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Period (mEq/min) (mEq/min) (mEq/min) The RAAS plays an important role in the day-to-day 1 6 virus like ebola purchase 250 mg disithrom overnight delivery. It favors Na conservation by Increase GFR by one third the kidneys when there is a Na or volume deficit in the 2 8 antibiotic 300 mg effective 500 mg disithrom. When there is an excess of Na or volume antibiotic resistance lab generic 250mg disithrom with mastercard, dimin- a Results from an experiment performed on a 10-kg dog. In response to an increase in GFR (produced by infusing a drug that di- the absence of aldosterone (e. If there had been no glomerulotubular balance and if tubular Na reabsorption had ciency—Addison’s disease—excessive amounts of Na are stayed at 5. If we assume that the ECF volume in the dog is 2 crease from a normal value of about 99. The dog would have been dead long before this could happen, which underscores the im- (see Table 24. Such a loss of Na would lead to a decrease in plasma and blood volume, cir- 1) A decrease in pressure in the afferent arteriole, with culatory collapse, and even death. Patients with Ad- 3) A decrease in fluid delivery to the macula densa re- dison’s disease often show a well-developed sodium ap- gion of the nephron, resulting, for example, from a decrease petite, which helps keep them alive. Retention of this sudation of fluid out of the vascular system, diarrhea, severe amount of fluid is not sufficient to produce obvious edema. Conversely, an increase in The fact that the person will not continue to accumulate the effective arterial blood volume inhibits renin release. Na and water is due to the existence of numerous factors Long-term stimulation causes vascular smooth muscle cells that are called into play when ECF volume is expanded; in the afferent arteriole to differentiate into granular cells these factors promote renal Na excretion and overpower and leads to further increases in renin supply. This phenomenon blood plasma acts on a plasma 2-globulin produced by the is called mineralocorticoid escape. Angiotensin I Intrarenal Physical Forces (Peritubular Capillary Starling is converted to the octapeptide angiotensin II as the blood Forces). An increase in the hydrostatic pressure or a de- courses through the lungs. This reaction is catalyzed by the crease in the colloid osmotic pressure in peritubular capil- angiotensin-converting enzyme (ACE), which is present laries (the so-called “physical” or Starling forces) results in on the surface of endothelial cells. In turn, an accumu- this system (renin, angiotensinogen, angiotensin-convert- lation of the reabsorbed fluid in the kidney interstitial ing enzyme) are present in some organs (e. The increased interstitial pressure causes a and brain), so that angiotensin II may also be formed and widening of the tight junctions between proximal tubule act locally. The result is increased back-leak of salt and water salt-conserving system. Angiotensin II has several actions into the tubule lumen and an overall reduction in net reab- related to Na and water balance: sorption. These changes occur, for example, if a large vol- 1) It stimulates the production and secretion of the al- ume of isotonic saline is infused intravenously. They also dosterone from the zona glomerulosa of the adrenal cortex occur if the filtration fraction (GFR/RPF) is lowered from (see Chapter 36). This mineralocorticoid hormone then the dilation of efferent arterioles, for example.
