pituitrin and Hypertrophy

Topics: Adenylyl Cyclases; Animals; Chlorpropamide; Crosses, Genetic; Diabetes Insipidus; Disease Models, Animal; Drug Synergism; Genes; Genetic Diseases, Inborn; Humans; Hybridization, Genetic; Hypertrophy; Hypothalamus; Kidney Concentrating Ability; Kidney Diseases; Kidney Medulla; Loop of Henle; Mice; Pituitary Gland; Rats; Vasopressins

The application of an orthostatic stress such as lower body negative pressure (LBNP) has been proposed to minimize the effects of weightlessness on the cardiovascular system and subsequently to reduce the cardiovascular deconditioning. The KAATSU training is a novel method to induce muscle strength and hypertrophy with blood pooling in capacitance vessels by restricting venous return. Here, we studied the hemodynamic, autonomic nervous and hormonal responses to the restriction of femoral blood flow by KAATSU in healthy male subjects, using the ultrasonography and impedance cardiography. The pressurization on both thighs induced pooling of blood into the legs with pressure-dependent reduction of femoral arterial blood flow. The application of 200 mmHg KAATSU significantly decreased left ventricular diastolic dimension (LVDd), cardiac output (CO) and diameter of inferior vena cava (IVC). Similarly, 200 mmHg KAATSU also decreased stroke volume (SV), which was almost equal to the value in standing. Heart rate (HR) and total peripheral resistance (TPR) increased in a similar manner to standing with slight change of mean blood pressure (mBP). High-frequency power (HF(RR)) decreased during both 200 mmHg KAATSU and standing, while low-frequency/high-frequency power (LF(RR)/HF(RR)) increased significantly. During KAATSU and standing, the concentration of noradrenaline (NA) and vasopressin (ADH) and plasma renin activity (PRA) increased. These results indicate that KAATSU in supine subjects reproduces the effects of standing on HR, SV, TPR, etc., thus stimulating an orthostatic stimulus. And, KAATSU training appears to be a useful method for potential countermeasure like LBNP against orthostatic intolerance after spaceflight.

Topics: Adult; Autonomic Nervous System; Cardiac Output; Dizziness; Exercise; Femoral Artery; Humans; Hypertrophy; Lower Body Negative Pressure; Male; Muscle Strength; Muscles; Norepinephrine; Physical Exertion; Posture; Regional Blood Flow; Renin; Vasopressins; Weightlessness Countermeasures

Chronic stimulation (24 h) with vasopressin leads to hypertrophy in H9c2 cardiomyoblasts and this is accompanied by continuous activation of phospholipase C. Consequently, vasopressin stimulation leads to a depletion of phosphatidylinositol levels. The substrate for phospholipase C is phosphatidylinositol (4, 5) bisphosphate (PIP

Topics: Animals; Cell Line; Diacylglycerol Cholinephosphotransferase; Hypertrophy; Myocytes, Cardiac; Phosphatidylinositols; Protein Kinase C; Proto-Oncogene Proteins c-fos; Rats; Type C Phospholipases; Vasopressins

We analyzed the outcome of nocturnal enuresis after adenotonsillectomy in children with sleep disordered breathing. We also evaluated differences in demographic, clinical, laboratory and polysomnography parameters between responders and nonresponders after adenotonsillectomy.. We prospectively evaluated children 5 to 18 years old diagnosed with sleep disordered breathing (snoring or obstructive sleep apnea syndrome) on polysomnography and monosymptomatic primary nocturnal enuresis requiring adenotonsillectomy to release upper airway obstruction. Plasma antidiuretic hormone and brain natriuretic peptide were measured preoperatively and 1 month postoperatively.. Sleep studies were done in 46 children and 32 also underwent blood testing preoperatively and postoperatively. Mean ± SD patient age was 8.79 ± 2.41 years and the mean number of wet nights weekly was 6.39 ± 1.26. Polysomnography revealed obstructive sleep apnea syndrome in 71.7% of patients and snoring in 28.3%. After adenotonsillectomy 43.5% of patients became dry. Preoperative polysomnography findings indicated that responders, who were dry, had significantly more arousals and obstructive apnea episodes but fewer awakenings than nonresponders, who were wet. Significant increases in plasma antidiuretic hormone and significant decreases in plasma brain natriuretic peptide were seen in all children with no difference between responders and nonresponders. No difference between the groups was noted in age, gender, race, body mass index, constipation, preoperative number of wet nights weekly or type of sleep disordered breathing.. Nocturnal enuresis resolved after adenotonsillectomy in almost half of the children with sleep disordered breathing. Those who became dry had more frequent arousal episodes caused by apnea events than those who remained wet.

