bluuebunny/crossref_metadata_2025 huggingface dataset:
Selective effects of sodium and chloride depletion on salt appetite in rats
Authors: Muntzel M. , Pouzet B. , Lacour B. , Hannedouche T. , Drueke T.
Published: December 2017

Findings from hypertension research indicate that dietary sodium chloride (NaCl), Na+, and Cl- independently influence blood pressure, electrolyte metabolism, and hormone secretion. In this context, we examined the effects of NaCl, Na+, and Cl- depletion, respectively, on the development of saline preference (salt appetite) in rats. Male Wistar rats were given a normal diet (1% NaCl) for 15 days and tested for salt appetite using a two-bottle choice test, one bottle containing water and the other 0.3 M saline. The animals were then divided into three groups (n = 11/group): one group received low NaCl, another received a Na(+)-deficient, normal-Cl-diet (low Na+), and a third received a Cl(-)-deficient, normal-Na+ diet (low Cl-). Salt appetite was again tested after 19 days on these diets. Both NaCl and Na+ depletion stimulated saline intake (P less than 0.01), whereas salt appetite did not change in the low-Cl- group. Water intake was not influenced by the regimens. In addition, no alterations were noted for weight, systolic blood pressure, plasma Na+ concentration, or blood pH. Dietary Cl-depletion, however, significantly reduced plasma Cl- concentration (P less than 0.05), and reduced plasma potassium in relation to rats depleted in Na+ (P less than 0.05). Plasma renin activity and urinary aldosterone were elevated in low-NaCl and Na(+)-depleted rats relative to the Cl(-)-depleted group (P less than 0.05). These results suggest that salt appetite is increased by dietary Na+ deficiency but not by Cl- deficiency. Salt appetite may be controlled by central or peripheral systems specifically sensitive to Na+ or by hormonal changes characteristic of Na+ depletion, such as the activation of renin and aldosterone observed in the low-NaCl and low-Na+ groups.
Role of vasopressin in acutely altered baroreflex sensitivity during hemorrhage in rats
Authors: Brizzee B. L. , Russ R. D. , Walker B. R.
Published: December 2017

Experiments were performed to examine the potential role of circulating arginine vasopressin (AVP) on baroreflex sensitivity during hypotensive and nonhypotensive hemorrhage in the conscious rat. Animals were chronically instrumented for measurement of cardiac output, blood pressure, and heart rate (HR). Three potential stimuli for release of AVP were utilized: 1) rapid 20% arterial hemorrhage that resulted in hypotension, 2) nonhypovolemic hypotension induced by intravenous infusion of nitroprusside, and 3) nonhypotensive hemorrhage (rapid 10% arterial blood withdrawal). Hypotensive hemorrhage was associated with significant reductions in blood pressure, cardiac output, HR, and calculated total peripheral resistance, an increase in baroreflex (BRR) bradycardia in response to pressor infusions of phenylephrine, and a moderate elevation in circulating AVP. Prior intravenous administration of a specific V1-vasopressinergic antagonist augmented the hypotensive response to hemorrhage; however, neither V1- nor V2-blockade affected hemorrhage-induced augmentation of the BRR. Inducement of hypotension by infusion of nitroprusside did not alter subsequent BRR sensitivity. Finally, nonhypotensive hemorrhage was associated with an increase in resting HR and augmented BRR sensitivity. However, in contrast to hypotensive hemorrhage, either V1- or V2-antagonism attenuated the increase in BRR sensitivity seen with 10% hemorrhage. These data suggest that, although AVP may play a role in blood pressure maintenance via its direct vasoconstrictor actions during hypotensive hemorrhage, the observed augmentation of BRR sensitivity associated with severe blood loss is not attributable to a vasopressinergic mechanism activated by circulating AVP. However, blood-borne AVP may contribute to BRR sensitivity alterations in response to mild blood loss.
Gestational maturation of placental glucose transfer capacity in sheep
Authors: Molina R. D. , Meschia G. , Battaglia F. C. , Hay W. W.
Published: December 2017

The net transfer rate of glucose to the fetus from the placenta (Rf,up) increases approximately 10-fold over the second half of pregnancy. To examine the mechanism underlying this increase, we measured Rf,up at different glucose concentration gradients between maternal arterial (GA) and umbilical arterial (Ga) glucose and at three fetal ages: midgestation (76.0 +/- 0.6 days, n = 6), late gestation (131.5 +/- 2.1 days, n = 8), and an intermediate age (103.3 +/- 1.9 days, n = 4). The GA -- Ga gradient was varied by changing Ga below and above control values with fetal insulin and glucose infusions, respectively, while GA was kept constant at 70 +/- 2 mg/dl by a glucose clamp procedure. The slope of the line relating Rf,up to GA -- Ga increased from 0.15 to 1.01 dl/min in the 76- to 131.5-day period, while the intercept in the GA -- Ga axis remained approximately constant at 34 mg/dl. This indicates a fivefold increase in the ability of the placenta to supply glucose to the fetus at fixed values of maternal and fetal glucose concentration (placental glucose transfer capacity). Concomitant with this increase, there was a significant (P less than 0.001) decrease in control Ga from 26.7 +/- 1.3 to 20.3 +/- 0.3 mg/dl, leading to a significant increase in the GA -- Ga gradient and an 11-fold increase in control Rf,up (from 1.53 to 16.77 mg/min). We conclude that, in the second half of pregnancy, fetal glucose demand grows much more rapidly than placental glucose transfer capacity and requires a decrease in fetal glucose concentration to balance glucose supply and demand.
Cholinergic reticular mechanisms influence state-dependent ventilatory response to hypercapnia
Authors: Lydic R. , Baghdoyan H. A. , Wertz R. , White D. P.
Published: December 2017

