptors for ANP.
Blood pressure in streptozotocin-treated Brattleboro and Long-Evans rats
Authors: Tomlinson K. C. , Gardiner S. M. , Bennett T.
Published: December 2017

The diabetogenic agent streptozotocin (STZ) was injected intraperitoneally in Long-Evans and arginine vasopressin (AVP)-deficient Brattleboro rats. Twenty-eight days later both strains had a bradycardia and systolic hypotension; STZ-treated Brattleboro rats also had diastolic hypotension. The vasopressin (V1-receptor) antagonist, d(CH2)5[Tyr(Et)]DAVP, had no effect on resting blood pressure (BP) or heart rate (HR) in either strain of rat, indicating the relative maintenance of diastolic BP in STZ-treated Long-Evans rats was not dependent on acute vascular actions of AVP. Captopril caused a modest hypotension in all groups of rats, indicating that BP was not differentially dependent on the renin-angiotensin system in the different groups. In the presence of captopril and the ganglion blocker, pentolinium tartrate, the AVP-mediated recovery in BP was impaired in STZ-treated Long-Evans rats. During administration of d(CH2)5[Tyr(Et)]DAVP and pentolinium, the angiotensin II (ANG II)-mediated BP recovery was smaller in both groups of STZ-treated rats, indicating that this abnormality was not likely to be caused by inhibition of renin release by AVP. The abnormalities in ANG II- and AVP-mediated recovery were prevented by insulin treatment.
Intracranial hypertension after cerebroventricular infusions in conscious rats
Authors: Morrow B. A. , Starcevic V. P. , Keil L. C. , Seve W. B.
Published: December 2017

Cerebrospinal fluid (CSF) pressure (PCSF) was recorded in conscious, relatively unrestrained, and freely behaving rats during a 24-h infusion of artificial CSF (25% synthesis rate) into one lateral ventricle or divided equally into both lateral ventricles. Fourier analysis of PCSF of uninfused rats showed a circadian rhythm; nighttime PCSF was higher (P less than 0.01) than daytime. Unilateral and bilateral infusions did not affect PCSF during the first 2 h, but it then increased in an exponential manner, doubling (P less than 0.01) in both groups by 4 h. The induced intracranial hypertension stabilized at 4 h in unilaterally infused rats, but the PCSF increased further in the bilateral group, so that the overall pressure for 24 h was higher (P less than 0.01. No symptoms emerged in uninfused or unilateral infused rats after 24 h, however, 5 of 13 bilaterally infused rats displayed neurological symptoms (P = 2.4%). These low-volume, long-term infusions may be a model of intracranial hypertension. One explanation for the PCSF increase is that artificial CSF diluted neurochemical control systems beyond autoregulatory capacity. This hypothesis accommodates the exacerbated PCSF rise in bilaterally infused rats, since the same volume bathed a larger ependymal-choroidal surface area.
Olfactory receptor response to CO2 in bullfrogs
Authors: Coates E. L. , Ballam G. O.
Published: December 2017

In vivo electrophysiological recordings of olfactory receptor cells of the bullfrog (Rana catesbeiana) exhibit a receptor response to CO2 concentrations as low as 0.5%. The amplitude of the electroolfactogram (EOG) increased with an increase in the CO2 concentration delivered to the olfactory epithelium. Likewise, there was a significant increase in the decay time (time from 90 to 10% peak EOG amplitude) with an increase in CO2. The EOG rise time (time from 10 to 90% peak EOG amplitude) and the EOG response latency (time from beginning of CO2 pulse to beginning of EOG response) significantly decreased, whereas the plateau time (time from 90% rising phase to 90% falling phase of the peak EOG amplitude) was not significantly altered by an increase in CO2. These results indicate that low concentrations of CO2, below normal end expiratory CO2 concentrations, stimulate olfactory receptor cells. These results support our proposal that the ventilatory depression observed in response to upper airway CO2 in reptiles and amphibians is mediated by CO2-sensitive olfactory receptor cells.
Increase in cytochrome oxidase capacity of BAT and other tissues in cold-acclimated gerbils
Authors: Bourhim M. , Barre H. , Oufara S. , Minaire Y. , Chatonnet J. , Cohen-Adad F. , Rouanet J. L.
Published: December 2017

To determine the effects of cold acclimation on the oxidative capacity of different tissues and their possible role in nonshivering thermogenesis (NST) in a desert rodent, the gerbil (Gerbillus campestris), measurements of cytochrome oxidase activity (COX) were performed on homogenates of liver, brown adipose tissue (BAT), and subsarcolemmal (SS) and intermyofibrillar (IMF) fractions of skeletal muscle. Total organ mass was also measured. Gerbils were maintained either at thermoneutrality (TN) or cold [4 degrees C, ambient temperature (Ta)] for 4 (CA4) or 8 (CA8) wk. A comparative study was made with mice (Mus musculus). Total and relative masses of BAT increased significantly in both gerbils and mice during cold acclimation, whereas muscle mass decreased in CA4 gerbils. Specific and total COX (TCOX) increased in the three tissues. A considerable increase (+170%, P less than 0.05) of TCOX and protein content in liver of CA4 gerbils compared with controls was observed, whereas no significant changes occurred in liver of CA4 mice. In muscle, an increase of TCOX in SS and a reduction in IMF cell compartments were noted. The increase in BAT oxidative capacity in CA4 gerbils represented only a small portion of that in liver (36%) and in SS fraction of muscle (41%) at the same stage of acclimation. The ability of the three tissues to contribute to components of thermogenesis in vivo was evaluated. The sum of oxidative capacity of the three tissues was largely above the peak metabolic rate (PMR), whereas that of muscle exceeded maximum shivering thermogenesis, which developed both in TN and CA4 gerbils.(ABSTRACT TRUNCATED AT 250 WORDS)