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In the third section of this chapter purchase lisinopril 17.5 mg with mastercard arteria epigastrica superficial, the pathogenesis purchase lisinopril 17.5 mg overnight delivery blood pressure medication omeprazole, causes 17.5 mg lisinopril for sale heart attack troublemaker, and clinical settings for hyperna- tremia and management strategies are described discount 17.5 mg lisinopril free shipping blood pressure 3 readings. In m ost steady-state situations, hum an water intake m atches water losses through all sources. W ater intake is determ ined by thirst (see Normal water intake (1. W ater intake is finely balanced by the need to m aintain physiologic serum osm o- lality between 285 to 290 m O sm /kg. Both water that is drunk and that is generated W ater of cellular through m etabolism are distributed in the metabolism extracellular and intracellular com part- (350–500 mL/d) m ents that are in constant equilibrium. Intracellular Extracellular Total body water Total body water equals approxim ately compartment compartment 42L (27 L) (15 L) (60% body weight 60% of total body weight in young m en, in a 70-kg man) about 50% in young wom en, and less in older persons. In a 70-kg m an, in tem perate conditions, total body water equals 42 L, 65% of which (22 L) is in the intracellular com partm ent and 35% (19 L) Fixed water excretion Variable water excretion in the extracellular com partm ent. Assum ing norm al glom erular filtration rate to be about 125 m L/m in, the total volum e of blood filtered by the kidney is Filtrate/d about 180 L/24 hr. H um an kidneys have two popula- tions of nephrons, superficial and juxtam edullary. This anatom ic arrangem ent has im por- tant bearing on the form ation of urine by the countercurrent m echanism. After two thirds of the filtered load (180 L/d) is isotoni- cally reabsorbed in the proxim al convoluted tubule, water is handled by three interrelated processes: 1) the delivery of fluid to the diluting segm ents; 2) the separation of solute and water (H 2O ) in the diluting segm ent; and 3) variable reabsorption of water in the collect- ing duct. These processes participate in the renal concentrating m echanism. D elivery of sodium chloride (N aCl) to the diluting segm ents of the nephron (thick ascending lim b of the loop of H enle and the distal convoluted tubule) is determ ined by glom erular filtration rate (GFR) and proxim al tubule function. G eneration of m edullary interstitial hypertonicity, is determ ined by norm al functioning of the thick ascending lim b of the loop of H enle, urea delivery from the m edullary col- lecting duct, and m edullary blood flow. Collecting duct perm eability is determ ined by the presence of antidiuretic horm one (ADH ) and norm al anatom y of the collecting system , leading to the form ation of a concentrated urine. GFR— glom erular H2O filtration rate; N aCl— sodium chloride; NaCl collecting duct H 2O — water. Determinants of delivery of H O NaCl H O 2 2 to distal parts of the nephron GFR NaCl Proximal tubular H2O and NaCl reabsorption H2O NaCl H2O Collecting duct impermeability depends on H2O Absence of ADH Absence of other antidiuretic substances FIGURE 1-4 Distal tubule M echanism of urine concentration: Urea overview of the passive m odel. Several m odels of urine concentration have been 2 put forth by investigators. The passive Cortex H2O m odel of urine concentration described by H2O Kokko and Rector is based on perm e- Na+ Na+ + + ability characteristics of different parts of K K 1 2Cl2– 2Cl2– the nephron to solute and water and on the Urea Outer medullary fact that the active transport is lim ited to NaCl + + Na Na collecting duct the thick ascending lim b. NaCl NaCl Urea concentration in the tubular fluid rises Urea 5 on account of low urea perm eability. Urea plays an im portant role in the Cortex generation of m edullary interstitial hypertonicity. A recycling m ech- anism operates to m inim ize urea loss. The urea that is reabsorbed Urea into the inner m edullary stripe from the term inal inner m edullary Urea collecting duct (step 3 in Fig. Som e of the urea enters the descending lim b of the loop of H enle and the thin ascending lim b of the loop of H enle. It is then carried Urea through to the thick ascending lim b of the loop of H enle, the distal Outer collecting tubule, and the collecting duct, before it reaches the stripe Outer inner m edullary