Breathing is impaired by the loss of wakefulness that accompanies sleep, certain comatose states, and anesthesia. Although state-dependent decrements in breathing and the ability to respond to hypercapnic stimuli are characteristic of most mammals, the neural mechanisms that cause state-dependent changes in respiratory control remain poorly understood. The present study examined the hypothesis that cholinergic mechanisms in the medial pontine reticular formation (mPRF) can cause state-dependent changes in breathing and in the hypercapnic ventilatory response (HCVR). Six cats were anesthetized with halothane and chronically instrumented for subsequent studies of breathing during wakefulness, non-rapid-eye-movement (NREM) sleep, rapid-eye-movement (REM) sleep, and during the REM sleep-like state caused by mPRF microinjections of carbachol or bethanechol. Minute ventilation was significantly decreased during the carbachol-induced REM sleep-like state (DCarb) compared with wakefulness. The HCVR in NREM, REM, DCarb, and after bethanechol was less than the waking HCVR. These results show for the first time that cholinoceptive regions in the mPRF can cause state-dependent reductions in normocapnic minute ventilation and in the ventilatory response to hypercapnia.
Mercury from dental "silver" tooth fillings impairs sheep kidney function
Authors: Boyd N. D. , Benediktsson H. , Vimy M. J. , Hooper D. E. , Lorscheider F. L.
Published: December 2017

In humans Hg vapor is released from "silver" amalgam fillings that contain 50% Hg by weight. Previous studies show that when 12 such fillings are placed in sheep teeth, the kidneys will concentrate amalgam Hg at levels ranging from 5 to 10 micrograms Hg/g renal tissue 4-20 wk after placement. In the present study 12 occlusal fillings were placed in each of six adult female sheep under general anesthesia, using standard dental procedures. Glass ionomer occlusal fillings (12) were inserted in two control sheep. At several days before dental surgery, and at 30 and 60 days after placement of fillings, renal function was evaluated by plasma clearance of inulin and by plasma and urine electrolytes, urea, and proteins. An average plasma inulin clearance rate of 69.5 +/- 7.2 ml/min before amalgam placement was reduced to 32.3 +/- 8.1 ml/min by 30 days and remained low at 27.9 +/- 8.7 ml/min after 60 days. Inulin clearance did not change in controls. After amalgam placement urine concentration of albumin decreased from 93.0 +/- 20.5 to 30.1 +/- 15.3 mg/l and urine Na+ concentration increased steadily from 24.8 +/- 7.7 to 82.2 +/- 20.3 mmol/l at 60 days. Concentrations of K+, urea, gamma-glutamyl transpeptidase, alkaline phosphatase, and total protein did not change significantly from 0 to 60 days in urine. Plasma levels of Na+, K+, urea, and albumin remained unchanged from 0 to 60 days after amalgam. Renal histology remained normal in amalgam-treated animals.(ABSTRACT TRUNCATED AT 250 WORDS)
Progesterone and modulation of endothelium-dependent responses in canine coronary arteries
Authors: Miller V. M. , Vanhoutte P. M.
Published: December 2017

Chronic treatment with estrogens enhances some endothelium-dependent relaxations. Whether or not progesterone would exert a similar effect is unknown. Experiments were designed to determine the effect of chronic treatment with progesterone on endothelium-dependent responses. Adult female dogs were ovariectomized and pellets containing carrier substance, estrogen, progesterone, or estrogen plus progesterone were implanted subcutaneously. After 14-21 days coronary arteries were removed, cut into rings, and suspended for the measurement of isometric force in organ chambers in the presence of indomethacin. Endothelium-dependent relaxations to ADP, bradykinin, or the calcium ionophore did not differ among groups. However, relaxations to acetylcholine and to the alpha 2-adrenergic agonist BHT-920 were greater in the estrogen-treated group than in the estrogen plus progesterone-treated group. In rings without endothelium, relaxations to nitric oxide and isoproterenol did not differ among groups. However, relaxations of the smooth muscle to ADP were greater in the progesterone-treated group than in the progesterone plus estrogen group. These results suggest that progesterone alone minimally affects endothelium-dependent responses. However, progesterone seems to antagonize the stimulatory effects of estrogen on two endothelium-dependent responses that are associated with pertussis toxin-sensitive guanine nucleotide regulatory proteins and the production of nitric oxide. These studies suggest that a specific receptor/second messenger system can be modulated by female reproductive steroid hormones.
Effect of acute renal denervation and ANF on renal function in adult spontaneously hypertensive rats
Authors: Pollock D. M. , Arendshorst W. J.
Published: December 2017

Experiments were designed to evaluate the influence of the renal efferent nerves on baseline renal function and on the renal response to atrial natriuretic factor (ANF) in euvolemic anesthetized 10- to 12-wk-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) and Munich-Wistar (MW) rats. Acute unilateral renal denervation produced increases in absolute and fractional excretion of sodium and water by the ipsilateral kidney that were similar in SHR and WKY rats; larger responses were observed in MW rats. Excretion by the contralateral innervated kidney was unchanged in each group. Intravenous infusion of ANF (0.25 microgram.kg-1.min-1) caused a diuresis and natriuresis that was similar in the three strains and independent of changes in glomerular filtration rate and renal blood flow. The excretory responses to ANF were larger in denervated than in innervated kidneys. The magnitude of the natriuresis and diuresis produced by ANF was directly related to the pre-ANF rate of urinary excretion, suggesting independent and additive effects of acute renal denervation and ANF on tubular reabsorption. The exaggerated response in the acutely denervated kidney can be explained by removal of a modulatory effect of the renal efferent nerves and associated increases in tubular flow and delivery to more distal ANF-sensitive sites. The denervation responses suggest that the renal efferent nerves have similar effects on sodium and water reabsorption in anesthetized SHR and WKY rats at 10-12 wk of age. The renal nerves and ANF appear to play a larger role in the acute control of sodium and water excretion in MW rats compared to rats of the Okamoto-Aoki strain.
Diurnal responses of mammals to acute exposure to a hyperdynamic environment
Authors: Fuller C. A. , Griffin D. W. , Horowitz J. M.
Published: December 2017

