[Water-saline balance in essential obesity].
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The experiments reported here attempted to examine in two groups of rats the effects on the taste preferences, food and fluid intake, energy balance and body weight gain of corticocerebellar lesions involving, primarily, the Lobulus VI (LVI) or the Lobulus Paramedianus (LP). The results showed that the lesions of LVI or LP did not affect the daily intake of total fluid and salty solution. The intake of sweet solution increased in both groups of lesioned rats, while the intake of deionized water and acid and bitter solutions decreased only in the LVI lesioned rats. Food intake decreased in the LVI-lesioned rats but not in the LP-lesioned animals. Body weight gain, efficiency of food utilization, caloric intake and body surface gain decreased in both groups. It seems therefore that the cerebellar cortex, which probably receives taste fibers, somehow influences taste preferences and water intake, and that it may be involved in the mechanisms of food intake, its utilization and body energy balance.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Hydroxyapatite (HA) coatings plasma sprayed without and with bond coats (titania, zirconia) onto titanium alloy (Ti6A14V) substrates under both atmospheric and low pressure plasma spray conditions were investigated in terms of their microstructure and their resorption resistance during immersion in simulated body fluid (Hank's balanced salt solution). The microstructures of test samples were characterized using SEM on as-sprayed and leached surfaces and on the corresponding cross sections. Selected coating systems were studied by 2-dimensional secondary ion mass spectroscopy imaging to obtain information on plasma spray induced diffusional processes at the coating interfaces, as well as the spatial distribution of minor and trace elements. Coatings consisting of thin (10-15 microm) titania/zirconia (eutectic ratio) and titania bond coats, combined with a 150- to 180-microm thick HA top coat, yielded peel strengths in excess of 32 N/m, as well as sufficient resorption resistance.
Hyponatremia is common following subarachnoid hemorrhage and has alternatively been attributed to either the inappropriate secretion of antidiuretic hormone or natriuresis causing intravascular volume contraction. We prospectively studied body sodium and intravascular volume regulation in 19 patients, beginning within 3 days after acute aneurysmal subarachnoid hemorrhage occurred, in order to determine the impact of hypervolemic therapy on both hyponatremia and volume contraction and to ascertain whether humoral factors account for hyponatremia. Serial measurements of plasma arginine vasopressin, atrial natriuretic factor, renin activity, aldosterone, and catecholamines were correlated with body sodium and fluid balance, change in blood volume, serum sodium concentration, and osmolality. Six patients (32%) developed hyponatremia, but only 2 had a negative sodium balance. In most patients, levels of atrial natriuretic factor were elevated, while plasma renin activity and aldosterone concentrations were generally suppressed. Plasma arginine vasopressin levels were not suppressed during hypo-osmolality and did not correlate with serum osmolality in hyponatremic patients. Only 1 patient had a decrease in blood volume, which was associated with marked rises in aldosterone and plasma renin activity, but normal serum sodium and plasma atrial natriuretic factor levels. We conclude that following subarachnoid hemorrhage: (1) Hypervolemic therapy prevents volume contraction but not hyponatremia, (2) humoral factors may favor both sodium loss and water retention, and (3) arginine vasopressin regulation is disturbed and may contribute to hyponatremia.
