bluuebunny/crossref_metadata_2025 huggingface dataset:
Pressor responsiveness in pseudopregnant and pregnant rats: role of maternal factors
Authors: Paller M. S. , Gregorini G. , Ferris T. F.
Published: December 2017

During pregnancy the pressor response to vasoconstrictor substances such as angiotensin II (ANG II) is diminished, and renal, uterine, and vascular prostaglandin (PG) production may increase. However, little is known about the factors that alter vascular reactivity or stimulate PG synthesis during pregnancy. To ascertain whether these factors are of maternal or fetal-placental origin, we studied vascular reactivity and urinary PGE excretion in pseudopregnant rats. Pseudopregnant rats had plasma progesterone and weight gain similar to that observed in pregnant rats. Urinary PG excretion in nonpregnant rats was approximately 70 ng/24 h and remained constant during a 12-day observation. In contrast, urinary PG excretion in both pregnant and in pseudopregnant rats rose to levels approximately twice control within 4-6 days. The pressor response to ANG II was diminished in pseudopregnant rats compared with nonpregnant rats. When the PG synthesis inhibitor meclofenamate was given there was no change in the pressor response to ANG II in nonpregnant animals, but in pseudopregnant animals meclofenamate produced a significant increase in the pressor response to ANG II. The pressor response to norepinephrine and arginine vasopressin (AVP) was not diminished in pseudopregnant animals, and meclofenamate did not increase the pressor response to these agents. Therefore, a developing fetus and placenta is not necessary for the decrease in pressor response to ANG II nor for the early increase in urinary PGE excretion. Like in pregnancy, the pressor response to ANG II was increased after meclofenamate in pseudopregnancy. Increased PG production may, therefore, be partly responsible for the decrease in pressor responsiveness to ANG II. However, pseudopregnancy, unlike pregnancy, did not affect pressor responsiveness to norepinephrine or AVP. Both maternal and fetal-placental factors seem required for the reduction in responsiveness to norepinephrine and AVP in pregnancy.
Role of hemodynamic factors in osmoregulatory alterations of rat pregnancy
Authors: Barron W. M. , Durr J. A. , Schrier R. W. , Lindheimer M. D.
Published: December 2017

Plasma osmolality (Posmol) decreases in pregnancy, possibly because of hemodynamically mediated arginine vasopressin (AVP) secretion, i.e., inadequate vascular filling and/or decreased blood pressure. This hypothesis was tested in Sprague-Dawley rats treated on gestational days 1-18 or 13-18 with 1) deoxycorticosterone acetate (DOCA) + standard chow (0.5% Na), 2) vehicle + standard chow, or 3) high-Na (1.25%) diet. Renal sodium "escape" and suppression of the renin-aldosterone system suggested "effective volume expansion," yet Posmol was similar in all pregnant groups, 7-10 mosmol/kg below levels in virgin controls, and plasma AVP was unaltered. Apparent osmotic thresholds for AVP secretion, similar in control and DOCA-treated gravid animals, were 8-10 mosmol/kg below those of untreated virgin rats. Norepinephrine + DOCA, administered to gravid animals consuming normal or high-Na chow, increased blood pressure approximately 10% above control levels, but this also failed to alter Posmol. These data suggest that mechanisms other than hemodynamically mediated AVP secretion are responsible for the osmoregulatory alterations accompanying rodent pregnancy.
Restoration of renal response to atrial natriuretic factor in experimental low-output heart failure
Authors: Redfield M. M. , Edwards B. S. , Heublein D. M. , Burnett J. C.
Published: December 2017

The renal response to atrial natriuretic factor (ANF) has been shown to be blunted in several experimental models of acute and chronic congestive heart failure. The mechanism responsible for this blunted response has been postulated to be activation of the renin-angiotensin system with associated potent antinatriuretic effects and/or the reduction in renal perfusion pressure (RPP) characteristic of heart failure. The present study was designed to examine the relative role of these two factors in mediating the blunted response to ANF in a model of acute low output heart failure produced by thoracic inferior vena cava constriction (TIVCC) in the anesthetized dog. TIVCC was produced in five groups of dogs. In group 1, ANF was infused after TIVCC to document the blunted natriuretic response. In group 2, ANF was infused after TIVCC in the presence of blockade of intrarenal angiotensin II (ANG II) by the intrarenal infusion of saralasin (Sar) at a dose without systemic effects. In group 3, ANF was infused after TIVCC in the presence of restoration of RPP by infusion of ANG II at a dose titrated to restore RPP to the level present before TIVCC. In group 4, ANF was infused in the presence of restoration of RPP with ANG II and blockade of intrarenal ANG II with Sar. Group 5 served as an additional control group where the effect of ANG II and Sar in TIVCC was examined in the absence of ANF. Restoration of RPP but not blockade of intrarenal ANG II resulted in a restoration of the response of sodium excretion and glomerular filtration rate to ANF. ANG II plus Sar in the absence of ANF did not produce a natriuresis. We conclude that RPP, more than intrarenal ANG II, modulates the blunted renal response to ANF observed in this model of acute low-output heart failure.
Sex differences in central adrenergic control of vasopressin release
Authors: Stone J. D. , Crofton J. T. , Share L.
Published: December 2017