Acute exposure to hyperdynamic environments elicits significant depressions in core temperature in both diurnal squirrel monkeys and nocturnal rats. This study describes time of day variations in core temperature responses in squirrel monkeys and rats exposed for 70 min to a hyperdynamic environment (2 g) produced via centrifugation. Experiments were performed during the middle of the light or dark phase. After a 70-min control period, squirrel monkey resting core temperature was 38.6 +/- 0.2 (SE) and 36.8 +/- 0.2 degrees C during the day and night, respectively. At the end of a 7-min exposure to 2 g, squirrel monkey core temperature decreased 1.3 +/- 0.2 degree C during the day but remained a constant 36.8 +/- 0.4 degrees C at night. Core temperature of rats exposed to an identical 70-min 2 g profile decreased 1.5 +/- 0.4 degree C from a resting 37.1 +/- 0.6 degrees C during the day and 2.3 +/- 0.2 degrees C from a resting 37.8 +/- 0.3 degrees C at night. Thus, in both species, there were clear day-night differences in response to hyperdynamic environments, with the greatest fall in core temperature occurring during the animal's active period.
Insulin sensitivity and liver insulin receptor structure in ducks from two genera
Authors: Constans T. , Chevalier B. , Derouet M. , Simon J.
Published: December 2017

Insulin sensitivity and liver insulin receptor structure were studied in 5-wk-old ducks from two genera (Muscovy and Pekin). In the fasting state, both duck types were equally resistant to exogenous insulin compared with chicken. Despite the low potency of duck insulin, the number of insulin receptors was lower in Muscovy duck and similar in Pekin duck and chicken liver membranes. After 125I-insulin cross-linking, the size of the alpha-subunit of the receptors from the three species was 135,000. Wheat germ agglutinin-purified receptors from the three species were contaminated by an active and unusual adenosinetriphosphatase (ATPase) contaminant (highest activity in Muscovy duck). Sequential purification of solubilized receptor from both duck types on lentil and then wheat germ agglutinin lectins led to a fraction of receptors very poor in ATPase activity that exhibited a beta-subunit size (95,000) and tyrosine kinase activity similar to those of ATPase-free chicken insulin receptors. Therefore the ducks from the two genera exhibit an alpha-beta-structure for liver insulin receptors and a clear difference in the number of liver insulin receptors. Their sensitivity to insulin is, however, similarly decreased compared with chicken.
Vasopressin-induced bradycardia in barodenervated rats
Authors: Brizzee B. L. , Adams E. M. , Walker B. R.
Published: December 2017

Experiments were performed on conscious chronically instrumented rats to determine the contribution of baroreceptor reflex (BRR)-independent mechanisms in the bradycardia associated with intravenous administration of arginine vasopressin (AVP). At least 2 wk prior to experimentation, the aortic and carotid baroreceptors were denervated in six rats. Following recovery, the maximum bradycardic responses to pressor doses of phenylephrine (PE) or AVP were determined on separate days in each animal. Pulse interval (PI) was calculated from heart rate (HR), and the slopes of PI vs. mean arterial blood pressure (MABP) and PI vs. dose were determined for each experiment by linear regression. There was no significant correlation of PI vs. MABP in response to bolus PE in these barodenervated rats. However, there was a significant correlation of PI vs. MABP and PI vs. dose in response to AVP in five of the six barodenervated rats. These data suggest that pressor levels of AVP may elicit bradycardia independent of the BRR. Another group of experiments was performed in the Langendorff-isolated rat heart preparation to assess the direct chronotropic effect of AVP. Hearts were not paced, and the coronary arteries were perfused at a constant flow. HR was determined at various concentrations of AVP (n = 4 at each dose). In addition, because unpaced hearts exhibited low intrinsic rates, the same protocol was performed in hearts receiving isoproterenol to elevate basal HR (n = 4 at each AVP dose). There was no chronotropic effect of AVP in isolated hearts with or without isoproterenol administration.(ABSTRACT TRUNCATED AT 250 WORDS)
Sexual function and neuropeptide Y levels in selected brain regions in male spontaneously hypertensive rats
Authors: Clark J. T. , Sahu A. , Mrotek J. J. , Kalra S. P.
Published: December 2017

