Sodium and water retention is characteristic of edematous disorders including cardiac failure, cirrhosis, nephrotic syndrome and pregnancy. In recent years the use of a sensitive radioimmunoassay for plasma vasopressin has implicated the role of nonosmotic vasopressin release in the water retention of these edematous disorders. In experimental studies and studies in humans it has been found that the nonosmotic release of vasopressin is consistently associated with activation of the sympathetic nervous and renin-angiotensin-aldosterone systems. Moreover, the sympathetic nervous system has been shown to be involved in the nonosmotic release of vasopressin (carotid and aortic baroreceptors) and activation of the renin-angiotensin system (renal beta-adrenergic receptors). These findings have led to our proposal that body fluid volume regulation involves the dynamic interaction between cardiac output and peripheral arterial resistance. In this context neither total extracellular fluid (ECF) volume nor blood volume are determinants of renal sodium and water excretion. Rather, renal sodium and water retention is initiated by either a fall in cardiac output (e.g. ECF volume depletion, low-output cardiac failure, pericardial tamponade or hypovolemic nephrotic syndrome) or peripheral arterial vasodilation (e.g. high-output cardiac failure, cirrhosis, pregnancy, sepsis, arteriovenous fistulae and pharmacologic vasodilators). With a decrease in effective arterial blood volume (EABV), initiated by either a fall in cardiac output or peripheral arterial vasodilation, the acute response involves vasoconstriction mediated by angiotensin, sympathetic mediators and vasopressin. The slower response to restoring EABV involves vasopressin-mediated water retention and aldosterone-mediated sodium retention. The renal vasoconstriction which accompanies those states that decrease EABV, by either decreasing cardiac output or causing peripheral arterial vasodilation, limits the distal tubular delivery of sodium and water thus maximizing the water-retaining effect of vasopressin and impairing the normal escape from the sodium-retaining effects of aldosterone. The elevated glomerular filtration rate and filtered sodium load in pregnancy allows increased distal sodium and water delivery in spite of a decrease in EABV, thus limiting edema formation during gestation.
This review has examined the pathophysiology of vasopressin in the edematous disorders of cardiac failure, cirrhosis, nephrotic syndrome and pregnancy and proposed a unifying hypothesis of body fluid volume regulation. A decrease in the EABV secondary to either a decreased cardiac output or a decrease in peripheral arterial resistance is proposed as the initiator of sodium and water retention. This decreased EABV leads to nonosmotic release of vasopressin and to activation of the sympathetic nervous and renin-angiotensinaldosterone systems. Nonosmotic release of vasopressin leads to water retention while increased secretion of aldosterone, and failure to escape from the hormones sodium-retaining effect, leads to sodium retention in edematous disorders.
Exceptions to the above statements may exist in nephrotic syndrome and pregnancy. In nephrotic syndrome, the kidney is diseased and intrarenal mechanisms may lead to expansion of the arterial vascular tree and suppression of the renin-angiotensin-aldosterone system. In pregnancy, the increased glomerular filtration rate and increased distal delivery of sodium and water “aldosterone escape” to occur.

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We studied the interaction between somatostatin receptors and inhibitory GTP binding protein in rat cerebrocortical membranes. Guanine nucleotides reduced [¹²⁵I-Tyr¹] somato-statin binding to cerebrocortical membranes in a dose-dependent manner with rank order of potency being guanyl-5′-yl-imidodiphosphate (Gpp (NH) p) >GTP>GMP. Maximum reduction of the binding to 32% of control was observed in the presence of 10^-5M Gpp (NH) p. Scatchard analysis of the labeled somatostatin binding revealed that the decrease in the binding by Gpp (NH) p was due to the decrease in the binding affinity for somatostatin. Divalent cations, such as Mg⁺⁺, Mn⁺⁺ and Ca⁺⁺, caused an increase in labeled somatostatin binding to membranes with the maximum binding observed at a concentration of 10, 10, 1 mM, respectively. However, Na⁺ decreased a labeled somatostatin binding in a dose-dependent manner, and half maximum inhibition of the binding was observed at 10mM Na⁺. Moreover, Gpp (NH) p and Na⁺ lowered labeled somatostatin binding in an additive fashion. When cerebrocortical membranes were treated at 37°C for 40min with various concentrations of Islet-Activating-Protein (IAP), which had been preactivated with dithiothreitol, sub-sequent labeled somatostatin binding to the membranes was decreased in a dose-dependent manner. 30μ/ml TAP treatment caused a decrease in the binding to 50% of control, which was characterized by the decreased binding affinity without a significant change in the binding capacity. Furthermore, exposure of IAP plus NAD to cerebrocortical membranes caused ADP-ribosylation of a membrane protein with Mr=41,000 on autoradiogram. Such an TAP treatment of cerebrocortical membranes abolished the inhibitory effect of somatostatin on vasoactive intestinal peptide-stimulated increase in adenylate cyclase activity. These results suggest that somatostatin receptors in the brain couple to inhibitory GTP binding protein, which mediates adenylate cyclase inhibition by somatostatin.

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Primary extramedullary plasmacytoma (PEMP) of the thyroid is rare. Only nine patients with PEMP of the thyroid have been reported in Japan to date. We describe an additional autopsy case with PEMP of the thyroid and review of the literature in Japan. A 67-year-old women complaining of swelling of the anterior neck exhibited thin scalp hair, edematous face and a giant, hard, nodular goiter. Laboratory examination showed elevated levels of ESR, collagenous reaction, gammaglobulin, and a M-bow of the IgG-k type in immunoelectrophoresis. No Bence-Jones protein was found in the urine. Thyroid function test revealed a subclinically hypothyroid state, showing a T₃ of 1.32 ng/ml, a T₄ of 10.0 μg/dl, a TSH of 23.4μU/ml and positive thyroid antibodies. The scintigram and the CT scan of the thyroid showed deviation of the trachea by the thyroid tumor and calcification within homogeneous thyroid gland. She underwent total thyroidectomy becasue of suspected malignancy. The histological examination of the removed thyroid weighing 117gr revealed a proliferation of plasma cells and lymphocytes and small amounts of atrophied thyroid follicles. The immunohistological examination of the removed thyroid showed the monoclonality to IgG-k chain. Plasma cells were stainable with methylgreen-pyronine. Twenty-six months after thyroidectomy, she died due to progressive emaciation, anemia, hypoalbuminemia and ascites. Postmortem examination revealed widespread metastasized plasma cell tumors in the liver, intestine, spleen and mesentry with ishemic changes in heart and kidney. Based on our autopsy case and the nine cases reported in Japan, clinical and histological characteristics of PEMP of the thyroid were discussed.

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