Central adrenoreceptor-mediated regulation of vasopressin secretion and cardiovascular function was studied in male rats and female rats in specific estrous cycle phases. In conscious, unrestrained rats with intracerebroventricular (icv) cannulas and femoral artery and vein catheters, plasma arginine vasopressin concentration (PAVP), mean arterial blood pressure (MABP), and heart rate (HR) were determined before and 5 and 15 min after icv injection of 10 micrograms norepinephrine or 50 micrograms phenylephrine. Norepinephrine (icv) increased PAVP in proestrus and metestrus four and three times (P less than 0.01 and 0.05, respectively) more than in males. Norepinephrine induced similar MABP elevations (P less than 0.01) in males and females in all cycle phases; HR decreased only in proestrus, estrus, and metestrus (P less than 0.01). The increase in PAVP after icv phenylephrine was four and three times greater in proestrous and diestrous females (P less than 0.01 and 0.05, respectively) than in males. The proestrous MABP rise was three times that in males (P less than 0.05); HR decreased similarly in diestrus, proestrus, and males. These results suggest gonadal steroid hormones influence adrenoreceptor-mediated control of vasopressin secretion, MABP, and HR.
Ventrolateral medullary neurons modulate pressor reflex to muscular contraction
Authors: Bauer R. M. , Iwamoto G. A. , Waldrop T. G.
Published: December 2017

Cardiorespiratory alterations during exercise are mediated through feedback from contracting muscles and descending drive from rostral brain sites such as the posterior hypothalamus. The role of medullary sites, which process this information, was examined in this study. In anesthetized cats, muscular contraction elicited by stimulation of L7 and S1 ventral roots and electrical stimulation of sites in the posterior hypothalamus both evoked increases in arterial pressure, heart rate, and minute ventilation. The reflex increase in arterial pressure produced by muscular contraction was attenuated significantly 15-20 min after bilateral microinjections of an excitatory amino acid (EAA) receptor antagonist, kynurenic acid (KYN), into the ventrolateral medulla (VLM). The reflex increase in arterial pressure evoked by muscular contraction returned to control levels 90 min after VLM microinjections of KYN. Microinjection of KYN into the VLM had no effect on the cardiorespiratory responses to posterior hypothalamic stimulation. These findings suggest that neurons in the VLM modulate the reflex pressor response evoked by muscular contraction. This reflex may be mediated through an interaction with EAA receptors on neurons in the VLM.
Effect of temperature on chemical control of ventilation in Mexican black iguanas
Authors: Dupre R. K. , Hicks J. W. , Wood S. C.
Published: December 2017

The impact of temperature on the chemical control of respiration in the Mexican black iguana Ctenosaura pectinata was examined by measuring ventilatory responses to graded hypoxia with and without 2.9% inspired CO2 at 25, 30, and 35 degrees C. Black iguanas increased pulmonary ventilation in response to hypoxia by increasing both tidal volume and respiratory frequency. Breathing 2.9% CO2 stimulated an increased pulmonary ventilation primarily through increases in tidal volume. The fractional O2 concentration at which ventilation began to increase (hypoxic threshold) varied with temperature, increasing from 0.067 at 25 degrees C to 0.085 at 30 degrees C and 0.112 at 35 degrees C. At 35 degrees C, breathing 2.9% CO2 promoted a further, although statistically insignificant, shift in the ventilatory hypoxic threshold to approximately 0.130 fractional inspired O2 concentration. A “gasping” ventilatory pattern was also observed, the frequency of which increased with progressive hypoxia and increasing temperature. These results suggest that the chemical control of ventilation in this lizard is susceptible to changes in temperature, although the mechanism underlying the temperature sensitivity remains obscure.
Membrane dynamics in insect malpighian tubules
Authors: Bradley T. J.
Published: December 2017

Urine formation in insects occurs in the Malpighian tubules by means of active ion transport and osmotically coupled water flow. The rates of urine formation can vary with time and can be modulated by diuretic hormones, developmental events, and intracellular parasitism. This paper reviews a number of recent studies in which it has been demonstrated that variations in transport rate are associated with substantial changes in tubule ultrastructure in the form of membrane insertion into and deletion from the apical microvilli. The principal driving force for fluid movement in Malpighian tubules is thought to be a common cation pump located in the apical membranes. It is proposed that modulation of the apical microvillar membrane may reflect regulation by the cells of the number of common cation pump units involved in fluid secretion.
Level of satiety: in vitro energy metabolism in brain during hypophagic and hyperphagic body weight recovery
Authors: Kasser T. R. , Harris R. B. , Martin R. J.
Published: December 2017

Rates of in vitro glucose and fatty acid oxidation were examined in four brain sites during hypophagic and hyperphagic recovery of normal body weight. Rats were fed 40, 100, or 160% of normal intake, via gastric intubation, for 3 wk. Another group of rats was starved until body weight loss was equivalent to weight loss in 40%-fed rats. Groups of rats were killed at the conclusion of tube feeding or fasting and at specific periods during recovery of body weight. Brain sites examined were the ventrolateral hypothalamus (VLH), ventromedial hypothalamus (VMH), a caudal brain stem site encompassing the area postrema-nucleus of the solitary tract (AP-NTS), and cortex. During recovery, rats previously fed 160% of normal intake (anorectic) maintained low rates of VLH fatty acid oxidation and were hypophagic until most excess fat was depleted. Conversely, rats previously fed 40% of normal intake (hungry) maintained high rates of VLH fatty acid oxidation and were hyperphagic until most deficient fat was repleted. Rats previously starved maintained high rates of VLH fatty acid oxidation during hyperphagic recovery, although levels of VLH fatty acid oxidation and food intake were initially low on refeeding. Rates of glucose oxidation in the brain sites examined did not relate well to energy balance status and the needed adjustments in food intake. The results indicated that the level of glucose oxidation in the VLH and AP-NTS responded to the level of energy immediately coming into the system (food intake).(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of prolonged exercise on puberty and luteinizing hormone secretion in female rats
Authors: Manning J. M. , Bronson F. H.
Published: December 2017

