Effect of hypothyroidism on the in vitro release of atrial natriuretic peptide in response to sodium challenge in rats.

The release of atrial natriuretic peptide (ANP) in vitro in response to the challenge of sodium chloride was investigated in hypothyroid rats. Male rats were injected with propylthiouracil (PTU, 20mg/kg BW, intraperitoneally), or PTU and thyroxine (T4, 20 micrograms/kg BW, subcutaneously) once daily for 14 days before decapitation. Rats injected with saline were used as control. The plasma samples were collected and extracted by Sep-Pak C18 cartridge. The concentrations of ANP in extracted plasma were measured by a radioimmunoassay (RIA). PTU-induced hypothyroidism resulted in decreased concentrations of plasma ANP. Replacement of T4 in PTU-treated hypothyroid rats restored the plasma concentrations of ANP to normal levels. Furthermore, we examined the right atrial ANP contents and the in vitro release of ANP in PTU-treated rats and control animals. The right atrium was excised and divided into 5 equal pieces, one was homogenized with 0.1 N HCl and extracted by Sep-Pak C18 immediately, and the others were incubated with Locke's solution at 37 degrees C. After basal incubation for 30 min, rat atrial tissues were then incubated with 154, 160, or 165 mM NaCl for 30 min. The concentrations of ANP in extracted atrial tissue and medium samples were also measured by RIA. Decreased atrial contents of ANP were noted in hypothyroid rats. The in vitro release of ANP in response to 165 mM sodium ion was significantly lower in PTU than in saline-injected animals. These results suggest that lower concentration of plasma ANP in hypothyroid rats is at least in part due to impairment of stimulation-secretion responses of right atria during thyroid hypofunction in rats.