Atrial natriuretic factor or peptide (ANP) is a peptide recently isolated from mammalian atria with potent natriuretic, vasorelaxant, and aldosterone-inhibitory properties. ANP may play an important role in the regulation of blood pressure and body salt and fluid balance. The presence of binding sites for ANP in the vasculature and adrenal glomerulosa of rats and in platelets in humans has been demonstrated. These sites are involved in the mediation of the vasorelaxant effect of ANP and its inhibitory action on aldosterone secretion. The role of binding sites on platelets is unknown, but the availability of platelets makes them a useful model for investigating the regulation of receptors for atrial natriuretic factor in humans. The effect of sodium depletion and loading and mineralocorticoids on the density of rat vascular and adrenal sites for ANP was examined, as well as changes that occur after development of renovascular and DOCA-salt hypertension in rats. Sodium loading in the presence of reduced renal mass (unilateral nephrectomy) or mineralocorticoid administration produced renin suppression and resulted in down-regulation of vascular ANP receptors. In one-kidney, one-clip Goldblatt hypertensive rats and in DOCA-salt hypertensive rats, two models of volume-expanded, non-renin-dependent experimental hypertension, the density of ANP binding sites in the mesenteric arterioles was significantly decreased. The sensitivity to ANP of precontracted aorta from renovascular and mineralocorticoid hypertensive rats was significantly reduced. No consistent changes occurred in the density of ANP binding sites in the adrenal glomerulosa.(ABSTRACT TRUNCATED AT 250 WORDS)
The present study is an attempt to demonstrate chemosensitive neurons within the area postrema (AP) electrophysiologically. Three types of chemosensitive neurons were identified: 1) glucose-responsive neurons that may participate in control of blood glucose and satiation, 2) sodium (osmotic pressure)-responsive neurons that may contribute to control of sodium and water balance of the body fluid and may be involved in salt appetite, 3) nausea-related neurons which respond to excess distension of stomach and LiCl as well. They may play a role in formation of conditioned taste aversion.
Brushite (dicalcium phosphate dihydrate, DCPD, CaHPO4 x 2H2O) was deposited electrolytically from calcium dihydrogen phosphate solution with and without potassium chloride (KCl) as a supporting electrolyte. The kinetics of brushite transformation to hydroxyapatite (HA, Ca5(PO4)3OH) in the presence of calcium and protein free, aqueous body fluid (Hank's balanced salt solution, HBSS) was investigated. We present evidence that the deposition of brushite in a KCl-supported electrochemical bath yields a modified brushite where some of the calcium is substituted by potassium. Transformation of both normal (i.e. potassium free) and modified brushite to hydroxyapatite upon exposure to calcium and protein-free aqueous fluid (HBSS) was followed by reflectance Fourier Transform Infrared (FTIR) spectroscopy and X-ray diffraction (XRD) techniques. Changes in the morphology of the coatings were studied using scanning electron microscopy (SEM). Results indicate that modified brushite undergoes faster transformation to hydroxyapatite in HBSS in comparison to normal brushite. Our results show that the presence of potassium ions in the brushite not only favors the formation of different intermediate phases but also alters transformation rates to HA.
The capability for a dialysis machine to use a measurement of the patient's status to automatically tune the dialysis session on-line is commonly addressed by physicians and bioengineers working in the hemodialysis field as "biofeedback." This paper presents the basics of mathematical modeling and control theory normally used in bioengineering, together with some advanced techniques, such as adaptive and multi-input/multi-output control systems. The architectural requirements for implementing biofeedback techniques in renal replacement therapy are then discussed, with due attention paid to the safety aspects, which play a central role in machines hosting such new techniques as well as their therapeutic mission. Finally, the blood volume tracking system, which is aimed at performing the intradialytic water removal, while maintaining a balance inside the body fluids compartments and thus preserving cardiovascular stability, is used as a paradigmatic example of such a class of advanced techniques. The significant results shown by the blood-volume-controlled treatments during a multicenter study focused on its clinical application (30% reduction of intradialysis collapses, 13% reduction of interdialysis symptoms) indicate the technical feasibility and the remarkable benefits of such systems, which get closer to a structurally complete artificial kidney.