Sexual function was examined in spontaneously hypertensive rats (SHR) from 8 to 20 wk of age and compared with normotensive Wistar-Kyoto (WKY) and Long-Evans rats (LE). Blood pressures (evaluated indirectly) were elevated in SHR (185 +/- 2 and 195 +/- 3 mmHg at 16 and 19 wk of age, respectively) relative to WKY and LE (135-144 mmHg). SHR exhibited good copulatory behavior but displayed fewer erections (less than 20% of the number displayed by WKY or LE) in ex copula tests. At the conclusion of the study (20 wk of age), body weights were lowest in SHR, intermediate in WKY, and greatest in LE. Relative weights of testes were greater in SHR, whereas relative weights of accessory organs, pituitary and adrenal glands, and kidneys were equivalent across strains, as were circulating levels of aldosterone. Circulating levels of testosterone were higher in SHR and WKY than in LE. Neuropeptide Y (NPY) levels in the median preoptic and arcuate nuclei were significantly greater in SHR than in WKY or LE, whereas NPY levels in the medial preoptic area and the suprachiasmatic, hypothalamic dorsomedial, and hypothalamic paraventricular nuclei were equivalent in SHR and WKY, with both greater than LE. No strain differences were evident in the medial nucleus of the amygdala, the bed nucleus of the stria terminalis, the median eminence, the anterior hypothalamic nucleus, or the hypothalamic dorsomedial nucleus.
Responses of sympathetic preganglionic neurons to rostral ventrolateral medullary stimulation
Authors: Morrison S. F. , Reis D. J.
Published: December 2017

Sympathoexcitatory pathways from the rostral ventrolateral medulla (RVL) play a significant role in maintaining the tonic discharge of sympathetic preganglionic neurons (SPNs) and, in turn, resting arterial pressure. We examined the responses of antidromically identified, splanchnic SPNs to single stimuli applied to the RVL. Four characteristic response patterns were observed. Forty-five percent (group 1) of responsive SPNs were excited with latencies between 15 and 41 ms (mean 27 ms). The spontaneous activity of these SPNs (mean 3.3 Hz) was strongly modulated by the baroreceptor reflex. Twenty-three percent (group 2) of SPNs were excited with a significantly longer latency (mean 108 ms) and frequently exhibited little spontaneous discharge. Twenty-one percent (group 3) were excited at both short (mean 29 ms) and long (mean 117 ms) latencies. Eleven percent (group 4) of responsive splanchnic SPNs had a biphasic response to RVL stimulation consisting of an early inhibition followed by a late, longer lasting increase in discharge probability. Spontaneous discharge of group 4 SPNs (mean 6.2 Hz) was significantly higher than other groups and was not related to the cardiac cycle (mean arterial pressure 105 mmHg). Microinjection of kainic acid into the RVL greatly reduced the short- and long-latency splanchnic nerve excitations evoked by RVL stimulation. The heterogeneity of the RVL stimulus-evoked responses in splanchnic SPNs may reflect specificity in the descending regulation of functionally distinct subsets of SPNs regulating the various tissues in the splanchnic distribution.
Beta 1- and beta 2-adrenoceptor subtypes in canine intrathoracic efferent sympathetic nervous system regulating the heart
Authors: Watson-Wright W. , Boudreau G. , Cardinal R. , Armour J. A.
Published: December 2017

The augmentation of cardiac inotropism induced by electrical stimulation of acutely decentralized efferent preganglionic sympathetic axons is reduced after the administration of timolol into the major ipsilateral intrathoracic ganglia. Thus it has been proposed that, in addition to nicotinic synapses, beta-adrenergic ones exist in intrathoracic ganglia that are involved in the efferent sympathetic regulation of the mammalian heart. Whether these are beta 1- as opposed to beta 2-adrenoceptor subtypes is unknown. In the present series of experiments, acutely decentralized canine efferent preganglionic sympathetic axons were stimulated before and after the administration of beta 1 (atenolol)- or beta 2 (ICI 118551)-selective adrenoceptor antagonists into the ipsilateral stellate and middle cervical ganglia to determine whether beta 1- or beta 2-adrenoceptors exist in intrathoracic ganglia that are involved in cardiac regulation. Augmentations of right and left ventricular inotropism induced by efferent preganglionic sympathetic axon stimulation were attenuated when either agent was administered into the major ipsilateral intrathoracic sympathetic ganglia. Myocardial liberation of norepinephrine evoked by these stimulations was also reduced after intraganglionic administration of either agent. These data indicate that canine intrathoracic neurons contain beta 1- and beta 2-adrenoceptors that are involved in the efferent sympathetic regulation of the heart.
Role of gram-negative and gram-positive gastrointestinal flora in temperature regulation of mice
Authors: Conn C. A. , Franklin B. , Freter R. , Kluger M. J.
Published: December 2017

An earlier study showed that the presence of gut flora elevates body temperature of mice and rats. In these experiments, we questioned whether the signal coming from the gut was endotoxin from gram-negative (Gm-) bacteria or some signal derived from gram-positive (Gm+) microorganisms. To test the idea that endotoxin is responsible for the effects of flora, we compared the temperature of the endotoxin-resistant mouse (C3H/HeJ) with that of endotoxin-sensitive strains of mice (C3H/SnJ and C3H/HeN). Temperature of C3H/HeJ was not different from that of C3H/SnJ or C3H/HeN during the light period but was significantly lower during the later hours of the dark period. We speculated that, if endotoxin leaking across the gut wall were responsible for elevating temperature, then reduction of gut flora with nonabsorbable antibiotics would depress the temperature of the endotoxin-sensitive mice more than that of the endotoxin-resistant mice. Because antibiotics lowered the temperature of both strains of mice to the same extent, the signal coming from the gut is unlikely to be endotoxin. To test whether Gm+ flora can be responsible for elevating temperature, we inoculated one group of germfree mice with Gm+ organisms. Their mean temperature was significantly higher than that of mice that remained germfree. Cecectomy had no effect on temperature, indicating that the special properties of the germfree cecum were not involved in lowering the temperature of germfree mice. These data support the hypotheses that Gm+ organisms are a major source of the stimulatory effect of flora on normal body temperature and that the presence of Gm- organisms is unnecessary.
Indirect coupling of organic anion secretion to sodium in teleost (Paralichthys lethostigma) renal tubules
Authors: Miller D. S. , Pritchard J. B.
Published: December 2017