collecting duct (pathway B). This process is facili- Urea medulla tated by the close anatom ic relationship that the hairpin loop of Inner stripe H enle and the vasa recta share. Urea Collecting duct Urea Urea Ascending vasa recta Pathway B Pathway A Urea Inner medulla FIGURE 1-6 1500 Changes in the volume and osmolality of 20 mL 0. The osmolality of the tubu- 1200 lar fluid undergoes several changes as it pass- es through different segments of the tubules. Tubular fluid undergoes marked reduction in 900 its volume in the proximal tubule; however, this occurs iso-osmotically with the glomeru- lar filtrate. In the loop of Henle, because of the aforementioned countercurrent mecha- 600 nism, the osmolality of the tubular fluid rises sharply but falls again to as low as 100 mOsm/kg as it reaches the thick ascend- 300 M aximal ADH ing limb and the distal convoluted tubule. In the absence of ADH, very Proximal tubule Loop of Henle Distal tubule Outer and little water is reabsorbed and dilute urine and cortical inner medullary results. On the other hand, in the presence collecting tubule collecting ducts of ADH, the collecting duct, and in some species, the distal convoluted tubule, become highly permeable to water, causing reabsorp- tion of water into the interstitium, resulting in concentrated urine. Antidiuretic horm one is Pineal responsible for augm enting the water perm eability of the cortical Baroreceptors Third ventricle and m edullary collecting tubules, thus prom oting water reabsorp- VP,NP tion via osm otic equilibration with the isotonic and hypertonic Supraoptic neuron interstitium , respecively. The horm one is form ed in the supraoptic Tanycyte and paraventricular nuclei, under the stim ulus of osm oreceptors SON and baroreceptors (see Fig. It is from the posterior pituitary that the antidi- Portal capillaries uretic horm one is released into the system ic circulation. Antidiuretic horm one (ADH ) is a cyclic hexapeptide (m ol. The biologically (164 AA) (Cleavage site) inactive m acrom olecule, pre-pro-vaso- pressin is cleaved into the sm aller, biologi- Signal peptide cally active protein. The protein of vaso- pressin is translated through a series of sig- nal transduction pathways and intracellular Pro-vasopressin AVP Gly Lys Arg Neurophysin II Arg Glycopeptide cleaving. Vasopressin, along with its bind- ing protein, neurophysin II, and the glyco- protein, are secreted in the form of neurose- cretory granules down the axons and stored Products of AVP NH2 + Neurophysin II + Glycopeptide in nerve term inals of the posterior lobe of pro-vasopressin the pituitary. ADH has a short half-life of about 15 to 20 m inutes and is rapidly m etabolized in the liver and kidneys. The m ultiple actions AQP-3 of vasopressin can be accounted for by its interaction with the V2 receptor found in the kidney. After stim ulation, vasopressin binds to the V2 receptor on the basolateral m em brane of the collecting Recycling vesicle duct cell. In ATP AQP-2 turn, cAM P activates a serine threonine kinase, protein kinase A AQP-2 (PKA). Cytoplasm ic vesicles carrying the water channel proteins m igrate through the cell in response to this phosphorylation PKA H O 2 process and fuse with the apical m em brane in response to increas- ing vasopressin binding, thus increasing water perm eability of the Gαs AQP-2 collecting duct cells. These water channels are recyled by endocyto- sis once the vasopressin is rem oved. The water channel responsible Gαs for the high water perm eability of the lum inal m em brane in Exocytic insertion response to vasopressin has recently been cloned and designated as aquaporin-2 (AQ P-2). The other m em bers of the aquaporin AVP Recycling vesicle fam ily, AQ P-3 and AQ P-4 are located on the basolateral m em - branes and are probably involved in water exit from the cell. The m olecular biology of these channels and of receptors responsible AQP-4 for vasopressin action have contributed to the understanding of the syndrom es of genetically transm itted and acquired form s of vaso- Basolateral Luminal pressin resistance. AQUAPORINS AND THEIR CHARACTERISTICS AQP-1 AQP-2 AQP-3 AQP-4 Size (amino acids) 269 271 285 301 Permeability to small solutes No No Urea glycerol No Regulation by antidiurectic hormone No Yes No No Site Proximal tubules; Collecting duct; principal cells Medullary collecting Hypothalamic— supraoptic, paraventricular nuclei; descending thin limb duct; colon ependymal, granular, and Purkinje cells Cellular localization Apical and basolateral Apical membrane and intracellu- Basolateral membrane Basolateral membrane of the prinicpal cells membrane lar vesicles Mutant phenotype Normal Nephrogenic diabetes insipidus Unknown Unknown FIGURE 1-10 Aquaporins and their characteristics.