Immature female rats were required to run for prolonged periods of time to obtain food. The amount of food they earned was adequate for full pubertal development and moderate growth under nonworking conditions, but both processes were blocked by the exercise requirement. Prolonged exercise also blocked the pulsatile release of luteinizing hormone (LH); only two LH pulses were seen in seven exercising females during a total of 24 h of monitoring at 8 wk of age. By comparison, almost 1 pulse/h was seen in postpubertal, normally growing females of this same age during metestrus. When the exercising females' running requirement was relaxed at 8 wk of age they experienced rapid catch-up growth and reproductive development. Both basal secretion and LH pulse frequency increased markedly within 48 h, and most of these females ovulated during the third dark period after relaxation. Altogether, the experimental paradigm and techniques employed here yield highly predictable results, and they should prove useful for exploring other neuroendocrine pathways through which excessive exercise antagonizes reproduction.
Homologous regulation of human platelet vasopressin receptors does not occur in vivo
Authors: Vittet D. , Launay J. M. , Chevillard C.
Published: December 2017

Large variations in the functional responsiveness of human platelets to arginine vasopressin (AVP), related to maximal platelet AVP-binding capacity, have been observed among individuals. The effects of dehydration and overhydration on maximal platelet AVP-binding capacity, plasma AVP, platelet-associated AVP, and AVP-induced platelet aggregation were examined in healthy human volunteers to determine whether homologous regulation of platelet AVP receptors occurs in vivo within the physiological range of circulating AVP fluctuations. Although significant variations of plasma AVP were observed under both conditions, no correlation could be found in the same individual with any change in 1) the maximal AVP-binding capacity, 2) platelet aggregatory responses to AVP, or 3) the platelet AVP fraction. Moreover, there was no relationship between the number of detectable platelet AVP receptors and the amount of AVP associated with platelets. These data show that homologous regulation of platelet AVP receptors by AVP does not occur in vivo over the time investigated, at least within the physiological range of AVP. Nonetheless, regulation at the platelet precursor stage appears to be highly probable in view of the relationship between plasma AVP and platelet AVP binding capacity observed among different individuals.
Effects of m-chlorophenylpiperazine on penile and bladder function in rats
Authors: Steers W. D. , de Groat W. C.
Published: December 2017

The effects of m-chlorophenylpiperazine (MCPP), a serotonin agonist, on spontaneous and evoked neural firing in nerves supplying the penis and bladder were examined in the urethan-anesthetized rat. MCPP (0.1-10 mg/kg iv) elicited, after a 2- to 4-min delay, an increase in spontaneous firing in cavernous nerves but no detectable firing in bladder nerves. The cavernous nerve firing was accompanied by an increase in intracavernous pressure and a depression of rhythmic bladder activity. Administration of ganglionic-blocking agents or transection of peripheral nerves revealed that the cavernous nerve discharge was mediated by activation of pre-ganglionic cholinergic pathways in the pelvic nerve. The effects of MCPP were noted in intact as well as in acute and chronic spinal rats and were prevented by the administration of the serotonin (5-HT) antagonist, metergoline (3 mg/kg im). These data indicate that pharmacological activation of 5-HT receptors, possibly of the 5-HT1B subtype, can facilitate the sacral preganglionic outflow to the penis and inhibit bladder activity.
Excitatory effect of substance P in parasympathetic ganglia of cat urinary bladder
Authors: Kawatani M. , Whitney T. , Booth A. M. , de Groat W. C.
Published: December 2017

Intra-arterial administration of substance P (0.1-50 micrograms/kg) to the urinary bladder of the cat produced slow-onset and sustained bladder contractions, asynchronous firing of bladder postganglionic nerves, and facilitation of nicotinic transmission in bladder ganglia. Intracellular recording from bladder ganglia in vitro revealed that substance P depolarized ganglion cells and initiated burst of action potentials (maximal frequency 6-7 Hz). The ganglionic excitatory effect of substance P in situ was blocked by gamma-aminobutyric acid (2-20 micrograms/kg) and the substance P antagonist [D-Arg1,D-Pro2,D-Trp7.9,Leu11]substance P (0.5-20 micrograms/kg) but was not altered by atropine (10-100 micrograms/kg), hexamethonium (0.5-2 mg/kg), norepinephrine (2-20 micrograms/kg), or leucine enkephalin (0.5-20 micrograms/kg). The bladder contractions elicited by substance P were not blocked by atropine, hexamethonium, or [D-Arg1,D-Pro2,D-Trp7.9,Leu11]substance P (0.1-10 micrograms/kg) but were blocked by another substance P antagonist, [D-Pro2,D-Phe7,D-Trp9]substance P. These data indicate that substance P has a direct postsynaptic excitatory effect on neurons in the vesical parasympathetic ganglia and on bladder smooth muscle cells. The differential effects of substance P antagonists on the excitatory responses at these two sites indicate the responses were mediated by different types of tachykinin receptors.
Increased urinary clearance of lysine vasopressin in the deoxycorticosterone acetate-hypertensive pig
Authors: Ling W. D. , Brooks D. P. , Crofton J. T. , Share L. , Bohr D. F.
Published: December 2017