Topics: Adolescent; Child; Child, Preschool; Comorbidity; Female; Humans; Hypertrophy; Male; Natriuretic Peptide, Brain; Nocturnal Enuresis; Palatine Tonsil; Polysomnography; Prospective Studies; Sleep Apnea, Obstructive; Snoring; Tonsillectomy; Vasopressins

Mesangial cell growth is a key feature of several glomerular diseases. Vascular endothelial growth factor (VEGF) is a potent mitogen of vascular endothelial cells and promoter of vascular permeability. Here, we examined the ability of vasopressin (AVP), which causes mesangial cell proliferation and hypertrophy, to stimulate VEGF secretion from cultured rat mesangial cells. AVP potently induced a time- and concentration-dependent increase in VEGF secretion in these cells, which was then inhibited by a V(1A) receptor-selective antagonist, confirming this is a V(1A) receptor-mediated event. VEGF also induced hyperplasia and hypertrophy in mesangial cells, which was completely abolished by an anti-VEGF antibody. In addition, AVP-induced hyperplasia and hypertrophy were completely inhibited by the V(1A) receptor-selective antagonist and partially abolished by the anti-VEGF antibody. These results indicate that AVP increases VEGF secretion in rat mesangial cells via V(1A) receptors and modulates mesangial cell growth not only by direct action but also through stimulation of VEGF secretion. This autocrine mechanism might contribute to glomerulosclerosis in renal diseases such as diabetic nephropathy.

Topics: Animals; Antibodies; Antidiuretic Hormone Receptor Antagonists; Autocrine Communication; Benzazepines; Cell Proliferation; Cells, Cultured; Collagen Type IV; Hyperplasia; Hypertrophy; Male; Mesangial Cells; Piperidines; Rats; Rats, Wistar; Receptors, Vasopressin; Vascular Endothelial Growth Factor A; Vasopressins

We compared the renal responses of rats on three diet regimens. Rats received either 8% protein food (low-protein, LP) for 10 weeks following weaning, 8% protein for 9 weeks followed by 1 week on 30% protein (short-term high-protein, SHP), or 30% protein for 10 weeks (high-protein, HP). Kidneys from HP rats were enlarged by approximately 50%, or 20% when corrected for body mass. Most of this hypertrophy resulted from enlargement of the inner stripe of the outer medulla, site of the thick ascending limbs (TAL), and TAL from HP rats were larger in diameter. SHP rats had TAL diameters similar to HP rats, but changes in renal mass or height of renal zones did not reach statistical significance. The activity of adenylyl cyclase (AC) in TAL, measured from the accumulation of cAMP in isolated tubules, increased with dose of both arginine vasopressin (AVP) and glucagon in all rats. However, HP rats had significantly higher hormone-induced AC activity than LP or SHP rats, which were not different from each other. Our results suggest that tubule hypertrophy may precede up-regulation of hormone-sensitive AC activity during the progression of renal response to elevated dietary protein.

Topics: Adenylyl Cyclases; Animals; Dietary Proteins; Glucagon; Hypertrophy; Kidney Medulla; Kidney Tubules, Distal; Rats; Rats, Sprague-Dawley; Time Factors; Vasopressins

Protein synthesis in H9c2 heart-derived myocytes responds biphasically to arginine vasopressin (1 microM). An initial 50% inhibition attributable to Ca(2+) mobilization from the sarcoplasmic/endoplasmic reticulum is followed by a recovery that subsequently converts to a 1.5-fold stimulation. This study was undertaken to ascertain whether vasopressin programs H9c2 cells to undergo hypertrophy or to proliferate and whether early translational inhibition is required for programming. Translational suppression was observed only at vasopressin concentrations (>1 nM) causing extensive (>50%) depletion of Ca(2+) stores and was diminished at supraphysiologic extracellular Ca(2+) concentrations. Stimulation of protein synthesis, by contrast, was unaffected by changes in extracellular Ca(2+), depended on gene transcription, was suppressed by a protein kinase C pseudosubstrate sequence (peptide 19-27), and was observed at pM vasopressin concentrations. Activation of MAP kinases, phosphoinositide 3-kinase, calcineurin, S6 kinase, or eIF4 could not be implicated in the stimulation, which persisted for 24 h. Vasopressin-treated H9c2 cells underwent hypertrophy by standard criteria. Cellular protein accumulation occurred at pM hormone concentrations, was blocked by peptide 19-27, was observed regardless of retinoic acid pretreatment to prevent myogenic transdifferentiation, and preceded full repletion of Ca(2+) stores. It is proposed that H9c2 cells, which possess all basic features of V1-vasopressin receptor signaling, provide a convenient model for investigating vasopressin-induced myocyte hypertrophy. Early translational suppression is not needed for vasopressin-induced H9c2 myocyte hypertrophy whereas activation of protein kinase C appears essential.