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Mu opioid receptor quence variants of GABA(A) alpha 6 generic lisinopril 17.5mg overnight delivery blood pressure medication young age, beta 2 discount 17.5mg lisinopril overnight delivery arrhythmia nursing diagnosis, and gamma2 gene gene variants: lack of association with alcohol dependence discount lisinopril 17.5mg with visa hypertension foods to eat. Alcohol Clin Exp Res 1999; Psychiatry 1997;2:490–494 generic 17.5mg lisinopril with visa heart attack 913. Human GABAA receptor alpha 1 receptor variation and alcohol dependence. Alcohol Clin Exp Res and alpha 3 subunits genes and alcoholism. Dopamine D4 recep- receptor gene (OPRM1) exon 1 polymorphisms: population tor gene: novelty or nonsense? Neuropsychopharmacology 1999; studies, and allele frequencies in alcohol- and drug-dependent 21(1):3–16. The molecular biology of neuronal nicotinic acetyl- ciation of a functional DRD2 variant (Ser311Cys) and DRD2 choline receptors. Am J Med Genet (Neuropsychi- four novel single nucleotide polymorphisms in the nicotinic acetylcholine receptor 2-subunit (CHRNB2) gene show no atr Genet) 1997;74:386–394. Evidence for genetic D2 receptor gene and alcoholism. Alcohol Clin Exp Res 1998: linkage to alcohol dependence on chromosomes 4 and 11 from 22(4):845–848. Identification of a J Med Genet (Neuropsychiatr Genet) 1998;81:216–221. Genome-wide search (DAT1) gene and the significant association with alcoholism. Quantitative trait loci mine in alcoholism: human and basic science studies. Alcohol analysis of human event-related brain potentials: P3 voltage. FISCHMAN Although the prevailing view for many decades was that severity ranging from occasional drug use to a dangerous drug dependent patients simply suffered from character but moderately severe state called 'abuse' in the American weakness, the persuasive data emerging from modern brain Psychiatric Association Diagnostic and Statistical Manual imaging techniques and the application of molecular biol- (DSM), to a severe compulsive state known as 'depen- ogy methods to animal models of compulsive drug use indi- dence' or 'addiction. The integration the usefulness of the term 'addiction' to denote this severe of a number of new technologies has allowed investigators state that occurs only in the minority of users who lose to combine behavioral and neurobiological approaches to control and become compulsive drug users with a chronic more completely evaluate multiple aspects of this difficult relapsing clinical course. The other point of view is that the term 'dependence' during the 1990s, the decade of the brain. The section con- creates confusion because it is already used to designate the centrates on advances most relevant to neuropsychopharma- state marked by drug-specific withdrawal symptoms that cology, integrating neurobiology, behavioral biology, and normally occur when regular drug use is abruptly termi- pharmacology. Knowledge of the pathophysiology of drug nated ('physical' dependence). Dependence also has a long- use disorders has greatly increased with the identification standing use as a personality disorder descriptor completely and cloning of receptors for the major drugs of abuse. Most important, patients with is also a much greater understanding of the brain circuits chronic pain receiving opiates often show signs of tolerance involved, including those common to different classes of and withdrawal symptoms without any behavior that could drugs. The efficacy of treatment has also increased through be categorized as abuse. Physicians who are confused by the availability of effective medications for alcohol, heroin, 'dependence' defined as a normal response and 'depen- and nicotine, as well as behavioral approaches used with dence' as a disorder have been known to mistakenly with- cocaine abusers. Also, there is greater acceptance of the hold pain medication to 'prevent addiction. There is general agreement that there are degrees of over proper terminology. For example, in the United States, over 4% of the general population is alcohol dependent and another 5 to The first step in the pharmacologic