We have previously reported an increased urinary excretion of vasopressin without a rise in circulating levels of this hormone in the deoxycorticosterone acetate (DOCA)-hypertensive pig (DH). The present study was designed to characterize the renal handling of vasopressin in DH that might account for this paradox. DOCA hypertension was produced in seven domestic female pigs by means of subcutaneous implants of Silastic rubber impregnated with DOCA. Thirty days after DOCA implantation, urinary clearances of inulin, para-aminohippurate (PAH), and vasopressin were measured in the conscious animals during infusion of a 5% dextrose solution, first without and then with lysine vasopressin. Subsequent to this study, four of the pigs were placed on a low-sodium (10 meq/kg food) diet for 4 wk. At the end of this period, the clearances were again evaluated. We observed an increased urinary vasopressin clearance (CLVP) in the DH associated with an increased urinary flow but without significant changes in the clearances of inulin or PAH. Dietary sodium restrictions reversed the hypertension and the increased urinary flow and returned the CLVP to normotensive levels. These results indicate that the increased urinary excretion of vasopressin in DH is because of an increased urinary clearance of this hormone. This increased urinary CLVP is the consequence of the high urine flow in these pigs.
Propranolol restores phosphaturic effect of PTH in short-term phosphate deprivation
Authors: Rybczynska A. , Hoppe A. , Knox F. G.
Published: December 2017

Phosphate deprivation causes a resistance to the phosphaturic effect of parathyroid hormone (PTH). The present study evaluated the role of the beta-adrenergic system in this resistance phenomenon. In clearance experiments performed on acutely thyroparathyroidectomized male Sprague-Dawley rats, the phosphaturic response to PTH was determined in the presence and absence of propranolol in rats fed a low-phosphate diet (LPD) for 0.5, 1, 2, 3, or 4 days. Fractional excretion of phosphate (FEPi) in control rats fed a normal-phosphate diet (NPD) increased from 4.37 +/- 1.6 to 38.5 +/- 3.4% in response to PTH infusion. Propranolol did not change FEPi in NPD animals in the absence or in the presence of PTH (2.0 +/- 1.1 vs. 36.7 +/- 1.6%). LPD resulted in a gradual decrease in the phosphaturic response to PTH infusion as compared with NPD animals. PTH increased FEPi to 24.2 +/- 6.0% after one-half day of LPD, but when the infusion was supplemented with propranolol, PTH increased FEPi to 38.0 +/- 4.7%, similar to that in NPD animals. In the group fed LPD for one day, PTH increased FEPi to 16.9 +/- 4.3%, whereas in the presence of propranolol FEPi was restored to a similar level as in the NPD group (36.0 +/- 5.9%). Two days of LPD markedly decreased FEPi in response to PTH to 7.9 +/- 3.8% as compared with NPD rats, and propranolol infusion did not change this value significantly. Three and 4 days of LPD induced complete resistance to the phosphaturic effect of PTH in the presence as well as in the absence of propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)
Ontogeny of vasoconstrictor neurohypophysial hormone function in rats
Authors: Kullama L. K. , Balaraman V. , Claybaugh J. R. , Ichimura W. M. , Nakamura K. T.
Published: December 2017

This in vitro study examined the ontogeny of arginine vasopressin (AVP) and arginine vasotocin (AVT) compared with norepinephrine (NE)-mediated contraction in rat thoracic aortas. Aortas from three age groups (2-3 days, 6-7 days, and 12 wk) of Sprague-Dawley rats were used. Ring segment resting length was adjusted to optimize tension developed to a dose that produces half-maximal tension of NE in Krebs solution (pH 7.4, 37 degrees C) and gassed with 95% O2-5% CO2. Cumulative dose-response curves were generated for KCl (5-100 mM), NE (10(-10)-10(-5) M), AVP, and AVT (both 10(-10)-10(-6) M) in the presence and absence of a selective V1 vasopressinergic inhibitor, [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine]arginine vasopressin ([d(CH2)5Tyr(Me)]AVP). A progressive increase in sensitivity among all age groups was found for KCl and NE. There was a slight decrease in sensitivity to both AVP and AVT in the 1st wk. Maximum contractile response to NE increased between 2-3 and 6-7 days, whereas no change was observed for KCl, AVP, or AVT. AVP- and AVT-mediated contractions were selectively inhibited by [d(CH2)5Tyr(Me)]-AVP. These results suggest 1) receptor-mediated contractility is present from 2 days of age for NE, AVP, and AVT; 2) sensitivity to KCl and NE increases progressively during postnatal development, whereas sensitivity to AVP and AVT slightly decreases in the 1st wk with no progressive age-related increase by 12 wk; 3) AVP and AVT mediate contraction via a similar V1-like receptor.
Evidence for presence of a new type of neurohypophysial hormone receptor in fish gill epithelium
Authors: Guibbolini M. E. , Lahlou B.
Published: December 2017

Arginine vasotocin (AVT) and isotocin (IT) induced direct inhibition of adenylate cyclase activity in gill plasma membranes of the rainbow trout adapted to freshwater (FW) and seawater (SW). The maximal inhibition was obtained with 10(-11)-10(-10) M (50% inhibitory concentration approximately 10(-13) M), values in agreement with the circulating levels of AVT in trout blood. Specific V1 or V2 agonists or antagonists (with reference to vasopressin) were used to define the specificity of the neurohypophysial peptide receptors involved in this inhibition. The V1 agonist [Phe2,Orn8]vasotocin ([Phe2]OVT) inhibited the basal and glucagon-stimulated adenylate cyclase activity, and this effect in SW (20%) was twice more than in FW (10%). The V2 agonist 1-deamino[Val4,Arg8]-vasopressin (dVDAVP), however, produced a stimulation that was of the same amplitude (10%) in both media. The V1 antagonist [(1-beta-mercapto-beta-beta-cyclopentamethylenepropionic acid), 1-(O-ethyl)Tyr2,Orn8]vasotocin (d(CH2)5[Tyr(Et)2]OVT) totally reversed the AVT- or IT-induced inhibition of basal or glucagon-stimulated cyclase activity, whereas the V1/V2 antagonist [(1-beta-mercapto-beta-beta-cyclopentamethylene propionic acid), 1-(O-ethyl)D-Tyr2,Val4,Arg8]vasopressin (d(CH2)5[D-Tyr(Et)2]-VAVP) (previously used as V2 antagonist in amphibians) had no such effect. When active, all analogues had their maximal activity at 10(-11)-10(-10) M (50% maximal activity approximately 10(-13) M), as observed with the natural peptides. These results, together with our previous observations, point to the gill epithelium as a direct target organ for neurohypophysial peptides and suggest that the hormone receptors involved in fish belong predominantly, if not exclusively, to a new type that we propose to designate as fish neurohypophysial hormone (NHF) receptors while awaiting further characterization.
Autoradiographic localization of atrial and brain natriuretic peptide receptors in rat brain
Authors: Brown J. , Czarnecki A.
Published: December 2017

