Miyuki Ishibashi

Plasma levels of atrial natriuretic peptide during normal pregnancy and in pregnancy complicated by hypertension

To clarify a possible role for atrial natriuretic peptide in the pathophysiology of pregnancy complicated by hypertension, we studied plasma levels of atrial natriuretic peptide in 176 pregnant women with or without hypertension. Plasma atrial natriuretic peptide levels in normal pregnant women showed a gradual increase as pregnancy advanced, but the mean (+/- SD) concentrations in women in each trimester (34.8 +/- 14.7 pg/ml in the first trimester, n = 35; 38.7 +/- 12.2 pg/ml in the second trimester, n = 34; and 43.1 +/- 20.0 pg/ml in the third trimester, n = 71) did not differ statistically from the mean plasma atrial natriuretic peptide level in nonpregnant women (38.2 +/- 13.6 pg/ml, n = 44). In contrast, plasma atrial natriuretic peptide levels were elevated in 9 of the 12 women who had hypertension. The mean plasma atrial natriuretic peptide concentration in these patients (162 +/- 95.2 pg/ml) was significantly (p less than 0.01) higher than in normal pregnant women and in nonpregnant controls. On the other hand, 11 pregnant women with proteinuria or edema but without hypertension had normal plasma atrial natriuretic peptide levels. These results suggest that plasma atrial natriuretic peptide levels are normal in women during uncomplicated pregnancy, while the levels are elevated in pregnancy complicated by hypertension. Increased atrial natriuretic peptide secretion in the latter condition may reflect a mechanism of compensation that operates in response to water and sodium retention.

Hyponatremia in small cell lung cancer: mechanisms not involving inappropriate ADH secretion

A 62‐year‐old man with small cell carcinoma (oat cell type) of the lung who had hyponatremia and renal sodium loss with inappropriate antidiuresis is reported. Plasma levels of arginine vasopressin (AVP) were not elevated inappropriately. Plasma levels of atrial natriuretic peptide (ANP), however, were high, and increased after water loading and hypertonic saline infusion. The renin‐aldosterone axis was normal, as were adrenal, thyroid, and renal functions. Water restriction to 500 to 700 ml/d resulted in a rise in serum sodium. Analysis of the tumor tissue failed to demonstrate the presence of AVP or ANP. The findings (1) suggest that hyponatremia and renal sodium loss with inappropriate antidiuresis observed in the patient is due to an antidiuretic substance distinct from AVP, and (2) point to the possibility that hypersecretion of ANP may play a role in the pathophysiology.

Multiple endocrine neoplasia type i with Cushing's disease, primary hyperparathyroidism, and insulin-glucagonoma

A case of multiple endocrine neoplasia type I (MEN I) consisting of Cushings disease, primary hyperparathyroidism, and insulin‐glucagonoma is described. This condition was treated successfully by transsphenoidal pituitary adenomectomy, subtotal parathyroidectomy, and enucleation of pancreatic tumors. Histologic features showed a basophilic adenoma in the pituitary, chief cell hyperplasia in the parathyroid, and islet cell adenomas in the pancreas. The rarity of multiple endocrine hyperfunctioning states and the pathophysiology created by the combination of these three diseases in this patient are of interest.

Atrial natriuretic peptide with artificial pacemakers

Abstract Accumulating evidence indicates that atrial natriuretic peptide (ANP) is a circulating hormone in humans. 1–4 Plasma levels of ANP increase in patients with various heart diseases such as paroxysmal atrial arrhythmias 2 and congestive heart failure. 3,4 If atrial stretching due to increased atrial pressure stimulates ANP secretion, 4 plasma ANP levels may be altered in patients with bradyarrhythmias and in those with pacemaker syndrome, a major clinical complication in patients in whom artificial pacemakers are implanted. 5 To clarify the role of ANP in the pathophysiology of these states, we examined plasma ANP levels in patients with bradyarrhythmias and in those treated with pacemakers of various modes.

Atrial natriuretic peptide and vasopressin during percutaneous transvenous mitral valvuloplasty and relation to renin-angiotensin-aldosterone system and renal function

To study the relation between plasma atrial natriuretic peptide (ANP) and cardiac pressure, and to assess the pathophysiologic significance of ANP in water and electrolyte metabolism, the changes in plasma levels of ANP and arginine vasopressin (AVP) were examined in 11 patients with mitral stenosis who underwent percutaneous transvenous mitral valvuloplasty, and compared with the changes in the renin-angiotensin-aldosterone system and renal function. Immediately after valvuloplasty, plasma ANP levels decreased significantly with a concomitant decrease in mean pressures in the left atrium, the pulmonary artery and the right atrium. Plasma ANP levels decreased to the normal range in 4 of the 6 patients with normal sinus rhythm, while all 5 patients with atrial fibrillation had higher levels despite a similar degree of decrease in atrial pressure. There were significant positive correlations between plasma ANP levels and the mean left atrial pressure (r = 0.61, p less than 0.01), the mean pulmonary arterial pressure (r = 0.49, p less than 0.01) and the mean right atrial pressure (r = 0.54, p less than 0.01). The mean plasma AVP levels, on the other hand, showed a transient increase after valvuloplasty from 0.5 +/- 0.1 to 1.2 +/- 0.4 pg/ml (p less than 0.05). The mean plasma renin activity (1.3 +/- 0.3 vs 2.7 +/- 0.8 ng/ml/hr, p less than 0.05) and plasma aldosterone concentration (8.6 +/- 2.3 vs 17.2 +/- 5.2 ng/dl, p less than 0.05) also increased significantly 30 minutes after valvuloplasty.(ABSTRACT TRUNCATED AT 250 WORDS)

Serum levels of neurophysin in pregnancy and in the postpartum period: Relation to 17β-estradiol levels

Changes in serum neurophysin levels were studied in women during normal pregnancy and after delivery. Neurophysin was elevated as early as the sixth week of gestation and gradually increased until, at the latest, the twentieth week. A significant positive correlation was obtained between serum concentrations of neurophysin and those of 17beta-estradiol. In serum samples with 17beta-estradiol levels exceeding 5 ng/ml, neurophysin was consistently elevated above the normal control range. After delivery, serum neurophysin concentrations declined quite rapidly. The levels returned to those of nonpregnant women by 6 days postpartum. These results support the view that a high rate of secretion of 17beta-estradiol may be one of the factors responsible for the elevated levels of serum neurophysin in pregnancy and that this effect disappears rapidly after the disposal of estrogen, independent of the duration of the elevated estrogen levels.