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These are enclosed in a double membrane; the inner membrane shows projections (cristae) (C13) into the inner space (matrix) antimicrobial conference 2013 order disithrom 100 mg with mastercard. The mitochondria are of various shapes (short and plump in the perikaryon antimicrobial nasal spray cheap generic disithrom uk, long and slender in the den- drites and the axon) and move constantly along fixed cytoplasmic paths between the Kahle virus 0000 disithrom 100mg overnight delivery, Color Atlas of Human Anatomy, Vol. Ultrastructure of the Nerve Cell, Function of Organelles 23 2 18 5 10 1 4 12 14 A Electron-microscopic view of a nerve cell (diagram) 17 14 11 11 6 7 17 1 3 4 5 B Detail of A 9 12 5 16 Protein synthesis 14 15 9 12 1 Oxidation DNA 7 ATP 3 4 13 6 C Function of Acid cell organelles esterases 17 8 11 Kahle, Color Atlas of Human Anatomy, Vol. In type I synapses, the synaptic cleft The axon ends with numerous small knob- is wider and the density of the postsynaptic like swellings, the axon terminals or boutons. In type II synapses, the synaptic the next neuron, the bouton forms the syn- cleft is narrower and the postsynaptic den- apse where excitation is transmitted from sity is about the same as the presynaptic one neuron to another. The synapse consists of the presynaptic com- ponent (bouton) (AB1) with the presynaptic Function (C) membrane (BC2), the synaptic cleft (B3), and There are excitatory and inhibitory synapses. Most of the inhibitory syn- neurotubules but contains mitochondria apses are found at the perikaryon or at the and small, mainly clear vesicles (BC5) which axon hillock, where excitation is generated are clustered near the presynaptic mem- and can be most effectively suppressed. The synaptic cleft con- While synaptic vesicles are usually round, tains filamentous material and communi- some boutons contain oval or elongated cates with the extracellular space. They are characteristic of in- synaptic and postsynaptic membranes ex- hibitory synapses. Asymmetric synapses hibit dense zones of apposition, which re- (type I) are often excitatory, whereas sym- semble those found at various cell junctions metric synapses (type II) are mostly inhibi- (zonulae or maculae adherentes, adherent tory. Synapsescanbeclassifiedaccordingtotheir localization, their structure, and their func- tion, or according to the neurotransmitter substances they contain. Localization (A) The boutons may be apposed to dendrites (AC7) of the receptor neuron (axodendritic synapses) (A8, C), to small projections of the dendritic membrane, spines (axospinoussyn- apses) (A9), to the perikaryon (axosomatic synapses) (A10), or to the initial segment of the axon (axoaxonal synapses) (A11). Structure (B) Depending on the width of the synaptic cleft and the properties of the apposing membranes, two types of synapses, type I Kahle, Color Atlas of Human Anatomy, Vol. Types of Synapses 25 9 7 1 7 8 9 10 A Electron-microscopic view of a dendrite (left) and a nerve cell (right) with synapses (according to Bak) 11 5 1 B Synapses, Gray type I (left) and type II (right) 2 6 3 3 2 4 2 4 12 5 13 7 4 2 C Electron microscopic view of a cross section of a dendrite with surrounding synapses (diagram according to Uchizono) Kahle, Color Atlas of Human Anatomy, Vol. The synaptic con- The catecholamines norepinephrine (NE) tact between parallel axons and dendrites is and dopamine (DA) also act as transmitters, called parallel contact or bouton en passant and so does serotonin (5-HT). Many dendrites have thornlike projec- ropeptides act not only as hormones in the tions (spines) that form a spinous synapse bloodstream but also as transmitters in the (A2) with the bouton. Several axons for transmitter synthesis are produced in and dendrites can join to form glomerulus- the perikaryon, while the transmitter sub- like complexes in which the different synap- stances themselves are synthesized in the tic elements are closely intertwined. The small and clear vesicles are probably affect each other in terms of fine- thought to carry glutamate and ACh, the tuning (modulating) the transmission of elongated vesicles of the inhibitory synapses impulses. The ves- icles pass through these spaces to reach the Electrical synapses presynaptic membrane and, upon excita- Adjacent cells can communicate through tion, empty their content into the synaptic pores (tunnel proteins), called gap junctions. The transmitter coupled; this facilitates the transmission of substances are delivered in certain quanta, impulses from one cell to another (e. Some of the transmitter in neurons are therefore also called electri- molecules return into the bouton by reup- cal synapses in contradistinction to the take (D5). Electrical coupling via gap junctions occurs not only between neurons but also between glial cells. Neurotransmitters (C, D) Transmission of impulses at the chemical synapses is mediated by neurotransmitters. The most widely distributed transmitter substances in the nervous system are acetylcholine (ACh), glutamate, gamma- aminobutyric acid (GABA), and glycine. Glutamate is the most common excitatory transmitter, GABA is a transmitter of the in- Kahle, Color Atlas of Human Anatomy, Vol. Types of Synapses, Neurotransmitters 27 2 1 B Complex synapse A Parallel contact (1) and spinous synapse (2) 6 C Different types of synaptic vesicles 5 3 4 D Model of a synapse (according to Akert, Pfenniger, Sandri and Moor) Kahle, Color Atlas of Human Anatomy, Vol.