Displacement of bound 125I-labeled atrial natriuretic peptide-(1-28) [alpha 125I-ANP-(1-28)] by alpha-ANP-(5-28) and porcine brain natriuretic peptide (BNP) was used to map receptors common to these peptides in rat brain by in vitro autoradiography. alpha-125I-ANP bound reversibly to subfornical organ, area postrema, median preoptic, supraoptic and paraventricular nuclei, and arachnoid mater. Binding at these sites was displaced similarly by 1 microM unlabeled alpha-ANP, alpha-ANP-(5-28), and BNP. Binding dissociation constants in the subfornical organ and arachnoid were 4.40 +/- 1.15 and 3.99 +/- 0.86 nM, respectively, for alpha-ANP, and 2.41 +/- 1.11 and 2.23 +/- 1.06 nM, respectively, for BNP. alpha-125I-ANP also bound to choroid plexus. Here 1 microM unlabeled alpha-ANP displaced significantly more radioligand than did 1 microM BNP, and the concentration displacing 50% of bound radioligand was 2.23 +/- 0.78 nM for alpha-ANP and 1.51 +/- 0.67 nM for BNP. alpha-ANP-(5-28) also displaced alpha 125I-ANP at all sites with significantly greater affinity than did unlabeled alpha-ANP. alpha-125I-ANP was not displaced by completely unrelated peptides. Therefore, both atrial and brain natriuretic peptides may be high-affinity ligands at common receptors in some cerebral localities.
Parabrachial nucleus modulation of vasopressin release
Authors: Ohman L. E. , Shade R. E. , Haywood J. R.
Published: December 2017

The present studies examine the contribution of the ventrolateral lateral parabrachial nucleus (VLLPBN) to the regulation of plasma arginine vasopressin (PAVP) release in response to either a baroreceptor or osmotic stimulus. These studies were carried out in rats with bilateral electrolytic lesions of the VLLPBN. Baroreceptor-induced stimulation of PAVP was achieved by decreasing blood pressure with combined blockade of the renin-angiotensin system with captopril (3 mg/kg iv) and the sympathetic nervous system with chlorisondamine, (11 mg/kg sc). Osmotic release of vasopressin was elicited by a 2-h intravenous infusion of hypertonic saline, (3.0 meq/ml, 0.01 ml/min). Blood pressure and heart rate were monitored throughout the experiments. Blood samples for determination of PAVP, plasma osmolality (posm), plasma sodium (PNa), and plasma potassium (PK) were taken before (base line) and after treatment in each study. The VLLPBN-lesioned rats secreted significantly more vasopressin in response to hypotension produced by combined renin-angiotensin and sympathetic nervous system blockade than did control rats. There was no significant difference between groups in Posm, PNa, or PK, or cardiovascular changes. In contrast, hypertonic saline infusion did not produce any differential changes between groups.
Renin secretion by fetal lamb kidneys in vitro
Authors: Rawashdeh N. M. , Rose J. C. , Kerr D. R.
Published: December 2017

We studied the content and secretion of renin by renal cortical slices obtained from ovine fetuses at 0.62-0.77 gestation (n = 5 immature) and at 0.84-1.00 gestation (n = 5 mature). Renin content of fresh slices and renin secretion after the incubation of slices in Robinson's medium with or without isoproterenol or dibutyryl (DB) adenosine 3',5'-cyclic monophosphate (cAMP) (10(-4)-10(-8) M) were measured. Renin content of immature fetal kidneys (ng.ml homogenate-1.h-1.mg-1) and basal renin secretion rate [ng (ANG I/h).mg tissue-1.h incubation-1] were 24.3 +/- 3.0 and 1.4 +/- 0.4, respectively. Both of these values were significantly lower (P less than 0.02) than the corresponding results obtained with mature fetal kidneys (67.0 +/- 4.5 and 3.4 +/- 0.5). Renin content and basal secretion rates were strongly correlated (r = 0.78, P less than 0.01). The addition of isoproterenol or DBcAMP induced a significant increase in renin secretion only when incubated with slices from mature fetuses. We conclude that there is a deficit in the beta-adrenoceptor-mediated renin release distal to cAMP formation in immature fetuses, which may be related to low renal content of renin at this stage of development.
Variable series elasticity accounts for Fenn effects of skeletal and cardiac muscles
Authors: Suga H.
Published: December 2017

The Fenn effect differs between skeletal and cardiac muscles in the magnitude of energy consumption of shortening contraction relative to isometric contraction at the same preload. The former is typically greater than the latter in the skeletal muscle, whereas the former is smaller than the latter in the cardiac muscle. The present theoretical study examined whether the different Fenn effects could be accounted for by different compliances of the series elasticity (SE) in different muscles. A two-element model consisting of an idealized contractile element (CE) and an SE was used. The compliance of the SE was assumed to be variable. Results show that the skeletal Fenn effect can be simulated when SE is stiff and the cardiac Fenn effect can be simulated when SE is compliant. Moreover, when SE is compliant the total work of CE approximates for force-length area, which has been proposed as a measure of the total mechanical energy and shown to correlate linearly with myocardial oxygen consumption.
Osmotic regulation of vasopressin and oxytocin release is rate sensitive in hypothalamoneurohypophysial explants
Authors: Yagil C. , Sladek C. D.
Published: December 2017