Recent findings in both rat and crab indicate that renal accumulation of p-aminohippurate (PAH) across the basolateral membrane can be coupled indirectly to the Na gradient through PAH-glutarate exchange and Na/glutarate cotransport. However, the role of this mechanism in net transepithelial PAH secretion was not examined. Therefore, proximal tubules from Southern flounder kidney were used to assess both the presence of indirect coupling in the fish and its relationship to net secretion. [14C]glutarate uptake by proximal tubular masses was concentrative, Na dependent, and Li inhibitable. Glutarate efflux from preloaded masses was stimulated by addition of PAH to the medium. Thus flounder tubules exhibited both Na/glutarate uptake and glutarate-PAH exchange. Furthermore, steady-state [3H]PAH accumulation was increased 50% by 10-50 microM glutarate, and this increase was abolished by Li, indicating indirect coupling of PAH entry to Na. To determine whether indirect coupling affected net secretion as well as tissue accumulation, the steady-state accumulation of an anionic dye, fluorescein (FL), was measured in individual renal tubules by use of epifluorescence microscopy and video-image analysis. FL accumulated in tubules to levels that were 20-40 times higher than the medium. In most fish, luminal fluorescence was measurably higher than cellular, and uptake in both compartments was markedly reduced by PAH and Li. Moreover, FL accumulation in cells and lumina was increased by 70-100% when 50 microM glutarate was added to the bathing medium. Thus glutarate not only stimulated uphill FL entry into the cells, but also stimulated active secretion into the tubular lumen.(ABSTRACT TRUNCATED AT 250 WORDS)
Inhibition of gluconeogenesis by extracellular ATP in isolated rat hepatocytes
Authors: Asensi M. , Lopez-Rodas A. , Sastre J. , Vina J. , Estrela J. M.
Published: December 2017

The aim of this study was to determine the effect of externally added ATP on gluconeogenesis by isolated hepatocytes from starved rats. High concentrations of extracellular ATP inhibited gluconeogenesis from lactate and pyruvate but not from glycerol or fructose. This inhibition was associated with an increase in intracellular adenosine contents. ADP, AMP, or adenosine but not guanosine 5'triphosphate, inosine 5' triphosphate, or adenine also inhibited gluconeogenesis. alpha, beta-Methylene-ATP, a nonmetabolizable structural analogue of ATP, did not affect the rate of gluconeogenesis. Intracellular ATP levels were increased by externally added ATP or adenosine, but ATP-to-ADP ratios in the cytosolic and mitochondrial compartments were diminished. Malate and phosphoenolpyruvate contents were decreased by extracellular ATP or adenosine. Our results show that inhibition of gluconeogenesis by high levels of extracellular ATP may be mediated by adenosine derived from ATP catabolism at the plasma membrane.
Dietary fat, hypothalamic glutamate decarboxylase, and food intake of streptozotocin-diabetic rats
Authors: Beverly J. L. , Oster M. H. , Castonguay T. W. , Stern J. S.
Published: December 2017

The association among changes in glucose status, glutamate decarboxylase (GAD) activity, and food intake was evaluated in several hypothalamic areas of streptozotocin-diabetic rats fed a low- (12% of calories as fat) or high-fat diet (59% of calories as fat). Control rats consumed approximately 90 kcal/24 h of either diet, whereas diabetic rats consumed approximately 150 kcal/24 h of the low-fat diet and approximately 100 kcal/24 h of the high-fat diet. At the end of the study, diabetic rats fed the high-fat diet weighed more and had higher retroperitoneal fat depot weights (P less than 0.05) than diabetic rats fed the low-fat diet. In diabetic rats, GAD activity was 15-20% higher in the ventromedial nucleus (P less than 0.01) but similar to controls in the lateral hypothalamus, paraventricular nucleus, and area postrema. Diet did not affect GAD activity in the brain areas studied. The increase in ventromedial nucleus GAD activity was not associated with the level of food intake and was the likely result of altered glucose homeostasis in diabetic rats.
Role of vasopressin in cardiovascular responses to acute and chronic hyperosmolality
Authors: Russ R. D. , Brizzee B. L. , Walker B. R.
Published: December 2017

Experiments were performed in conscious chronically instrumented rats to determine the role of arginine vasopressin (AVP) in the cardiovascular adjustments to acute and chronic increases in plasma osmolality. Animals were implanted with pulsed Doppler flow probes and arterial and venous catheters for the determination of cardiac output, mean arterial blood pressure (MABP), and heart rate and for the calculation of total peripheral resistance and baroreflex sensitivity (BRS). Before and after raising plasma osmolality by either 48-h water deprivation or acute hypertonic saline infusion, specific V1- or V2-vasopressinergic receptor antagonists or vehicle were administered to the animals, and the cardiovascular responses were noted. MABP was significantly elevated in water-deprived animals. These animals also exhibited significantly increased BRS, which was further increased by administration of the V1-receptor antagonist. Animals subjected to acute hypertonic saline infusion also demonstrated increased MABP, although the infusion, unlike water deprivation, did not affect BRS. We observed no significant effects on any other variable measured. We conclude that AVP plays a relatively minor role in the cardiovascular adjustments to acute and chronic hyperosmolality.
Blockade of type A, not type B, CCK receptors attenuates satiety actions of exogenous and endogenous CCK
Authors: Moran T. H. , Ameglio P. J. , Schwartz G. J. , McHugh P. R.
Published: December 2017