Topics: Animals; Calcium; Cell Membrane Permeability; Cell Size; Clone Cells; Hypertrophy; Myocardium; Protein Biosynthesis; Protein Kinase C; Proteins; Rats; Substrate Specificity; Vasopressins

Little is known regarding the effect of chronic changes in neuronal activity on the extent of collateral sprouting by identified CNS neurons. We have investigated the relationship between activity and sprouting in oxytocin (OT) and vasopressin (VP) neurons of the hypothalamic magnocellular neurosecretory system (MNS). Uninjured MNS neurons undergo a robust collateral-sprouting response that restores the axon population of the neural lobe (NL) after a lesion of the contralateral MNS (). Simultaneously, lesioned rats develop chronic urinary hyperosmolality indicative of heightened neurosecretory activity. We therefore tested the hypothesis that sprouting MNS neurons are hyperactive by measuring changes in cell and nuclear diameters, OT and VP mRNA pools, and axonal cytochrome oxidase activity (COX). Each of these measures was significantly elevated during the period of most rapid axonal growth between 1 and 4 weeks after the lesion, confirming that both OT and VP neurons are hyperactive while undergoing collateral sprouting. In a second study the hypothesis that chronic inhibition of neuronal activity would interfere with the sprouting response was tested. Chronic hyponatremia (CH) was induced 3 d before the hypothalamic lesion and sustained for 4 weeks to suppress neurosecretory activity. CH abolished the lesion-induced increases in OT and VP mRNA pools and virtually eliminated measurable COX activity in MNS terminals. Counts of the total number of axon profiles in the NL revealed that CH also prevented axonal sprouting from occurring. These results are consistent with the hypothesis that increased neuronal activity is required for denervation-induced collateral sprouting to occur in the MNS.

Topics: Animals; Axons; Axotomy; Central Nervous System; Electron Transport Complex IV; Functional Laterality; Histocytochemistry; Hypertrophy; Hyponatremia; Hypothalamo-Hypophyseal System; In Situ Hybridization; Male; Microscopy, Electron; Nerve Regeneration; Neurons; Oxytocin; Paraventricular Hypothalamic Nucleus; Peptides; Pituitary Gland; Rats; Rats, Sprague-Dawley; RNA, Messenger; Supraoptic Nucleus; Time Factors; Vasopressins

Diabetic nephropathy represents a major complication of diabetes mellitus (DM), and the origin of this complication is poorly understood. Vasopressin (VP), which is elevated in type I and type II DM, has been shown to increase glomerular filtration rate in normal rats and to contribute to progression of chronic renal failure in 5/6 nephrectomized rats. The present study was thus designed to evaluate whether VP contributes to the renal disorders of DM. Renal function was compared in Brattleboro rats with diabetes insipidus (DI) lacking VP and in normal Long-Evans (LE) rats, with or without streptozotocin-induced DM. Blood and urine were collected after 2 and 4 weeks of DM, and creatinine clearance, urinary glucose and albumin excretion, and kidney weight were measured. Plasma glucose increased 3-fold in DM rats of both strains, but glucose excretion was approximately 40% lower in DI-DM than in LE-DM, suggesting less intense metabolic disorders. Creatinine clearance increased significantly in LE-DM (P < 0.01) but failed to increase in DI-DM. Urinary albumin excretion more than doubled in LE-DM but rose by only 34% in DI-DM rats (P < 0.05). Kidney hypertrophy was also less intense in DI-DM than in LE-DM (P < 0.001). These results suggest that VP plays a critical role in diabetic hyperfiltration and albuminuria induced by DM. This hormone thus seems to be an additional risk factor for diabetic nephropathy and, thus, a potential target for prevention and/or therapeutic intervention.

