A case of progressive systemic sclerosis (PSS) with silent thyroiditis and anti-bovine thyrotropin antibodies.

We have examined a patient with progressive systemic sclerosis (PSS) who had increased serum T3 (235 ng/dl) and T4 (13.2 micrograms/dl) and low 24-h thyroidal 123I-uptake (1.2%).

[Release mechanisms of inactive renin from rat renal cortical slices: role of the submandibular gland].

In our previous studies, we showed an in vivo stimulating effect of the extract of the rat submandibular gland on plasma inactive renin release. In this study, we evaluated the effects of the rat submandibular gland extract and of some plasma active renin stimulants on inactive renin release from rat renal cortical slices. Adult male Wistar rats (250-350g) were kept on a regular diet (Na 260mg/100g) and nephrectomized under pentobarbital anesthesia (50mg/kg, i.

[Roles of the kidney in activation and release of plasma inactive renin in the rat].

Plasma inactive as well as active renin is supposed to originate from the kidney, though there is little direct evidence. As we have previously reported (Sakanaka et al., Folia Endocrinol.

[Role of the submandibular glands in in vivo mechanisms of plasma inactive renin release in the rat].

In our present studies, we evaluated the role of the submandibular glands (SMG) on plasma inactive renin (PIR) releasing mechanisms in rats using some agents which are known to stimulate plasma active renin (PAR) release. The results were analyzed between sialoadenectomized (SX) and sham-operated (control: C) rats. Twenty-four h after the operation, PAR releasing agents, furosemide (FRO) 2.

Increased furosemide-sensitive sodium influx into erythrocytes in non-insulin-dependent diabetes mellitus associated with hypertension.

Our previous study demonstrated increased sodium (Na+) influx into ouabain-treated erythrocytes in diabetic patients with hypertension. The present study was designed to estimate the effect of furosemide on the Na+ influx in non-insulin-dependent diabetes mellitus (NIDDM) with hypertension. Both Na+ influx in the absence of furosemide (total Na+ influx; TNaI) and furosemide-sensitive Na+ influx (FSNaI) were increased in patients with essential hypertension (group 1, n = 22) than those in non-diabetic, normotensive control subjects without family history of hypertension (control group, n = 26, P less than 0.