Explants of the hypothalamoneurohypophysial system (HNS) from rats were maintained in perifusion culture and exposed to 15-18 mosmol/kgH2O changes in the osmolality of the culture medium achieved by increasing or decreasing the NaCl concentration. The rate of change in osmolality was either 0.14 +/- 0.01 mosmol/min (2%/h), 0.27 +/- 0.02 mosmol/min (5%/h), or 1.7 +/- 0.2 mosmol/min (30%/h). Vasopressin (VP) and oxytocin (OT) release into the culture medium was determined. Increased VP release was detected after all three rates of increase, but the peak response occurred sooner and in response to a smaller increment in osmolality during the 5% rate of increase compared with the 2% rate of increase. Peak VP release occurred during the first 10 min of the 30% pulse and was significantly greater than the response to the 2 and 5% rates (P less than 0.05). The increase in VP release was sustained throughout the 3 h of hypertonicity during the 2% pulse, but not during the 5 and 30% osmotic pulses. A significant decrease in VP release was observed on returning the osmolality to basal at both the 2 and 5% rate, but this inhibition was followed by a rebound in VP release that started during the decrease in osmolality and significantly exceeded basal VP release. A significant inhibition of VP release also was observed when explants were exposed to hypotonic pulses at the 2 and 5% rate. At both rates, the inhibition of VP release corresponded to a 5- to 7-mosmol/kgH2O decrease in osmolality.(ABSTRACT TRUNCATED AT 250 WORDS)
Weight gain and brown fat composition of mice selected for high body weight fed a high-fat diet
Authors: Desautels M. , Dulos R. A.
Published: December 2017

Mice selected for high body weight (QL522) had increased food intake, body weight gain, and fat deposition relative to mice without weight selection (QL521). Brown adipose tissue (BAT) thermogenic capacity, as determined by the tissue content of protein, DNA, and succinate dehydrogenase and by mitochondrial uncoupling protein content was similar or slightly higher in 2- and 10-mo-old QL522 mice relative to age-matched QL521 mice. When food intake of QL522 mice was restricted to the level of QL521 mice, body weight gain and fat deposition over 28 days were then comparable to those of QL521 mice. Food restriction had no effect on BAT composition of QL522 mice. Both QL521 and QL522 mice increased calorie intake by 40-50% when offered a palatable high-fat supplement (HF), but only QL522 mice increased weight gain and fat deposition significantly. QL521 mice fed a high-fat supplement showed a significant increase in brown fat succinate dehydrogenase content, whereas QL522 mice showed significant increases in brown fat weight, protein, and succinate dehydrogenase content relative to mice fed stock diet. Nonshivering thermogenic capacity, as assessed by norepinephrine-stimulated oxygen uptake in anesthetized animals at 30 degrees C was similar between QL521 and QL522 mice eating stock diet and was significantly increased by the high-fat supplement in both strains. Thus mice selected for high body weight are very susceptible to diet-induced obesity, and we have no evidence that a reduction in brown fat thermogenic capacity contributes to the increased fat deposition of QL522 mice as they grow old or when they are offered palatable energy-dense supplements.
Mitochondrial and peroxisomal fatty acid oxidation in elasmobranchs
Authors: Moyes C. D. , Buck L. T. , Hochachka P. W.
Published: December 2017

In heart and red muscle of dogfish (Squalus acanthias), the maximal activities of the fatty acid catabolizing enzyme carnitine palmitoyltransferase (CPT) are less than 5% the rate in the same tissues of teleosts (carp, Cyprinus carpio; trout, Salmo gairdneri). CPT activities in these tissues of hagfish (Eptatretus stouti) are approximately 10% the rate in teleosts. However, the maximal activities of the beta-oxidation enzyme beta-hydroxyacyl-CoA dehydrogenase (HOAD) in dogfish red muscle and heart are similar to these tissues in the other species. This paradox prompted a more detailed study on the capacity of mitochondria from dogfish cardiac and red skeletal muscles to utilize fatty acids, possibly by a CPT-independent pathway. Free fatty acids were not oxidized by mitochondria from red muscle (hexanoate, octanoate, decanoate, and palmitate) or from heart (octanoate, palmitate). Neither hyposmotic incubation nor addition of 5 mM ATP could stimulate oxidation of octanoate or palmitate in either preparation, suggesting that these tissues have little capacity to oxidize fatty acids by a carnitine-independent pathway. Palmitoyl carnitine oxidation was detectable at very low rates in these mitochondria only with hyposmotic incubation. Octanoyl carnitine was oxidized at greater rates than palmitoyl carnitine, 10% the rate of pyruvate in both tissues, suggesting that medium-chain fatty acids could be physiologically relevant fuels in elasmobranchs if available to heart and red muscle. One potential source of medium-chain fatty acids is hepatic peroxisomal beta-oxidation, which occurs in dogfish liver at maximal activities similar to carp and trout liver. However, based on relative rates of oxidation, it is likely that dogfish heart and red muscle metabolism are fueled primarily by carbohydrate and ketone bodies.
Physiological regulation of the renal vasopressin receptor-effector pathway in dogs
Authors: Kinter L. B. , Caldwell N. , Caltabiano S. , Winslow C. , Brooks D. P. , Huffman W. F.
Published: December 2017