Recent work has suggested a role for an endogenous release of cholecystokinin (CCK) acting at either type A or type B CCK receptors in the control of food intake. In an effort to investigate whether the mechanisms by which exogenously administered and endogenously released CCK inhibits food intake are similar and depend upon interactions with either type A or type B CCK receptors, we examined in rats the ability of the type A (L 364718) and type B (L 365260) CCK receptor antagonists to 1) block the inhibition of glucose consumption produced by an intraperitoneal injection of 4 micrograms/kg of CCK and 2) increase glucose consumption in the absence of exogenous CCK after a 6-h daytime deprivation. Increasing dosages (10-100 micrograms/kg) of the type A CCK antagonist resulted in a dose-related blockade of the inhibition of intake produced by CCK, and the 100 micrograms/kg dose of the A antagonist significantly increased glucose intake above baseline levels. In contrast, no dose (10-1,000 micrograms/kg) of the B antagonist blocked the inhibitory action of exogenous CCK at any time point. In the absence of exogenous CCK, the 32 and 100 micrograms/kg doses of L 364718 increased intake above baseline levels. No dose (3.2-320 micrograms/kg) of the type B antagonist, L 365260, affected intake in this paradigm. These results suggest that the mediation of the feeding-inhibitory effects of exogenous and endogenous CCK are similar and depend upon activation of type A CCK receptors.
Thirst and brain angiotensin in cattle
Authors: Blair-West J. R. , Denton D. A. , McKinley M. J. , Weisinger R. S.
Published: December 2017

Cows that were normally hydrated or deprived of water were given intravenous or intracerebroventricular (icv) infusions of angiotensin I converting-enzyme inhibitors (CEI) or angiotensin II antagonists. Normally hydrated Na-deficient cows increased water intake in a dose-related manner in response to icv infusion of angiotensin I (n = 5). The response to 3 micrograms/h angiotensin I was abolished by concurrent icv infusion of the CEI captopril at 3 mg/h but not by intravenous infusion of captopril at 120 mg/h, which reduced Na appetite (n = 5). The icv infusion of captopril at 12 mg/h did not reduce the water intake of cows that were water restricted for 26.5 h (n = 4) or water restricted and Na deficient (n = 4). The icv infusion of the more lipophilic CEI ramipril at 3 mg/h (n = 7) did not reduce the water intake of normally hydrated or dehydrated cows but reduced the "need-free" intake of Na solution by dehydrated cows. The icv infusion of the nonpeptide antagonist Du Pont 753 at 3 mg/h (n = 7) reduced water intake in dehydrated cows. The results indicate that brain angiotensin may be involved in thirst in cattle. The data suggest that this brain angiotensin II may be formed by a pathway that does not include converting enzyme and that is sited inside the blood brain barrier, possibly in the median preoptic nucleus.
Swimming changes vascular fatty acid composition and prostanoid generation of rats
Authors: Ohkubo T. , Jacob R. , Rupp H.
Published: December 2017

To define the effects of physical activity on vascular fatty acid composition and prostanoid generation, spontaneously hypertensive and normotensive rats were made to swim at 34-35 degrees C for 5-7 wk. Fatty acids were determined by gas chromatography and prostanoids by high-performance liquid chromatography and electrochemical detection. A characteristic feature of swimming rats was a markedly reduced linoleic acid content in the iliac artery and the aorta; in normotensive swimming rats stearic acid and arachidonic acid contents were increased. These changes could not be attributed to a heat loss during swimming or to depressed growth characteristics. A chemical sympathectomy using guanethidine (60 mg/kg body wt daily) did not prevent the alterations in fatty acid composition. A higher arachidonic acid content was correlated with an increased generation of 6-ketoprostaglandin F1 alpha in the aorta of untreated rats and sympathectomized rats. It is concluded that swimming can alter the vascular fatty acid composition in a manner which results in an increased potential for prostacyclin production.
CCK-receptor antagonists attenuate suppression of sham feeding by intestinal nutrients
Authors: Yox D. P. , Brenner L. , Ritter R. C.
Published: December 2017

To test the possibility that endogenous cholecystokinin (CCK) participates in suppression of sham feeding by intraintestinal nutrient infusions, we examined the effect of CCK-receptor antagonists on the suppression of sham feeding by intraintestinally infused oleic acid, maltose or L-phenylalanine (L-Phe). In addition, we monitored amylase activity in the intestinal lumen during some sham feeding experiments and measured plasma CCK in parallel experiments using intestinally infused animals that were not feeding. Suppression of sham feeding by oleic acid or maltose was attenuated by CCK-receptor antagonists, while suppression of sham feeding by L-Phe was not. Oleate infusion increased plasma CCK concentration and luminal amylase activity. Oleate-induced increase in luminal amylase activity was attenuated by a CCK-receptor antagonist. Intraintestinal maltose or L-Phe did not increase plasma CCK concentration or luminal amylase activity, suggesting that they did not release endocrine CCK. These results suggest 1) that endogenous CCK mediates suppression of sham feeding by oleate and maltose but not by L-Phe and 2) that CCK participating in suppression of feeding by intestinal stimuli might not be of endocrine origin.
Feeding suppression elicited by electrical and chemical stimulations of monkey hypothalamus
Authors: Takaki A. , Aou S. , Oomura Y. , Okada E. , Hori T.
Published: December 2017

