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Abstract. To assess whether atrial natriuretic peptide (ANP) and arginine vasopressin (AVP) participate in impaired water excretion in patients with hypothyroid states (HS), an oral acute water loading (WL) test (20 ml/kg.BW/45 min) was performed before and after L-thyroxine (T4) treatment in 5 hypothyroid patients. Plasma ANP, AVP, osmolality (Posm), total protein and renal water excretion were simultaneously determined, and these data were compared to the data from five normal subjects (NS). The impaired water excretion rate in HS was entirely improved in the euthyroid states (ES) after T4 therapy for at least 7 months. Plasma ANP in HS was lower than that in NS (5.9± 0.9 vs. 16.5 ± 3.6 pmol / L, P<0.05), but increased after T4 treatment (21.2±5.7 pmol / L, P<0.05). Plasma AVP in HS (1.6± 0.5 pmol / L) showed a tendency to be lower than those in ES and NS (2.9 ± 0.4 and 2.9 ± 0.7 pmol / L), but did not respond to a fall in Posm after WL, unlike ES and NS. Significant positive correlation were noticed between Posm and plasma AVP in ES and NS, but not in HS. These results suggest that not only the impaired release and/or metabolisms of AVP and ANP, but also derangement of renal water and electrolytes handling might induce attenuation of CHZO formation in hypothyroid states.

To assess the central role of interleukin 1-beta (IL-1 beta) in the release of ACTH, vasopressin (AVP) and atrial natriuretic peptide (ANP) and in the regulation of blood pressure and thermogenesis, 3 ng (0.173 pM) x 100-1 x BW-1 (LIL), 30 ng (1.73 pM) x 100g-1 x BW-1 (MIL), and 150 ng (8.63 pM) x 100g-1 x BW-1 (HIL) of human IL-1 beta dissolved in sterile saline were injected intracerebroventricularly to conscious rats. In the control rats, saline alone (5 microliters) was administered. In three other groups, rats were pretreated with indomethacin, a cyclooxygenase inhibitor, given i.v. (1 mg x 100g-1 x BW-1); medium and high doses of IL-1 beta or its vehicle were given. In the LIL group, IL-1 beta increased blood pressure, body temperature and plasma AVP and ANP without any changes in heart rate (HR) and plasma ACTH. In the MIL group, plasma ACTH was increased, and changes in the other parameters were similar to those in the LIL group. In the HIL group, however, the pressor and thermogenetic responses were attenuated; plasma AVP, ACTH, and ANP were increased; and HR was unchanged. In the control (CON) group, none of these parameters was changed throughout the studies. Indomethacin abolished the AVP and ACTH responses to IL-1 beta, but potentiated the pressor and hypothermic responses and increased plasma ANP. These data suggest that the actions of IL-1 beta on AVP and ACTH release and thermogenesis, but not on blood pressure and the release of ANP, are modulated by the stimulated central production of prostaglandins.

In order to investigate the role of central alpha 1- and alpha 2-adrenoceptors in the control of vasopressin (ADH) release and the cardiovascular system, norepinephrine (NE) (1.4 microgram/kg), methoxamine (1.4 microgram/kg), yohimbine (60 micrograms/kg), and prazosin (40 micrograms/kg) were administered via the cerebral ventricles in urethane-chloralose-anesthetized dogs after morphine sedation (n = 42). In the control study 0.9% saline was administered. NE resulted in a significant fall in blood pressure, heart rate, and ADH release. Methoxamine tended to activate the cardiovascular system, but did not affect the release of ADH significantly. Prazosin decreased blood pressure significantly with a significant rise in heart rate and ADH release. Pretreatment with prazosin did not block significantly the effect of NE on blood pressure, heart rate, and ADH release. Yohimbine did not affect the cardiovascular system and ADH release significantly. Pretreatment with yohimbine completely blocked the effect of NE on ADH release, and brought about a slight rise in blood pressure and heart rate. In none of the experiments could changes in ADH release be attributed to changes in plasma osmolality. These results indicate that central alpha 1-adrenoceptors might act to activate the cardiovascular system, but have no effects on ADH release in anesthetized dogs. On the other hand, central alpha 2-adrenoceptors might act to reduce ADH release and to depress the cardiovascular system.

A 64-year-old man was admitted to the emergency center of Furukawa City Hospital because of common cold-like symptoms and hypotension. He was diagnosed as fulminant myocarditis with cardiogenic shock and arrhythmia elicited by influenza virus subtype A. Cardiac angiography, echocardiography and biopsy also showed myocarditis, and serum antibody titer to influenza virus subtype A was increased to 4-fold in paired serums. Treatments of both percutaneous cardio-pulmonary support (PCPS) and intra-aortic balloon pumping (IABP) were carried out to sustain the general circulation. PCPS treatment was discontinued on the 25th day of the admission, but IABP was continued. Finally, he died of multiple organ failure. The autopsy revealed myocardial necrosis with a slight fibrosis and a small amount of lymphocytic infiltration into the ventricular wall, which were compatible with restrictive myocarditis. Moreover, immunohistochemical analysis also showed the presence of viral antigens in cardiac myocytes. This case clearly showed that PCPS and IABP can be beneficial to sustain the general circulation in fulminant myocarditis, but cardiac pumping function failed completely to recover from myocardial damage.

To assess the mutual relationship between acute osmotic stimulation and arginine vasopressin (AVP) gene expression, 2 ml/100 g body weight of 0.9 M NaCl was intraperitoneally administered into conscious rats. They were decapitated to collect blood and brain samples before and 15 min and 1, 3, 6, and 9 h after the injection. The total RNA from the hypothalamus or whole brain tissue was used to determine AVP mRNA by Northern blot analyses with a complementary DNA probe. Plasma AVP and osmolality increased rapidly and transiently 15 min and 1 and 3 h after the injection. AVP mRNA was detected in the hypothalamus but not in the brain tissue without hypothalamus under basal and stimulated conditions. Brain AVP mRNA increased 2.2-fold at 3 h and 1.7-fold at 6 h (P < 0.05-0.01). These increases appeared to be due to the appearance of AVP mRNA with the shorter migration in the gel. These results suggest that an acute osmotic challenge increases AVP mRNA with size heterogeneity within the hypothalamo-hypophyseal tract.

To assess the interaction of endothelin (ET) with atrial natriuretic peptide (ANP) on cardiovascular and renal function, arginine vasopressin (AVP) release, and the renin-angiotensin-aldosterone system, either a low or high dose of ET (4 or 12 pmol.kg-1.min-1) was administered with ANP (26 pmol.kg-1.min-1) for 45 min after the initial infusion of ANP alone in anesthetized dogs. In the other groups, either ANP or saline alone was administered for 90 min. ANP alone decreased blood pressure (BP), cardiac output (CO), plasma aldosterone, and plasma renin activity (PRA), increased urinary Na and K excretion (UNaV and UKV, respectively) and urine flow (UF), but did not affect plasma AVP. The low dose of ET had no effect on these ANP-induced changes. However, the high dose of ET curtailed the responses to ANP, increased BP and PRA, and decreased UNaV, UKV, and UF associated with decreased renal plasma flow and glomerular filtration rate. High ET also further potentiated the decrease in CO and the increase in total peripheral resistance induced by ANP and increased plasma AVP. These results indicate that a dose of ET one-half that of ANP (on the molar ratio) may have completely counteracted vascular, hormonal, and renal responses to ANP.

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