As noted ear- Cl- lier antibiotic resistance cost generic disithrom 500 mg with mastercard, the proximal straight tubule has transport properties H+ similar to those of the proximal convoluted tubule infection vs intoxication purchase disithrom 500mg fast delivery. The thin descending antibiotic resistance oxford discount 500 mg disithrom overnight delivery, thin ascending, and thick ascending limbs of the loop of Henle all display different permeability and A cell model for ion transport in the thick FIGURE 23. CHAPTER 23 Kidney Function 395 Tubular Distal convoluted Blood dominantly permeable to Cl. Diffusion of these ions out of the cell produces a transepithelial potential difference, urine tubule cell with the lumen about 6 mV compared with interstitial space around the tubules. This potential difference drives Blocked by ATP + 2 2 Na small cations (Na , K , Ca , Mg , and NH4 ) out of thiazides ADP + Pi K+ the lumen, between the cells. The tubular epithelium is ex- tremely impermeable to water; there is no measurable wa- Na+ K+ ter reabsorption along the ascending limb despite a large Cl- transepithelial gradient of osmotic pressure. Cl- TUBULAR TRANSPORT IN THE DISTAL NEPHRON The so-called distal nephron includes several distinct seg- ments: distal convoluted tubule; connecting tubule; and FIGURE 23. Note that the distal nephron includes the collecting duct system, which, strictly speaking, is not part of the nephron, but from a functional perspective, this the lumen into the cell by a Na-Cl cotransporter that is in- is justified. Transport in the distal nephron differs from that hibited by thiazide diuretics. Na is pumped out the baso- in the proximal tubule in several ways: lateral side by the Na /K -ATPase. Water permeability of 1) The distal nephron reabsorbs much smaller amounts the distal convoluted tubule is low and is not changed by of salt and water. The Cortical Collecting Duct Is an Important 2) The distal nephron can establish steep gradients for Site Regulating K Excretion salt and water. For example, the [Na ] in the final urine Under normal circumstances, most of the excreted K may be as low as 1 mEq/L (versus 140 mEq/L in plasma) and comes from K secreted by the cortical collecting ducts. By contrast, the proximal tubule reabsorbs Na and collecting ducts may secrete so much K that more K is water along small gradients, and the [Na ] and osmolality excreted than was filtered. With severe K depletion, the of its tubule fluid are normally close to that of plasma. This explains why the distal nephron can establish steep volves active uptake by a Na /K -ATPase in the basolat- gradients for small ions and water, whereas the proximal eral cell membrane, followed by diffusion of K through tubule cannot. Outward diffusion of K 4) Na and water reabsorption in the proximal tubule from the cell is favored by concentration gradients and op- are normally closely coupled because epithelial water per- posed by electrical gradients. By contrast, Na and water reab- dient opposing exit from the cell is smaller across the lumi- sorption can be uncoupled in the distal nephron because nal cell membrane than across the basolateral cell water permeability may be low and variable. The luminal cell membrane po- coarse operation that reabsorbs large quantities of salt and tential difference is low (e. By contrast, distal reabsorption because this membrane has a high Na permeability and is is a finer process. Recall that the The collecting ducts are at the end of the nephron sys- entry of Na into a cell causes membrane depolarization tem, and what happens there largely determines the excre- (see Chapter 3). Transport in the collect- The magnitude of K secretion is affected by several ing ducts is finely tuned by hormones. Increased amounts of The Luminal Cell Membrane of the Distal Na in the collecting duct lumen (e. In 2) The lumen-negative transepithelial electrical poten- this nephron segment, Na and Cl are transported from tial promotes K secretion. The ability to concentrate the urine decreases the urine principal cell amount of water we are obliged to find and drink each day. Na+ ATP + Arginine Vasopressin Promotes the Excretion Na of an Osmotically Concentrated Urine ADP + Pi K+ Changes in urine osmolality are normally brought about largely by changes in plasma levels of arginine vasopressin + K+ (AVP), also known as antidiuretic hormone (ADH) (see K Chapter 32).
