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In this process the amino group from GABA is transferred onto the TCA cycle intermediate a-ketoglutarate purchase viagra super active 100 mg on line,producing glutamate and succinic semialdehyde buy viagra super active 25 mg otc. The latter is in turn converted by the enzyme succinic semialdehyde dehydrogenase (SSADH) into succinate,which re-enters the TCA cycle. Other potential routes of GABA production have been described Ð involving deamination and decarboxylation reactions from putrescine,spermine,spermidine and ornithine Ð but the vast majority of GABA is generated by means of the GABA-shunt. GABA-T and SSADH are also present in the mitochondria of glial cells and are responsible for the degradation of GABA recovered from the extracellular space (see below). In this case the glutamate formed from the action of GABA-T is converted into glutamine by the cytosolic enzyme glutamine synthetase (GS). Glial glutamine serves as an important precursor for both neuronal glutamate and GABA. It is transported from glia into neurons where the mitochondrial enzyme phosphate-activated glutaminase (PAG) converts it back into glutamate. This neuronal glutamate can then be converted to GABA,either directly or following metabolism via the TCA cycle. The inter- conversion of glutamate and a-ketoglutarate is achieved by two further groups of AMINO ACIDS: INHIBITORY 227 Figure 11. Enzymes responsible for the syntheisis (GAD) and metabolism (GABA-T and SSADH) of GABA,and their relationship to the TCA cycle and the amino acids glutamate and glutamine. In glia,glutamate can be converted to glutamine by glutamine synthetase (GS). Dark-grey boxes denote enzymes present in both neurons and glia,light-grey boxes denote enzymes present only in neurons enzymes found in the mitochondria of both neurons and glia: the multi-enzyme complex glutamate dehydrogenase (GDH),and several aminotransferases (including aspartate and alanine aminotransferases) whose action is analogous to that of GABA-T. Regulation of GAD Of key importance in the synthesis of GABA is the short-term regulation of GAD activity. Increasing the availability of glutamate does not lead to an increase in the production of GABA,suggesting that GAD may normally be saturated with its substrate. GAD exists in two states; an inactive apoenzyme (apoGAD) lacking the co-factor and active 228 NEUROTRANSMITTERS,DRUGS AND BRAIN FUNCTION Figure 11. GABA produced by both GAD67 and GAD65 can be used as a neurotransmitter but GAD65 is preferentially associated with synaptic vesicles. Synaptically released GABA is recovered into neurons and glia by GABA transporters (not shown is the possible release of GABA by reversal of these transporters). Glutamine produced in glial cells is exported to neurons and converted to glutamate (after Soghomonian and Martin 1998) holoenzyme (holoGAD) complexed with PLP. During the synthetic process GAD can undergo cycles of interconversion between these states.

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This excess fluid Two types of alveolar hypoxia are encountered in the travels through the interstitium to the perivascular and peri- lungs generic viagra super active 25 mg with visa, with different implications for pulmonary vascular bronchial spaces in the lungs buy viagra super active 50 mg low price, where it then passes into the resistance. In regional hypoxia, pulmonary vasoconstric- lymphatic channels (see Fig. The lungs have a more tion is localized to a specific region of the lungs and diverts extensive lymphatic system than most organs. Lymphatic channels, like small pulmonary blood monary arterial pressure, and when alveolar hypoxia no vessels, are held open by tethers from surrounding connec- longer exists, the vessels dilate and blood flow is restored. Generalized hy- poxia occurs when the partial pressure of alveolar oxygen Fluid Imbalance Leads to Pulmonary Edema (PAO2) is decreased with high altitude or with the chronic hypoxia seen in certain types of respiratory diseases (e. Generalized hy- the lung interstitial spaces and alveoli, and usually results poxia can lead to pulmonary hypertension (high pul- when capillary filtration exceeds fluid removal. Pulmonary monary arterial pressure), which leads to pathophysiologi- edema can be caused by an increase in capillary hydrostatic CHAPTER 20 Pulmonary Circulation and the Ventilation-Perfusion Ratio 343 CLINICAL FOCUS BOX 20. These struc- Hypoxia has opposite effects on the pulmonary and sys- tural changes occur in both large and small arteries. Hypoxia relaxes vascular smooth mus- there is abnormal extension of smooth muscle into pe- cle in systemic vessels and elicits vasoconstriction in the ripheral pulmonary vessels where muscularization is not pulmonary vasculature. Hypoxic pulmonary vasoconstric- normally present; this is especially pronounced in precap- tion is the major mechanism regulating the matching of re- illary segments. These changes lead to a marked increase gional blood flow to regional ventilation in the lungs. With severe, chronic hy- regional hypoxia, the matching mechanism automatically poxia-induced pulmonary hypertension, the obliteration of adjusts regional pulmonary capillary blood flow in re- small pulmonary arteries and arterioles, as well as pul- sponse to alveolar hypoxia and prevents blood from per- monary edema, eventually occur. Regional hy- part, by the hypoxia-induced vasoconstriction of pul- poxic vasoconstriction occurs without any change in monary veins, which results in a significant increase in pul- pulmonary arterial pressure. Hypoxia-induced pulmonary hypertension strict with hypoxia; however, only the arterial side under- affects individuals who live at a high altitude (8,000 to goes major remodeling. The postcapillary segments and 12,000 feet) and those with chronic obstructive pulmonary veins are spared the structural changes seen with hypoxia. Because of the hypoxia-induced vasoconstriction and vas- With chronic hypoxia-induced pulmonary hyperten- cular remodeling, pulmonary arterial pressure increases. An increase in wall thickness results pertrophy and failure, the major cause of death in COPD from hypertrophy and hyperplasia of vascular smooth patients. In- Protein leakage makes pulmonary edema more severe be- creased capillary hydrostatic pressure is the most frequent cause additional water is pulled from the capillaries to the cause of pulmonary edema and is often the result of an ab- alveoli when plasma proteins enter the interstitial spaces and normally high pulmonary venous pressure (e. Increased capillary permeability occurs with pul- stenosis or left heart failure). Loss of surfactant causes high surface tension, lowering in- terstitial hydrostatic pressure and resulting in an increase of capillary fluid entering the interstitial space. A decrease in plasma colloid osmotic pressure occurs when plasma protein concentration is reduced (e.