The effects of electrical (ES) and chemical stimulations of the hypothalamus were investigated in monkeys during bar-press feeding. ES elicited both prolonged and nonprolonged types of suppression of bar-press feeding in hungry animals. Prolonged type suppression persisted for greater than 1 min beyond one or more post-ES trials and was found after ES of the dorsomedial hypothalamus (DMH), the ventromedial hypothalamus (VMH), and the ventromedial part of the lateral hypothalamic area (LHA). Non-prolonged type suppression was observed only during ES at some sites of both in hypothalamic and extrahypothalamic areas. A microinjection of glutamate into the VMH and the DMH, but not into the LHA, was able to reproduce the ES-induced prolonged type suppression. In contrast, the ES of the LHA, but not the VMH and DMH, in a satiated state provoked feeding. The results, together with the previous findings, suggest that the neuronal inhibitory mechanism of feeding exists in the VMH and DMH, while both the neuronal facilitatory and axonal inhibitory mechanisms in the LHA are involved in the feeding regulation, and these mechanisms of the LHA are affected by the hunger/satiety state.
Oxidative and glycolytic pathways in rat (newborn and adult) and turtle brain: role during anoxia
Authors: Xia Y. , Jiang C. , Haddad G. G.
Published: December 2017

Using enzyme histochemistry and in vitro electrophysiological recordings in brain slices, we studied 1) the relative activity of cytochrome c oxidase (Cytox) and hexokinase (HK) and 2) cellular function by examining ionic homeostasis across cell membranes in the turtle and newborn (5 days old) and adult rat central nervous system. We found that Cytox was higher in the rostral than in the caudal brain regions of the adult rat and that the activity in the newborn is at least as high as in the adult rat. In contrast, adult turtles had very low Cytox activity throughout the central nervous system. Compared with that in the adult rat, HK activity in the newborn was generally lower in the rostral brain and cerebellum but similar or higher in the brain stem and spinal cord. In the turtle, HK activity was higher in the cerebellum, brain stem, and ventral horn of the spinal cord than in those in the rat. During anoxia, extracellular K+ increased by approximately 10-fold (from 3.2 to approximately 32 mM) in the adult brain stem but only by 2.6 mM in newborn rats. After glycolysis was blocked with iodoacetic acid (10-20 mM), extracellular K+ increased remarkably in both adult and newborn rats to approximately 35 mM. In contrast, the turtle brain tissue showed a slight and insignificant increase in extracellular K+ during complete anoxia or with iodoacetic acid; there was a modest increase in K+ when anoxia and iodoacetate were administered together. We conclude that 1) the newborn rat brain must rely either on higher glycolytic capacity or on a reduction of metabolic rate during O2 deprivation and 2) the turtle brain can subsist on nonglucose fuels or on fuels not requiring the citric acid cycle and the electron transfer chain.
Human thermoregulatory responses during cold water immersion after artificially induced sunburn
Authors: Pandolf K. B. , Gange R. W. , Latzka W. A. , Blank I. H. , Young A. J. , Sawka M. N.
Published: December 2017

Thermoregulatory responses during cold-water immersion (water temperature 22 degrees C) were compared in 10 young men before as well as 24 h and 1 wk after twice the minimal erythemal dose of ultraviolet-B radiation that covered approximately 85% of the body surface area. After 10 min of seated rest in cold water, the mean exercised for 50 min on a cycle ergometer (approximately 51% of maximal aerobic power). Rectal temperature, regional and mean heat flow (hc), mean skin temperature from five sites, and hearrt rate were measured continuously for all volunteers while esophageal temperature was measured for six subjects. Venous blood samples were collected before and after cold water immersion. The mean skin temperature was higher (P less than 0.05) throughout the 60-min cold water exposure both 24 h and 1 wk after sunburn compared with before sunburn. Mean hc was higher (P less than 0.05) after 10 min resting immersion and during the first 10 min of exercise when 24 h postsunburn was compared with presunburn, with the difference attributed primarily to higher hc from the back and chest. While rectal temperature and heart rate did not differ between conditions, esophageal temperature before immersion and throughout the 60 min of cold water immersion was higher (P less than 0.05) when 24 h postsunburn was compared with presunburn. Plasma volume increased (P less than 0.05) after 1 wk postsunburn compared with presunburn, whereas plasma protein concentration was reduced (P less than 0.05). After exercise cortisol was greater (P less than 0.05) 24 h postsunburn compared with either presunburn or 1 wk postsunburn.(ABSTRACT TRUNCATED AT 250 WORDS)
Autonomic cardiovascular responses to smoke exposure in conscious rats
Authors: Nakamura T. , Hayashida Y.
Published: December 2017