Angiotensinogen, the precursor molecule for angiotensins I, II and III, and the enzymes renin, angiotensin-converting enzyme (ACE), and aminopeptidases A and N may all be synthesised within the brain. Angiotensin (Ang) AT(1), AT(2) and AT(4) receptors are also plentiful in the brain. AT(1) receptors are found in several brain regions, such as the hypothalamic paraventricular and supraoptic nuclei, the lamina terminalis, lateral parabrachial nucleus, ventrolateral medulla and nucleus of the solitary tract (NTS), which are known to have roles in the regulation of the cardiovascular system and/or body fluid and electrolyte balance. Immunohistochemical and neuropharmacological studies suggest that angiotensinergic neural pathways utilise Ang II and/or Ang III as a neurotransmitter or neuromodulator in the aforementioned brain regions. Angiotensinogen is synthesised predominantly in astrocytes, but the processes by which Ang II is generated or incorporated in neurons for utilisation as a neurotransmitter is unknown. Centrally administered AT(1) receptor antagonists or angiotensinogen antisense oligonucleotides inhibit sympathetic activity and reduce arterial blood pressure in certain physiological or pathophysiological conditions, as well as disrupting water drinking and sodium appetite, vasopressin secretion, sodium excretion, renin release and thermoregulation. The AT(4) receptor is identical to insulin-regulated aminopeptidase (IRAP) and plays a role in memory mechanisms. In conclusion, angiotensinergic neural pathways and angiotensin peptides are important in neural function and may have important homeostatic roles, particularly related to cardiovascular function, osmoregulation and thermoregulation.
The influence of aging on the renin-angiotensin-aldosterone system was evaluated by comparing young (20 to 30 yr) with elderly (62 to 70 yr) healthy subjects. Despite comparable body sodium-fluid balance in the two age groups, serum renin concentration, plasma renin activity and aldosterone concentrations were lower in the elderly. The age-related decreases in circulating renin and aldosterone concentrations were slight while subjects were supine and receiving normal sodium intake; when upright and during sodium depletion, they were more pronounced. Inverse renin-blood pressure interrelations were noted during two of four study conditions involving normal sodium intake or mild sodium depletion (r = --0.44 and --0.47, respectively), but not during progressive sodium depletion. Plasma renin levels were decreased in the elderly regardless of the presence or absence of an inverse relationship with blood pressure. Aldosterone and cortisol responses to corticotropin infusion were unaltered in the elderly. It is concluded that aging may cause a decrease in circulating renin, with parallel lowering of plasma aldosterone concentrations.
1. The renal medulla plays an important role in regulating body sodium and fluid balance and blood pressure homeostasis through its unique structural relationships and interactions between renomedullary interstitial cells (RMIC), renal tubules and medullary vasculature. 2. Several endocrine and/or paracrine factors, including angiotensin (Ang)II, endothelin (ET), bradykinin (BK), atrial natriuretic peptide (ANP) and vasopressin (AVP), are implicated in the regulation of renal medullary function and blood pressure by acting on RMIC, tubules and medullary blood vessels. 3. Renomedullary interstitial cells express multiple vasoactive peptide receptors (AT1, ETA, ETB, BK B2, NPRA and NPRB and V1a) in culture and in tissue. 4. In cultured RMIC, AngII, ET, BK, ANP and AVP act on their respective receptors to induce various cellular responses, including contraction, prostaglandin synthesis, cell proliferation and/or extracellular matrix synthesis. 5. Infusion of vasoactive peptides or their antagonists systemically or directly into the medullary interstitium modulates medullary blood flow, sodium excretion and urine osmolarity. 6. Overall, expression of multiple vasoactive peptide receptors in RMIC, which respond to various vasoactive peptides and paracrine factors in vitro and in vivo, supports the hypothesis that RMIC may be an important paracrine target of various vasoactive peptides in the regulation of renal medullary function and long-term blood pressure homeostasis.
Sodium chloride ingestion is stimulated during conditions of sodium deficiency to maintain body fluid and electrolyte balance. Recent studies have indicated that salt appetite in rats is often inversely related to peripheral and central secretion of the hormone oxytocin (OT). We studied the potential role of central OT on salt and water ingestion by treating rats intracerebroventricularly with OT conjugated to the A chain of the plant cytotoxin ricin (rAOT) to produce a chronic selective inactivation of brain cells containing OT-receptive elements. The rats treated with rAOT and control rats treated with the ricin A chain alone were given 5-hr two-bottle (water and 0.5 M NaCl) drinking tests 30 min after they were made hyperosmolar by injections of hypertonic (2M) mannitol solution, which elevated plasma osmolality but reduced plasma Na+ concentration. In the control rats only water intake was stimulated in response to the induced hyperosmolality, but in the rAOT-treated rats hypertonic mannitol caused a robust salt appetite as well as thirst. Analogous results were obtained in rats treated with two different OT-receptor antagonists prior to induction of hyperosmolality with mannitol. In contrast to these results, when hyperosmolality was induced by administration of equivalently hypertonic (1M) NaCl, which elevated both plasma osmolality and plasma Na+ concentration, only water intake but not salt intake was stimulated in both control and OT-receptor antagonist-treated rats. When salt appetite was stimulated by the physiological stimulus of polyethylene glycol-induced hypovolemia, hypertonic mannitol similarly inhibited salt ingestion in control animals but not in rAOT-treated rats, whereas hypertonic NaCl inhibited subsequent salt ingestion in both groups. These results suggest that salt appetite is regulated by both Na(+)- and osmolality-sensing mechanisms in rats. In addition, they indicate that central OT likely mediates a significant component of osmolality-related inhibition of salt appetite but does not appear to be essential for Na(+)-related inhibition of this important homeostatic behavior.