Topics: Albuminuria; Animals; Creatinine; Diabetes Insipidus; Diabetes Mellitus, Experimental; Diabetic Nephropathies; Glomerular Filtration Rate; Glycosuria; Hypertrophy; Kidney; Kidney Failure, Chronic; Male; Nephrectomy; Organ Size; Rats; Rats, Brattleboro; Rats, Long-Evans; Vasopressins

We investigated the effects of YM087, a potent nonpeptide V1A and V2 vasopressin (AVP)-receptor antagonist, in binding and functional studies on rat vascular smooth-muscle cells (VSMCs). V1A AVP receptors on VSMCs were characterized by using the radioligand [3H]AVP. Specific binding of [3H]AVP was time dependent, reversible, and saturable. A single class of high-affinity binding sites with the expected V1A profile was identified. YM087 showed high affinity for V1A receptors with an inhibitory dissociation constant (Ki) value of 0.24 nM. In addition, YM087 potently and concentration-dependently inhibited AVP-induced increase in intracellular free calcium concentration and activation of mitogen-activated protein kinase. When added to growth-arrested VSMCs, AVP concentration-dependently induced hyperplasia and hypertrophy. YM087 prevented AVP-induced hyperplasia and hypertrophy of these cells in a concentration-dependent manner. YM087 had no agonistic activity in any biological assays used. These results suggest that YM087 displays high affinity for V1A receptors on VSMCs and high potency in inhibiting the AVP-induced physiological response. YM087 is a potent pharmacologic probe for investigating the physiologic and pathophysiologic roles of AVP in several diseases.

Topics: Animals; Benzazepines; Binding, Competitive; Calcium; Calcium-Calmodulin-Dependent Protein Kinases; Cell Culture Techniques; DNA; Enzyme Activation; Hyperplasia; Hypertrophy; Muscle, Smooth, Vascular; Protein Biosynthesis; Rats; Receptors, Vasopressin; Vasopressins

In previous studies we found that vasopressin stimulation of both cyclic AMP (cAMP) formation in cortical collecting tubules (CCT) and sodium reabsorption in isolated perfused kidneys was markedly exaggerated in rats with mineralocorticoid hypertension. In the present study, we tested the response (cAMP accumulation) of cortical and outer medullary collecting tubules (OMCT) to vasopressin in two rat models that are resistant to deoxycorticosterone acetate (DOCA)-induced hypertension, the Wistar-Furth strain and NaCl-deficient rats. The blood pressure of normal outbred Wistar rats rose to hypertensive levels (systolic pressure more than 165 mm Hg) during a 5-week treatment with DOCA (10 mg/week) and 1% saline to drink. Significant hypertrophy of the heart and kidneys was also observed. Vasopressin (10(-8) M)-induced cAMP formation was enhanced 3.4-fold in the CCT (OMCT unchanged) of hypertensive rats compared with normotensive controls. Significant hypertrophy (as indexed by tubule diameter) of the CCT but not the OMCT was also observed in DOCA-salt hypertensive rats. Restriction of dietary NaCl (0.13% in chow, tap water to drink) completely prevented DOCA-induced hypertension, organ and CCT hypertrophy, and enhancement of vasopressin-stimulated cAMP formation in the CCT. In Wistar-Furth rats, DOCA-salt treatment did not alter blood pressure or cause significant organ hypertrophy. However, DOCA-salt treatment enhanced vasopressin-stimulated cAMP formation by 4.1-fold in CCT of Wistar-Furth rats, with significant tubular hypertrophy in the CCT but not the OMCT. We conclude that DOCA-induced hypertension and changes in CCT function are dependent on excess dietary NaCl.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Blood Pressure; Cyclic AMP; Desoxycorticosterone; Hypertension; Hypertrophy; Kidney Tubules, Collecting; Male; Rats; Rats, Inbred WF; Sodium, Dietary; Vasopressins