Physiological regulation of receptor-effector pathways is recognized as a significant factor determining target organ selectivity and sensitivity in several hormonal systems. Whether or not physiological regulation of the renal vasopressin (V2) receptor-effector pathway participates in the control of body fluid homeostasis is unknown. We evaluated four states likely to be associated with altered sensitivities of the renal V2 receptor-effector pathway as follows: dehydration (18-h hydropenia), volume expansion, exogenous arginine vasopressin (AVP) infusion (10 ng/kg + 0.25 ng.kg-1.h-1), and cyclooxygenase blockade (indomethacin, 2 mg/kg + 2 mg.kg-1.h-1) for effects on the antidiuretic efficacies and potencies of putative V2-receptor antagonists in conscious dogs. The antidiuretic efficacies of desGly9[Pmp1-D-Tyr(Et)2Val4]AVP [Smith Kline & French (SK&F) 101926; 0.01-1,000 micrograms/kg] ranged from that of a full agonist to that of an antagonist, depending on the physiological state studied. The vasopressin antagonist potency of SK&F 101926 was increased 150-fold in association with extracellular volume expansion and decreased by blockade of renal cyclooxygenase activity. This spectrum of activities is that anticipated for a partial agonist under conditions where receptor number and/or sensitivity of receptor-effector coupling is increased or decreased, respectively. Thus volume expansion and increased circulating vasopressin concentration are associated with effective decreases, whereas hydropenia and cyclooxygenase blockade are associated with effective increases in sensitivity of the renal V2 receptor-effector pathway in the dog kidney. We conclude that the V2 receptor-effector pathway is a site of integration of physiological mechanisms participating in the control of body fluid homeostasis in conscious dogs.
Temperature regulation in biotelemetered spontaneously hypertensive rats
Authors: Morley R. M. , Conn C. A. , Kluger M. J. , Vander A. J.
Published: December 2017

Core temperature of the spontaneously hypertensive rat (SHR) was not found to be different from the core temperature of the control rat, the Wistar-Kyoto rat (WKY), when the rats were left undisturbed in their home cages. When the rats were exposed to a variety of stressful environments, including cage switching, exposure to an open field, and handling, both SHR and WKY rats showed an increase in temperature. For the set of rats supplied by Charles River, the SHR temperature response to the stress was identical to the WKY rats' temperature response. For the set of rats supplied by Taconic Farms, the SHR was found to have a greater temperature response to the acute stress and the open-field stress. The Taconic Farms rats were also exposed to restraint stress, which resulted in a rise in temperature that was greater for the SHR when compared with the WKY. Because we have observed the increased lability in body temperature of the SHR compared with the WKY rats during restraint, we believe that it is important that studies with these strains of rat be done using minimal or no restraint.
Transuterine ion movement and electrical potential difference in pregnant guinea pigs
Authors: Dale P. S. , McNaughton T. G. , Power L. A. , Gilbert R. D. , Power G. G.
Published: December 2017

An investigation of the site and mechanism responsible for the maternal-fetal electrical potential difference (PD) was done in 11 anesthetized guinea pigs at 54-56 days gestation. We removed the most distal fetus and placenta from one uterine horn and secured a catheter, thermistor, and Ag-AgCl electrode in the resulting pouch. The pouch was filled with Earle's solution. We placed another thermistor and electrode in the maternal abdomen. The PD between electrodes was monitored continuously; periodic samples of maternal blood and intrauterine fluid were taken. Thirty minutes after the uterus was filled, the PD (uterine cavity negative) averaged 29.6 +/- 4.5 (95% confidence interval of the mean) mV. Over 4 h, intrauterine K+ concentration [( K+]) decreased from 4.9 to 2.6 +/- 0.5 meq/l, against a chemical and electrical gradient. In eight animals, we measured bidirectional Na+ flux using 22Na and 24Na. The flux ratio was not distinguishable from unity despite a significant PD. Our data indicate that the maternal-fetal PD is probably generated by the endometrial epithelium and that Na+ and K+ both move across the epithelium by active transport or cotransport rather than simple diffusion.
Cardiovascular and neuroendocrine responses to baroreceptor denervation in baboons
Authors: Shade R. E. , Bishop V. S. , Haywood J. R. , Hamm C. K.
Published: December 2017

The purpose of this study was to describe the hormonal and blood pressure responses to partial (carotid sinus) and complete (carotid sinus + aortic arch) baroreceptor denervation in baboons. Experiments were performed in eight adult male baboons maintained on a tether system for the continuous measurement of mean arterial blood pressure (MAP) and heart rate (HR). Bilateral carotid sinus denervation (CSD) immediately increased MAP from 83 +/- 2.2 to 124 +/- 7.3 mmHg. MAP gradually decreased over the next 14 days to intact levels. There were also transient decreases in HR variability and increases in blood pressure variability after CSD. Subsequent denervation of the aortic arch to produce sinoaortic denervation (SAD) resulted in another abrupt large increase in MAP followed by a small but significant increase in MAP of 11 mmHg that was maintained for up to 4 wk after SAD. The short-term variability of HR and blood pressure was chronically decreased and increased, respectively, after SAD. Plasma renin activity, vasopressin, and epinephrine were not changed from intact levels either after CSD or SAD. Plasma norepinephrine was only transiently increased by CSD and chronically elevated by 72% over intact levels after SAD. Thus CSD in the baboon does not produce a sustained increase in MAP. SAD chronically increases MAP and is associated with evidence for an increased sympathetic tone. There is no indication that either increased renin secretion or vasopressin secretion contributes to the chronic cardiovascular effects of SAD in baboons.
A distributed model of fluid and mass transfer in peritoneal dialysis
Authors: Seames E. L. , Moncrief J. W. , Popovich R. P.
Published: December 2017