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Individual differences in levels of pain antimicrobial resistance generic disithrom 500 mg amex, in the transition from acute to chronic pain antibiotic neurotoxicity order disithrom in india, in susceptibility to neuropathic pain after nerve damage and in analgesic effectiveness may have a genetic basis antibiotics for steroid acne discount 100mg disithrom with amex. There is marked variability in animal genetic strains in terms of the sequelae of tissue and nerve damage and even in their responses to morphine. Given the huge range of human phenotypes, this may indicate important individual differences in susceptibility to pain and analgesia but we have no way of monitoring this possibility. Dray, A, Urban, L and Dickenson, AH (1994) Pharmacology of chronic pain. McMahon, SB, Lewin, GR and Wall, PD (1993) Central excitability triggered by noxious inputs. Edited by Roy Webster Copyright & 2001 John Wiley & Sons Ltd ISBN: Hardback 0-471-97819-1 Paperback 0-471-98586-4 Electronic 0-470-84657-7 Section N SM IT S A IO Neurotransmitters, Drugs and Brain Function. Edited by Roy Webster Copyright & 2001 John Wiley & Sons Ltd ISBN:Hardback 0-471-97819-1 Paperback 0-471-98586-4 Electronic 0-470-84657-7 22 Sleep and aking R. STANFORD INTRODUCTION There have been many references in this book to the role of neurotransmitters in the control of CNS excitability. It is therefore appropriate, but possibly foolhardy, to see if the two natural extremes of that excitability, namely sleep and waking, can be explained in terms of neurotransmitter activity. Of course, these states are not constant:our sleep can be deep or light and, even when we are awake, our attention and vigilance fluctuate, as the reading of these pages will no doubt demonstrate. Also, the fact that we sleep does not mean that our neurotransmitters are inactive:this would imply that sleep is a totally passive state, whereas all the evidence suggests that it is an actively induced process, subject to refined physiological control. In order to explain the physiological characteristics of the sleep±waking cycle, as well as how this might be controlled by different neurotransmitters and modified by drugs, we need to know which areas and pathways in the brain are vital to the induction and maintenance of this rhythmic behaviour. Essentially, these brain systems can be resolved into two interacting networks. One is responsible for the basic circadian rhythm and ensures that our sleeping and waking periods normally occur at regular intervals. A second system fine-tunes this process and ultimately determines our precise functional status on the sleep±waking continuum. THE NEURAL BASIS OF CIRCADIAN RHYTHMS It is most probable that sleep and waking stem from an inherent cycle of neuronal activity that can be influenced dramatically by changes in sensory stimulation. This is demonstrable not only in humans and laboratory animals, but also in invertebrates. Thus, while we cannot be sure that other animals sleep in the same way that we do, they do show a circadian cycle of motor activity. In some (nocturnal) species, such as the rat, this activity is actually highest during darkness. Even aplysia, the sea hare, has such a rhythm but this is more like that of humans in being maximally active during daylight (diurnal). These rhythms seem to be innately programmed although they can be adjusted. Interestingly, when humans are in a time-free environment, the change in the rhythm of Neurotransmitters, Drugs and Brain Function. Webster &2001 John Wiley & Sons Ltd 478 NEUROTRANSMITTERS, DRUGS AND BRAIN FUNCTION body temperature does not follow the change in the sleep±waking cycle. Generally, it becomes shorter (to as little as 20 h), rather than longer, which suggests that these cycles are regulated in different ways. Entrainment has also been shown in aplysia which, after exposure to a normal dark±light cycle, retains a cyclic pattern of activity for a number of days even if subjected to continuous light. These genes have been studied most extensively in insects but they have also been found in humans. Their protein products enter the cell nucleus and regulate their own transcription.
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