BACKGROUND: The renin-angiotensin system (RAS) functions as both a circulating endocrine system and a tissue paracrine/autocrine system. As a circulating peptide, angiotensin II (Ang II) plays a prominent role in blood-pressure control and body fluid and electrolyte balance by acting on the AT1 receptor in the brain and peripheral tissues. As a paracrine/autocrine peptide, locally formed Ang II also plays additional roles in tissues involving the regulation of regional haemodynamics, cell growth and remodelling, and neurotransmitter release. Evidence is emerging that Ang II is not the only active peptide of the RAS, and other Ang II fragments may also have important biological activities. OBJECTIVES: To provide a morphological basis for understanding novel actions of angiotensin-converting enzyme (ACE), Ang II and related peptides in tissues, this article will review the localization of ACE and AT1, AT2 and AT4 receptors in the central nervous system, blood vessels and kidney. RESULTS AND CONCLUSION: Autoradiographic mapping of the major components of the RAS has proved a valuable strategy to reveal, or suggest, cellular sites of novel actions for Ang II and related peptides in tissues. First, colocalization of ACE and AT1 receptors in the substantia nigra, the caudate nucleus and putamen of human and rat brain, which contain the dopamine-synthesizing neurons, suggests that the central RAS may be important in modulating central dopamine release. Secondly, the distribution of AT4 receptors with a striking association with cholinergic neurons, motor and sensory nuclei in the brain reveals that Ang IV may modulate central motor and sensory activities and memory. Thirdly, the occurrence of high levels of ACE and AT1 and/or AT2 receptors in the adventitia of blood vessels suggests important paracrine roles of the vascular RAS. Finally, the identification of abundant AT1 receptor and elucidation of its roles in the renomedullary interstitial cells of the kidney may provide a new impetus to study further the role of Ang II in the regulation of renal medullary function and blood pressure. Overall, circulating and locally produced Ang II and related peptides may exert a remarkable range of actions in the brain, kidney and cardiovascular system through multiple angiotensin receptors.
This double-blind, placebo-controlled human study was performed to determine the endocrine responses to intravenously administered indomethacin at two dose rates (0.36 or 0.72 mg/kg bolus followed by 0.071 or 0.143 mg/kg/hr for 150 min.). A 5% hypertonic saline infusion was used for further assess the hormonal systems regulating body fluid and electrolyte balance. Plasma renin activity (PRA) and concentrations of aldosterone and vasopressin (AVP) were unaffected by indomethacin. Hypertonic saline caused a 5% increase in plasma sodium and a 4.2% increase in serum osmolality, with a concomitant two-fold rise in plasma AVP levels and significant declines in PRA and aldosterone. Indomethacin had no effects on these responses, and did not affect plasma catecholamine concentrations, but the hypertonic saline infusion doubled the noradrenaline levels in plasma. Atrial natriuretic peptide (ANP)-like immunoreactivity in plasma was not affected by indomethacin nor by hypertonic saline. The higher dose rate of indomethacin resulted in significant stimulation of growth hormone release, but plasma prolactin levels were not influenced. Thus acute intravenous administration of indomethacin proved to be devoid of significant effects on the multihormonal system regulating fluid and electrolyte balance.