Autonomic cardiovascular responses and the change in renal sympathetic nerve activity (RSNA) in response to smoke exposure were investigated in unrestrained conscious rats. Smoke exposure caused a prominent increase in RSNA (to 557.3 +/- 221.9% of the control level) and plasma norepinephrine [from 0.18 +/- 0.08 (control) to 0.66 +/- 0.22 ng/ml (at peak response of smoke exposure)], a slight increase in arterial blood pressure (from 89.6 +/- 3.3 to 103.6 +/- 3.8 mmHg), and marked bradycardia (from 386.6 +/- 12.8 to 231.3 +/- 20.6 beats/min). Respiratory rate in conscious rats was initially increased (from 1.6 +/- 0.1 to 6.1 +/- 0.3 breaths/s) but was decreased (to 0.9 +/- 0.1 breaths/s) at the peak phase of the cardiovascular responses to smoke inhalation. Blood gases and pH reflected these changes in respiratory rate to some extent. Sinoaortic denervation did not attenuate the bradycardia (from 402 +/- 17.5 to 255.8 +/- 16.2 beats/min) or increase in RSNA (to 413.4 +/- 74.9%) that occurred during smoke inhalation. Atropine sulfate abolished the bradycardic response (from 440.4 +/- 13.8 to 485.4 +/- 8.6 beats/min). Initial tachypnea was also observed in both sinoaortic denervated rats and atropine-treated rats. Anesthesia, induced by pentobarbital sodium (30 mg/kg iv) or alpha-chloralose (65 mg/kg iv), abolished the bradycardia, the increase in RSNA, and the change in respiratory rate caused by smoke exposure. Ablation of the olfactory lobes also greatly attenuated the smoke-induced increase in RSNA (to 150.9 +/- 22.9%), bradycardia (from 372.9 +/- 19.6 to 376.3 +/- 24.1 beats/min), and the respiratory change.(ABSTRACT TRUNCATED AT 250 WORDS)
Immunity to nerve growth factor and the effect on motor unit reinnervation in the rabbit
Authors: Finkelstein D. I. , Luff A. R. , Schuijers J. A.
Published: December 2017

The trophic effects of nerve growth factor (NGF) on sympathetic, peripheral afferent, and other neural crest-derived cells have been intensively investigated. More recently, NGF has been shown to have an influence on motoneurons. This study was undertaken to investigate whether NGF had any influence on the mechanical or histological properties of reinnervated motor units. Three groups of rabbits were used: normal rabbits, rabbits in which the nerve to medial gastrocnemius (MG) was cut and allowed to reinnervate for 56 days, and rabbits in which the MG nerve reinnervated in the presence of immunity to NGF. Immunity to NGF did not affect the ability of motor axons to reinnervate a muscle, nor were the contractile characteristics of the motor units altered. The size of horseradish peroxidase-labeled motoneurons was not influenced by immunization against NGF; however, the distribution of afferent neuron sizes was altered. Conduction velocity of motor axons proximal to the neuroma was significantly faster after immunization against NGF. Transection and subsequent reinnervation by a peripheral nerve normally causes an increase in myelin thickness proximal to the neuroma. However, immunization against NGF appeared to decrease the magnitude of myelin thickening. It was concluded that immunization against NGF affects motor axonal conduction velocity via an influence on the neural crest-derived Schwann cells.
Effects of brain stem lesions on 10-Hz and 2- to 6-Hz rhythms in sympathetic nerve discharge
Authors: Zhong S. , Barman S. M. , Gebber G. L.
Published: December 2017

We studied the effects of brain stem lesions or transection on the 10-Hz and 2- to 6-Hz rhythms in sympathetic nerve discharge (SND) in baroreceptor-denervated unanesthetized decerebrate cats. The results indicate that these two rhythms depend in part on different brain stem regions. The 10-Hz rhythm was eliminated by ablation of the rostral ventrolateral medulla (RVLM), medullary raphe complex, or pontine parabrachial and Kolliker-Fuse complex (PB/KF) or by pontomedullary border transection. Except for RVLM lesions, these procedures did not disrupt the 2- to 6-Hz rhythm in SND. In fact the power in SND at frequencies less than 6 Hz was increased by raphe or PB/KF lesions. Total power in SND was not significantly affected by raphe or PB/KF lesions, but mean arterial pressure was significantly reduced. Field potentials recorded from the RVLM (11 of 26 sites) and raphe (10 of 20 sites) were correlated to the 10-Hz rhythm in SND, further supporting a role of these areas in either generating or relaying this rhythm to sympathetic nerves. In contrast, field potentials recorded from the PB/KF were not correlated to the 10-Hz rhythm in SND. Thus this region may provide a tonic drive to the 10-Hz generator located elsewhere in the brain stem.
Expiratory bulbospinal neurons of dogs. II. Laterality of responses to spatial and temporal pulmonary vagal inputs
Authors: Tonkovic-Capin M. , Zuperku E. J. , Bajic J. , Hopp F. A.
Published: December 2017

Pulmonary mechanoreceptors with vagal fibers produce a combination of excitation and inhibition in the majority of the expiratory bulbospinal (EBS) neurons of dogs. Both aspects of this transpulmonary pressure-dependent neuronal response appear to be slowly adapting and activated at low pressure levels, suggesting the involvement of the slowly adapting pulmonary stretch receptors (PSRs). The purpose of the present study was to determine the contribution of different afferent pathways to each of the response components and to characterize the spatial and temporal processing of ipsi-, contra-, and bilateral vagal afferent inputs by two types of EBS neurons. For this purpose low-intensity electrical stimulation of the intact, desheathed, vagus nerves was used in thiopental sodium-anesthetized paralyzed dogs. The phrenic neurogram was used to synchronize both ventilation and stimulation. During test respiratory cycles, pulse trains (4-5 s duration) were applied during the neural expiratory phase to each and both vagus nerves. The mean discharge frequency (Fn) during the stimulus period was obtained from cycle-triggered histogram data. Plots of Fn vs. stimulus strength and Fn vs. stimulus frequency suggest that inhibition of both type D and type A EBS neurons is mediated mainly by the ipsilateral vagus nerve, and that the excitation of type D neurons is mediated bilaterally. These conclusions are also supported by inflation responses obtained before and after unilateral vagotomies. Differences in latencies and spatial and temporal summation characteristics suggest the possible involvement of different 1) types of PSRs, 2) central pathways, and/or 3) synaptic mechanisms in the biphasic response of the caudal ventral EBS neurons to lung inflation.