Recent experiments have shown that the kidney adapts to chronic variations in urine concentration. Glomerular filtration rate (GFR), kidney weight relative to body weight, thickness of inner stripe of the outer medulla, volume of epithelium in early thick ascending limb, and internephron heterogeneity are all decreased by chronic water diuresis and increased by chronic stimulation of urine concentration. It was further shown that the intrarenal pattern of hypertrophy observed after high protein (HP) intake, but not that observed after compensatory hypertrophy or normal growth with age, is exactly similar to that observed after chronic stimulation of urine concentration. Since solute-free water reabsorption (TcH2O) is markedly enhanced by HP diet, this suggests that the increases in GFR and renal mass observed after HP intake are, at least in part, an adaptive response of the kidney to increased urinary concentrating activity. The beneficial effects are induced by protein restriction in chronic renal failure (CRF) could thus be due, in part, to the reduction of this concentrating activity. This hypothesis was confirmed by an experiment performed in rats with experimental chronic renal failure (CRF) in which a chronic increase in water intake, reducing urine osmolality and TcH2O, without any change in food composition or consumption, reduced proteinuria, systemic hypertension, kidney hypertrophy, incidence of glomerulosclerosis, and mortality.

Topics: Adaptation, Physiological; Animals; Dietary Proteins; Glomerular Filtration Rate; Hypertrophy; Kidney; Kidney Concentrating Ability; Kidney Failure, Chronic; Organ Size; Rats; Rats, Brattleboro; Vasopressins

In this investigation we have observed the effects of withholding water for 5 days, the effects of long-term (5 weeks) lesions of the tissue surrounding the preoptic recess in the anteroventral third ventricle (AV3V region), and the interaction of the effects of long-term AV3V lesions and water deprivation on paraventricular nuclei. The purpose of these observations was to see if recovery of the antidiuretic response after AV3V lesions is associated with recovery of fine structural responses in these neurosecretory cells. Paraventricular neurosecretory cells of rats deprived of water for 5 days were hypertrophied in controls and in rats with AV3V lesions. Areas of cell bodies and their nuclei were increased, as were the number of Golgi stacks and electron dense (immature) neurosecretory granules. A greater percentage of nucleoli were adjacent to the nuclear envelope. Paraventricular neurons of rats with AV3V lesions also had fine structural changes characteristic of increased secretory activity, even in animals with free access to drinking water. The areas of cells and their nucleoli in coronal sections, and the number of Golgi stacks and electron-dense neurosecretory granules per cell were significantly increased in both treatment groups with AV3V lesions. There was a greater increase in the numbers of Golgi stacks and immature neurosecretory granules tended to be more numerous in water-deprived lesioned rats than in water-deprived controls. We suggest that recovery of body fluid balance in rats with chronic AV3V lesions involves enhanced secretory activity of neurosecretory cells in paraventricular nuclei, possibly stimulated via undamaged descending connections from the subfornical organ and by ascending pathways activated by cardiovascular volume receptors.

Topics: Adaptation, Physiological; Animals; Hypertrophy; Microscopy, Electron; Neuronal Plasticity; Paraventricular Hypothalamic Nucleus; Pituitary Gland, Posterior; Preoptic Area; Rats; Rats, Inbred Strains; Vasopressins; Water Deprivation; Water-Electrolyte Balance

To determine if unilateral hypothalamic lesions block adrenal compensatory hypertrophy (ACH), such lesions were produced unilaterally under stereotaxic guidance using direct cathodal current in rats just after the left adrenal gland was removed. The animals were sacrificed one week later and the degree of the ACH of the remaining adrenal gland was determined. Animals without lesions uniformly showed ACH in terms of an absolute increase in adrenal weight of the remaining gland as compared to the one excised or if calculated as mg adrenal weight/100 g body weight. On the other hand, lesions in the region lateral to the paraventricular nucleus, lateral to the median eminence or in the region between these two loci prevented ACH in roughly 50% of the animals whether the lesion was placed on the same or opposite side of the hypothalamus. Some lesions in the mid-line in the vicinity of the paraventricular nucleus also resulted in blockade of ACH. We speculate that the blockade is due to a partial elimination of CRF and/or vasopressin/oxytocinergic pathways which are activated by the fall in plasma corticosterone after removal of an adrenal gland.