A mathematical model has been developed to study peritoneal fluid and solute transfer. The model uses the concept of a distributed capillary system within the peritoneal tissue. The model accounts explicitly for transport across the capillary membrane, through interstitial tissue, and across the mesothelium. The capillary and mesothelial membranes are modeled using pore theory and a dual pathway (through pores and across cells) for fluid transfer. The nonperitoneal tissues are modeled as a single body pool. Lymphatic uptake from the peritoneal cavity is included. Model parameters were found from the literature and by simultaneously fitting experimental data for dialysate volume and dialysate concentrations of blood urea nitrogen, glucose, creatinine, and inulin. The model was also shown to predict concentration gradients within several tissues surrounding the peritoneal cavity. Variation of the model parameters revealed the importance of the mesothelial cell layer in peritoneal ultrafiltration. The results of model simulations indicate an initial transfer of fluid from the tissue space to the peritoneal cavity followed by transcapillary fluid transfer.
Ethanol attenuates endotoxin-enhanced glucose utilization
Authors: Molina P. E. , Lang C. H. , Bagby G. J. , Spitzer J. J.
Published: December 2017

Ethanol (EtOH) is known to alter various aspects of cellular metabolism. Among these, the blunting of the increased rate of glucose production and utilization by the host after the administration of endotoxin may be an important factor in the increased susceptibility to infections. Therefore the present study was conducted to determine which tissues are responsible for the attenuation of the endotoxin-induced increase in whole body glucose utilization after acute EtOH administration. In vivo glucose metabolic rate (Rg) of different organs was investigated in conscious rats by the tracer 2-deoxy-D-glucose technique. Rats received a slow intravenous bolus injection of EtOH (275 mg/100 g body wt of a 20% wt/vol solution) followed by a continuous infusion (25 mg/100 g body wt) that was maintained throughout the experimental period. Thirty minutes after initiation of the EtOH treatment, Escherichia coli endotoxin (100 micrograms/100 g body wt) was administered intravenously. Time-matched control animals received an equal volume of saline. EtOH alone affected Rg only in gastrocnemius muscle (30% decrease) and adipose tissue (twofold increase). Endotoxin alone increased Rg in all tissues examined except in heart and brain. Prior administration of EtOH inhibited the endotoxin-induced increased Rg in skeletal muscle (regardless of fiber type), ileum, liver, adipose tissue, and kidney, blunted the increase in spleen and lung, and did not alter the increased Rg in skin. Brain showed a 20% decrease in Rg in response to EtOH and endotoxin administration. The EtOH-attenuated increase in glucose utilization in the macrophage-rich tissues of endotoxin-treated rats may be a reflection of an impaired capacity of these tissues to respond to infection.
Effects of temperature and acid-base state on hippocampal population spikes in hamsters
Authors: Eckerman P. , Scharruhn K. , Horowitz J. M.
Published: December 2017

Previous studies have shown that changes in temperature, within the range encountered by hamsters entering hibernation, alter the evoked response of hippocampal pyramidal cells to stimulation of an afferent pathway. The present study was designed to determine whether these alterations are due to changes in the acid-base status of the neural tissue brought about by changes in temperature. Extracellular-evoked responses were recorded from hamster hippocampal slices after Schaffer collateral stimulation. The pH was changed by varying the concentration of CO2 aerating the bathing medium. Buffers contained either 26 or 40 mM bicarbonate ion. The width of the population spike (the synchronous firing of pyramidal cells) was measured as pH was varied between 7.5 and 7.1, with slice temperature set at either 25 or 20 degrees C. There was a significant increase in spike width as temperature was lowered to 20 degrees C, but no significant change in spike width or amplitude as pH or bicarbonate was varied. The effect of temperature (20 degrees C for half-maximal stimulation, and from 20 to 25 degrees C for just maximal stimulation) on spike width and amplitude thus does not appear to be due to pH- or bicarbonate-induced changes.
Beta 2-adrenergic stimulation does not prevent potassium loss from exercising quadriceps muscle
Authors: Rolett E. L. , Strange S. , Sjogaard G. , Kiens B. , Saltin B.
Published: December 2017

During exercise K+ is released from contracting muscle and plasma K+ concentration rises. Because beta 2-adrenergic agonists stimulate K+ uptake by skeletal muscle in vitro, we tested whether terbutaline, a selective beta 2-agonist, would reduce the loss of K+ from working muscle. Dynamic quadriceps muscle exercise was performed by 12 healthy male volunteers for 50 or 80 min at an average workload of 38 W. A steady K+ loss estimated at 0.16 +/- 0.02 mmol.min-1.kg working muscle-1 and a 0.30 +/- 0.05 mM elevation of arterial plasma K+ concentration were observed. The addition of terbutaline during exercise caused leg blood flow to increase 13% from 5.10 +/- 0.16 to 5.75 +/- 0.13 l/min and arterial K+ concentration to fall monoexponentially by 0.90 +/- 0.05 mM with a rate constant of 0.26 min-1. Terbutaline increased, rather than decreased, the washout of K+ from working quadriceps by 40% to an average value of 0.23 +/- 0.02 mmol.min-1.kg muscle-1. In an additional subject who exercised to exhaustion, terbutaline failed to diminish muscle K+ loss. We conclude that terbutaline does not augment Na(+)-K+ pump activity to a degree sufficient to prevent K+ loss from exercising muscle in humans. On the other hand, the rapid reduction in plasma K+ concentration observed with beta 2-adrenergic stimulation is compatible with an uptake of K+ by nonexercising tissue at an estimated maximal rate of 0.5 micromol.g-1.min-1.