Transcript figure 9.1

Chapter 9
Companion site for Basic Medical Endocrinology, 4th Edition
Author: Dr. Goodman
FIGURE 9.1
Distribution of body water and principal electrolytes. Note that water and electrolytes equilibrate
freely between plasma and interstitial fluid, but only water equilibrates between the intracellular and
extracellular compartments. The electrochemical gradient for sodium is maintained by the activity of
the sodium/potassium ATPase.
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FIGURE 9.2
Schematic representation of renal tubules and their component parts. (Modified from Kriz, W.
(1988) A standard nomenclature for structures of the kidney. Am. J. Physiol. 254: F1–F8.)
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FIGURE 9.3
The countercurrent multiplier in the loop of Henle. Selective permeability of the tubular epithelium
and active transport of sodium by the thick ascending limb create osmotic gradients. Tubular to
interstitial flow of water concentrates sodium in the descending limb. Sodium movement across the
water impermeable ascending limb creates the osmotic gradient in the interstitium. Yellow arrows
indicate the direction of flow. Note that active sodium transport in the thick ascending limb creates
the gradient in the interstitium and makes the tubular fluid hypoosmotic by the time it emerges from
Henle’s loop.
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FIGURE 9.4
The V1 receptor mediates the pressor actions of AVP/ADH, and the V2 receptor mediates the water
conservation effects. The two receptors signal by way of different G-proteins.
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FIGURE 9.5
Principal cells of the collecting duct before (A) and (B) after ADH. ADH binds to V2 receptors to
induce formation of cAMP, which promotes insertion of aquaporin 2 (AQP2) into the luminal
membrane making it permeable to water. In the presence of ADH, water can pass through the
principal cell from lumen to interstitium driven by the osmotic gradient. Deep in the medulla, urea
transporters also are inserted in the luminal membrane in addition to AQP2. Expression of
Aquaporins 3 and 4 (Aq 3 & 4) in the basolateral membranes allows osmotic equilibration between
intercellular and interstitial water.
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FIGURE 9.6
Relation between ADH and osmolality in plasma of unanesthetized rats. Note the appearance of
thirst (increased drinking behavior) when plasma osmolality exceeds 290 mOsm/kg. (From
Robertson, G.L. and Berl, T. (1996) In The Kidney, 5th ed., Brenner and Rector, eds., 881.
Saunders, Philadelphia, with permission.)
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FIGURE 9.7
A. Sagital view of the brain showing the circumventricular organs and their relation to ADHproducing cells. PVN = paraventricular nucleus; OVLT = organum vasculosum of the lamina
terminalis; SON = supraoptic nucleus; AP = area postrema. (Adapted from Netter, F.H. (2003) In
Netter’s Atlas of Human Neuroscience, David L. Felten and Ralph Jozefowicz, eds. Icon Learning
Systems; Teterboro, NJ.) B. Neural and hormonal input to ADH secreting cells.
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FIGURE 9.8
Relation between changes in blood osmolality, pressure, or volume and ADH concentration in
plasma of unanesthetized rats. (From Dunn, F.L., Brennan, T.J., Nelson, A.E., and Robertson, G.L.
(1973) The role of blood osmolality and volume in regulating vasopressin secretion in the rat. J.
Clin. Invest., 52: 3212, with permission.)
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FIGURE 9.9
The effects of increases or decreases in blood volume or blood pressure on the relation between
ADH concentrations and osmolality in the plasma of unanesthetized rats. Circled numbers indicate
percent change from normal (N). (Modified from Robertson, G.L. and Berl, T. (1996) In The Kidney,
5th ed., 881. Saunders, Philadelphia, with permission.)
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FIGURE 9.10
Two-step formation of angiotensin II. Amino acids are represented by the single letter amino acid
code, D = aspartic acid, F = phenylalanine, H = histidine, I = isoleucine, L = l eucine, P = proline, R
= arginine, S-serine, V = valine, Y = tyrosine.
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FIGURE 9.11
The juxtaglomerular apparatus. Red arrows indicate the direction of blood flow. (Modified from
Davis, J.O. (1975) Regulation of aldosterone secretion. In Handbook of Physiology, Sect 7:
Endocrinology, Vol. IV: Adrenal Gland. American Physiological Society, Washington, DC, with
permission.)
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FIGURE 9.12
Angiotensin II increases sodium reabsorption by stimulating sodium proton exchange in the luminal
brush border and sodium bicarbonate cotransport in the basolateral membrane. Hydrogen ions and
bicarbonate are regenerated in the cell cytosol from CO2 and water.
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FIGURE 9.13
Actions of angiotensin.
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FIGURE 9.14
Negative feedback control of renin and angiotensin secretion. The monitored variable is blood
volume detected as decreases in sodium chloride at the macula densa, decreased pressure in the
afferent arterioles, and decreased pressure in the carotid sinuses, aortic arch, and thoracic low
pressure receptors. Coordinated actions of angiotensin restore plasma volume and abolish the
stimuli for renin secretion. Note that angiotensin II contributes directly and indirectly to maintenance
of blood volume, but its influence in this regard is inadequate in the absence of aldosterone (see
Chapter 4).
Companion site for Basic Medical Endocrinology, 4th Edition. by Dr. Goodman
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FIGURE 9.15
Electron microscopic section through rat cardiac atrium showing working cardiac myocytes (x
4,500). G = Storage granules; GC = Golgi complex; My = myofribril; N = nucleus. (From de Bold,
A.J. and Bruneau, B.G. (2000) Natriuretic peptides. In Fray, J.C.S., ed. Handbook of Physiology,
Section VII, The Endocrine System, Volume 3, Endocrine Regulation of Water and Electrolyte
Balance . American Physiological Society/Oxford University Press, 377–409.)
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FIGURE 9.16
The natriuretic peptides. Amino acids are represented by the single letter amino acid code Amino
acidsare represented by the single amino acid code: A = alanine, C = cysteine, D = aspartic acid, F
= phenylalanine, G = glycine, H = histidine, I = isoleucine, K = lysine, L = leucine, M = methionine,
N = asparagine, Q = glutamine, R = arginine, S = serine, V = valine.
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FIGURE 9.17
Actions of atrial natriuretic factor (ANF).
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FIGURE 9.18
Direct and indirect actions of ANF on the kidney.
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FIGURE 9.19
Negative feedback regulation of ANF secretion.
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FIGURE 9.20
Hormonal responses to hemorrhage.
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FIGURE 9.21
Hormonal responses to dehydration.
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FIGURE 9.22
Responses of normal subjects to low or high intake of sodium chloride for five days. Plasma sodium
concentrations were maintained within less than 2% by compensating rates of sodium excretion.
The small increases or decreases in hematocrit and plasma protein concentrations indicate
contraction of the plasma volume in the low sodium group and expansion in the high sodium group.
The changes in hormone concentrations are in response to the small changes in osmolality and
volume. Plasma renin activity is a measure of renin concentration expressed as ng of angiotensin I
formed per ml of plasma in one hour. (Drawn from the data of Sagnella, G.A., Markandu, N.D.,
Shore, A.C., Forsling, M.L., MacGregor, G.A. (1987) Plasma atrial natriuretuc peptide: Its
relationship to changes in sodium intake, plasma renin activity and aldosterone secretion in man.
Clin. Sci. 72: 25–30.)
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