Topics: Adaptation, Physiological; Adrenal Glands; Adrenalectomy; Adrenocorticotropic Hormone; Animals; Brain Mapping; Hypertrophy; Hypothalamo-Hypophyseal System; Hypothalamus; Rats; Rats, Inbred Strains; Vasopressins

Topics: Adrenal Cortex; Aldosterone; Animals; Arginine Vasopressin; Cytoplasmic Granules; Diabetes Insipidus; Diet, Sodium-Restricted; Hypertrophy; Juxtaglomerular Apparatus; Male; Microscopy, Electron; Rats; Rats, Brattleboro; Rats, Mutant Strains; Renin; Vasopressins

Topics: Aldosterone; Alkalosis; Angiotensin II; Biopsy; Blood Pressure; Child, Preschool; Diet Therapy; Female; Follow-Up Studies; Growth Disorders; Humans; Hyperaldosteronism; Hyperplasia; Hypertrophy; Hypokalemia; Juxtaglomerular Apparatus; Kidney Concentrating Ability; Kidney Diseases; Norepinephrine; Potassium; Renin; Secretory Rate; Sodium Chloride; Spironolactone; Syndrome; Vasopressins

Topics: Animals; Cerebral Ventricles; Fluorescent Antibody Technique; Hypertrophy; Hypothalamo-Hypophyseal System; Neural Pathways; Neurons; Neurophysins; Neurosecretion; Scrapie; Sheep; Sheep Diseases; Vasopressins

Topics: Animals; Axons; Basement Membrane; Capillaries; Hypertrophy; Hypophysectomy; Hypothalamo-Hypophyseal System; Intercellular Junctions; Microscopy, Electron; Nerve Regeneration; Neurosecretory Systems; Oxytocin; Pituitary Gland, Posterior; Rats; Synaptic Vesicles; Vasopressins

Topics: Adolescent; Diabetes Insipidus; Diuretics; Female; Humans; Hydrochlorothiazide; Hydronephrosis; Hypertrophy; Infant; Kidney Diseases; Male; Postoperative Complications; Sodium; Ureteral Obstruction; Ureterocele; Urinary Bladder Diseases; Urography; Vasopressins; Water

Topics: Animals; Castration; Disease Models, Animal; Drug Antagonism; Female; Follicle Stimulating Hormone; Gonadotropins, Pituitary; Hypertrophy; Indoles; Melatonin; Mice; Ovarian Diseases; Ovulation; Oxytocin; Physiology, Comparative; Pineal Gland; Rodentia; Serotonin; Tissue Extracts; Vasopressins

Topics: Adrenal Glands; Adrenalectomy; Adrenocorticotropic Hormone; Animals; Corticotropin-Releasing Hormone; Dehydration; Diabetes Insipidus; Female; Formaldehyde; Hypertrophy; Hypothalamo-Hypophyseal System; Hypothalamus; Karyometry; Kidney Diseases; Male; Melanocyte-Stimulating Hormones; Mice; Neurosecretion; Organ Size; Pituitary Gland; Pituitary-Adrenal System; Stress, Physiological; Vasopressins

Topics: Animals; Blood; Cell Nucleolus; Diabetes Insipidus; Hypertrophy; Hypothalamo-Hypophyseal System; Hypothalamus; Kidney Concentrating Ability; Kidney Tubules; Mice; Neurosecretion; Osmolar Concentration; Rodent Diseases; Urine; Vasopressins

Topics: Adrenocortical Hyperfunction; Animals; Body Weight; Diabetes Insipidus; Diuresis; Genes, Dominant; Genes, Lethal; Glomerular Filtration Rate; Hypertrophy; Kidney Concentrating Ability; Kidney Glomerulus; Kidney Tubules; Mice; Organ Size; Syndactyly; Vasopressins

Topics: Animals; Arteries; Cytoplasmic Granules; Hyperplasia; Hypertrophy; Juxtaglomerular Apparatus; Male; Rats; Vasopressins

Topics: Adrenal Glands; Adrenocorticotropic Hormone; Castration; Chorionic Gonadotropin; Dinitrophenols; DNA; Estrogens, Conjugated (USP); Female; Gonadotropins; Growth Hormone; Humans; Hypertrophy; Metabolism; Mitochondria; Ovary; Parathyroid Hormone; Pharmacology; Rats; Research; RNA; RNA, Mitochondrial; Thyrotropin; Triiodothyronine; Vasopressins

Topics: Adrenal Cortex Hormones; Adrenal Gland Diseases; Adrenal Glands; Adrenocorticotropic Hormone; Animals; Atrophy; Hypertrophy; Hypophysectomy; Kidney; Liver; Pituitary-Adrenal Function Tests; Postoperative Complications; Rats; Stomach; Thymus Gland; Vasopressins

Topics: Arginine Vasopressin; Deamino Arginine Vasopressin; Humans; Hypertrophy; Kidney Function Tests; Male; Prostatic Hyperplasia; Vasopressins