Thyroid hormones and atrial natriuretic hormone secretion: study in hyper- and hypothyroid patients

1992 ◽  
Vol 127 (1) ◽  
pp. 23-26 ◽  
Author(s):  
Ermanno Rolandi ◽  
Bruno Santaniello ◽  
Marcello Bagnasco ◽  
Angelo Cataldi ◽  
Cristina Garibaldi ◽  
...  

Plasma atrial natriuretic hormone (ANH) values were evaluated in 28 hyperthyroid patients and in 11 hypothyroid patients and compared with 20 healthy subjects. In hyperthyroid patients plasma ANH basal levels were significantly (p<0.01) higher (14.2±1.6 pmol/l) than in controls (7.8±0.4 pmol/l) and in hypothyroid patients (6.4±0.3 pmol/l). No significant differences were found between controls and hypothyroid patients. The propranolol-induced decrease in heart rate in hyperthyroid patients did not significantly affect the plasma ANH values. Conversely, after the methimazole-induced euthyroidism a return within the normal range of ANH values was observed. The thyroxine replacement in hypothyroid patients determined a small but significant (p<0.05) increase in plasma ANH values. Observed data suggest that in humans thyroid hormones may influence plasma ANH concentrations independently of their effect on heart rate.

1989 ◽  
Vol 257 (4) ◽  
pp. E583-E587 ◽  
Author(s):  
Y. Shenker

To evaluate the effect of very low-dose infusion of atrial natriuretic hormone (ANH) on aldosterone regulation, seven normal young men were infused for 2.5 h with 0.47 pmol.kg-1.min-1 of human [Ser-Tyr28]ANH or placebo. During the last 0.5 h 4 pmol.kg-1.min-1 of angiotensin II were also infused. ANH plasma levels increased from 3.46 +/- 0.25 to a maximum of 6.80 +/- 0.88 pmol/l, which is well within normal limits. Plasma aldosterone decreased almost 40%, from 40.7 +/- 5.7 to 25.9 +/- 4.9 ng/dl after 2 h. ANH infusion caused a slight decrease in blood pressure and slight increase in renal excretion of sodium and potassium. These results suggest that even small changes in ANH levels, within the normal range, have physiological significance, particularly in aldosterone regulation.


1987 ◽  
Vol 252 (6) ◽  
pp. E740-E745 ◽  
Author(s):  
J. A. Sanfield ◽  
Y. Shenker ◽  
R. J. Grekin ◽  
S. G. Rosen

Six normal human subjects each underwent sequential 80-min infusions of saline and epinephrine (EPI) at 0.55 and 2.75 micrograms X min-1 X m-2 to determine the role of EPI in the control of atrial natriuretic hormone (ANH) in humans. Plasma immunoreactive-ANH (IR-ANH) levels nearly doubled in response to the infusion of EPI at 0.55 microgram X min-1 X m-2 (P less than 0.05) and then plateaued; heart rate accelerated significantly (P less than 0.01) with increasing plasma EPI levels, whereas systolic blood pressure increased only with higher plasma EPI levels (P less than 0.05). To determine whether beta-adrenergic mechanisms mediate the EPI-induced increase in IR-ANH, six additional subjects each received infusions on two separate days of saline for 240 min and the beta-adrenergic antagonist propranolol followed by propranolol plus EPI at 2.75 micrograms X min-1 X min-2 each for 80 min. Neither saline nor propranolol plus EPI caused a significant increase in plasma IR-ANH. We conclude that EPI increases plasma IR-ANH through beta-adrenergic mechanisms in humans. beta-Adrenergic-mediated increases in plasma IR-ANH levels appear to be unrelated to changes in the heart rate.


Life Sciences ◽  
1987 ◽  
Vol 41 (13) ◽  
pp. 1635-1644 ◽  
Author(s):  
Yoram Shenker ◽  
Friedrich K. Port ◽  
Richard D. Swartz ◽  
Milton D. Gross ◽  
Roger J. Grekin

1988 ◽  
Vol 152 (2) ◽  
pp. 893-897 ◽  
Author(s):  
Adam Johnson ◽  
Ferzan Lermioglu ◽  
Uttam C. Garg ◽  
Rebecca Morgan-Boyd ◽  
Aviv Hassid

Author(s):  
Howard R. Champion ◽  
Nova L. Panebianco ◽  
Jan J. De Waele ◽  
Lewis J. Kaplan ◽  
Manu L. N. G. Malbrain ◽  
...  

1992 ◽  
Vol 126 (3) ◽  
pp. 217-223 ◽  
Author(s):  
Tokihisa Kimura ◽  
Kozo Ota ◽  
Masaru Shoji ◽  
Minoru Inoue ◽  
Kazutoshi Sato ◽  
...  

To assess whether arginine vasopressin and atrial natriuretic hormone participate in impaired urinary dilution and excretion in glucocorticoid deficiency secondary to hypopituitarism. an acute oral water load of 20 ml·kg−1 BW was undertaken in the absence and presence of an oral hydrocortisone (60 mg) treatment in patients with ACTH deficiency (N= 7) and panhypopituitarism (N = 2). Plasma arginine vasopressin and atrial natriuretic hormone and renal water handling were simultaneously determined and compared with those in similarly water-loaded normal subjects. Plasma arginine vasopressin did not fall in response to decreased blood osmolality after an acute water load in the absence of hydrocortisone; plasma atrial natriuretic hormone did not change despite blood volume expansion; and impairment in urinary dilution and excretion remained. On the other hand, in the presence of hydrocortisone, plasma arginine vasopressin fell in response to a decrease in plasma osmolality and plasma atrial natriuretic hormone increased, thereby restoring urinary dilution and excretion. These results demonstrate that the impaired arginine vasopressin response to acute water loading play an essential role in deranged renal water and electrolyte handling in the state of glucocorticoid deficiency; the impaired release of atrial natriuretic hormone also may affect these disorders.


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