treatment of alcoholism 10 million people drink hazardously at least several times is to help patients safely detoxify from alcohol. The economic and medical costs of alcohol- historically, alcohol detoxification has occurred in inpatient ism and alcohol abuse continue to escalate. Most recent setting, increasingly alcohol detoxification is being con- figures put the economic costs of alcohol-related expenses ducted in ambulatory settings. Except in the case of medical at $176 billion annually in the United States (2). This in- or psychiatric emergencies, outcome studies generally show cludes the economic costs of increased health care expenses, that successful detoxification can safely and effectively be lost productivity at work, and legal expenses. Similarly, al- carried out in ambulatory setting using medications such though there have been some reductions in the number of as benzodiazepines (5,6). In addition, the use of anticonvul­ motor vehicle deaths attributed to excessive alcohol drink- sants has received recent interest. Benzodiazepines Current psychosocial approaches to alcohol addiction are moderately effective, with perhaps as many as half the pa- Benzodiazepines are �-aminobutyric acid (GABA) agonists tients receiving treatment becoming abstinent or signifi- that metaanalysis of placebo-controlled double-blind studies cantly reducing episodes of binge drinking (4). In the past have consistently shown to be safe and effective (7). Benzo­ two decades significant progress has been made in under- diazepines differ widely in their pharmacologic half-life, and standing the pharmacology of alcohol and why some people this has been a factor in the choice of which benzodiazepines become dependent. This has led to the development of sev- to use for detoxification. For example, one popular ap­ eral medications that have been shown in research studies proach is to use a benzodiazepine with a long half-life such to improve treatment outcomes. This chapter reviews some as chlordiazepoxide as a loading dose and let the benzodiaze­ of the possible neurobiological mechanisms involved in al- pine self-taper (8). We introduce precludes problems with patience noncompliance. A second future directions for research such as the use of combina- approach is to use shorter acting benzodiazepines and titrate tions of medications that may have additive or synergistic the dose depending on symptoms. In a recent study, oxaze­ effects on improving treatment, and discuss the role of psy- pam was used as needed depending on the severity of with­ chosocial support to facilitate the effectiveness of pharmaco- drawal symptoms as assessed by the Clinical Institute With- therapy. As needed oxazepam resulted in effective alcohol withdrawal management with a lower total amount of oxazepam over a shorter duration compared to routine dosing (9). Volpicelli: Department of Psychiatry, University of Pennsylva- Anticonvulsants nia, Veterans Affairs Medical Center, Philadelphia, Pennsylvania. Anticonvulsants have the 1446 Neuropsychopharmacology: The Fifth Generation of Progress advantage of no abuse potential and a theoretical advantage drinking (17–33). These studies have consistently demon­ of reducing kindling, a sensitization of withdrawal symp­ strated that alcohol enhances the release of endogenous toms that occurs after multiepisodes of alcohol withdrawal. For example, Gia­ of less hostility in the phenobarbital group (10). Carbamaze­ noulakis and colleagues (34) have found that in humans pine has also been used as an alternative to benzodiazepines peripheral levels of �-endorphin increase in family his­ to attenuate alcohol withdrawal symptoms (11). Although tory–positive subjects following a moderate dose of alcohol, its mechanism of action remains unknown, research gener­ whereas there is no increase in �-endorphin for social drink­ ally shows that carbamazepine is as effective as benzodiaze­ ers without a family history of alcoholism. Disadvantages of carbamazepine include a rather nar­ lich and colleagues (36) have also demonstrated that alco­ row therapeutic window, the need to monitor serum levels, hol-induced �-endorphin responses both prior to and and hepatotoxic effects. For patients with a history of alco­ following alcohol administration are significantly heritable. Nonpreferring (NP) rats exhibit differences in the densities of � opioid receptors in certain brain reward regions compared to alcohol-preferring rats.