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Below or The kidneys use about 8% of total resting oxygen above the autoregulatory range of pressures generic viagra super active 100mg otc, blood flow and consumption generic viagra super active 50 mg on line, but they receive much more oxygen than GFR change appreciably with arterial blood pressure. Consequently, renal extraction of oxygen is Two mechanisms account for renal autoregulation: the low, and renal venous blood has a bright red color (be- myogenic mechanism and the tubuloglomerular feedback cause of a high oxyhemoglobin content). In the myogenic mechanism, an increase in cal arrangement of the vessels in the kidney permits a pressure stretches blood vessel walls and opens stretch-ac- large fraction of the arterial oxygen to be shunted to the tivated cation channels in smooth muscle cells. Therefore, ing membrane depolarization opens voltage-dependent the oxygen tension in the tissue is not as high as one 2 2 Ca channels and intracellular [Ca ] rises, causing might think, and the kidneys are certainly sensitive to is- smooth muscle contraction. Blood Flow Is Higher in the Renal Cortex In the tubuloglomerular feedback mechanism, the transient increase in GFR resulting from an increase in and Lower in the Renal Medulla blood pressure leads to increased solute delivery to the Blood flow rates differ in different parts of the kidney (Fig. Blood flow is highest in the cortex, averaging 4 to tubular fluid [NaCl] at this site and increased NaCl reab- 5 mL/min per gram of tissue. By mechanisms that are permits a high rate of filtration in the glomeruli. Blood still uncertain, constriction of the nearby afferent arteriole flow (per gram of tissue) is about 0. The relatively low blood flow in the medulla feedback sensitivity varies directly with the local concen- helps maintain a hyperosmolar environment in this region tration of angiotensin II. The tubuloglomerular feedback 386 PART VI RENAL PHYSIOLOGY AND BODY FLUIDS mechanism is a negative-feedback system that stabilizes renal blood flow and GFR. Autoregulatory If NaCl delivery to the macula densa is increased exper- range imentally by perfusing the lumen of the loop of Henle, fil- 1. This sug- gests that the purpose of tubuloglomerular feedback may be to control the amount of Na presented to distal nephron segments. Regulation of Na delivery to distal Renal blood flow parts of the nephron is important because these segments have a limited capacity to reabsorb Na. Without renal autoregulation, increases in arterial blood pressure would lead to dramatic increases in GFR and potentially serious losses of NaCl and water from the ECF. Sympathetic nerve stimulation causes renal vasocon- 0 40 80 120 160 200 240 striction and a consequent decrease in renal blood flow. Mean arterial blood pressure (mm Hg) Renal sympathetic nerves are activated under stressful condi- Renal autoregulation, based on measure- tions, including cold temperatures, deep anesthesia, fearful FIGURE 23. In the autoregulatory range, renal blood flow and GFR conditions, the decrease in renal blood flow may be viewed stay relatively constant despite changes in arterial blood pressure. The circles indicate that vessel radius (r) and heart, which are more important for short-term survival. Since resistance to blood flow varies as r , including adenosine, angiotensin II, endothelin, epineph- changes in vessel caliber are greatly exaggerated in this figure. Other substances cause vasodilation in the kidneys, includ- ing atrial natriuretic peptide, dopamine, histamine, kinins, nitric oxide, and prostaglandins E2 and I2. An increase in sympathetic nerve activ- ity or plasma angiotensin II concentration stimulates the production of renal vasodilator prostaglandins.

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