Atrial natriuretic peptide does not affect corticotropin-releasing factor-, arginine vasopressin- and angiotensin II-induced adrenocorticotropic hormone release in vivo or in vitro.

The effect of synthetic atrial natriuretic peptide (ANP) was examined on the in vivo and in vitro release of ACTH. Intravenous ANP (4 micrograms/kg body weight) administration did not affect the corticotropin releasing factor (CRF, 4 micrograms/kg body weight)-, arginine vasopressin (AVP, 2 micrograms/kg body weight)- and angiotensin II (A II, 4 micrograms/kg body weight)-induced ACTH release in unanesthetized freely moving rats. ANP did not inhibit the basal, CRF- and AVP-induced release of ACTH in pituitary cell cultures.

Effects of (D-ala2, met5)-enkephalinamide and naloxone on ACTH and corticosterone secretion.

An intravenous administration of (D-ala2, met5)-enkephalinamide (DALA) caused a significant elevation of plasma ACTH and corticosterone at 10 to 20 min after injection in unanesthetized freely moving rats. An intraperitoneal administration of cyproheptadine tended to reduce plasma ACTH and corticosterone levels at 60 min after injection, but it did not attenuate the DALA-induced ACTH and corticosterone elevation. A large dose of naloxone (1-10 mg/kg body weight) caused a significant elevation in plasma corticosterone, but naloxone at 10 mg/kg body weight reduced the basal ACTH level and DALA-induced ACTH elevation.

Effect of indapamide on atrial natriuretic polypeptide receptor in spontaneously hypertensive rat kidney.

The effect of a hypotensive state on atrial natriuretic polypeptide (ANP) receptors of the kidney treated by indapamide was investigated in spontaneously hypertensive rats (SHRs). SHRs aged 12 weeks were injected intraperitoneally with indapamide (10mg/kg/day) for 10 days and an ANP radiolabeled receptor assay (RRA) was done on the 11th day. The systolic blood pressure of SHRs injected with indapamide (IDP group) was statistically lower than that of SHRs injected with 2% gum Arabic solution (control group).

Brain corticotropin releasing factor in the spontaneously hypertensive rat.

Corticotropin releasing factor and vasopressin were measured in major brain regions including the neurohypophysis in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) during development of hypertension. The highest concentration of corticotropin releasing factor was found in the hypothalamus in both strains. Corticotropin releasing factor was decreased in most major brain regions of SHR.

Effect of synthetic atrial natriuretic polypeptide on hemorrhage-induced adrenocorticotropin secretion of the rat.

The effect of synthetic alpha-human atrial natriuretic polypeptide (alpha-hANP) on the in vivo and in vitro release of ACTH and corticosterone was examined. In the in vivo study ACTH and corticosterone responses to rapid 2-ml/rat hemorrhage were measured in sixteen conscious rats after alpha-hANP administration. The hemorrhage increased plasma ACTH and corticosterone concentrations in the control group of rats (p greater than 0.

Multiple endocrine neoplasia with Cushing's syndrome due to paraganglioma producing corticotropin-releasing factor and adrenocorticotropin.

A male patient with corticotropin-releasing factor (CRF) and adrenocorticotropin (ACTH)-producing syndrome is described. Soon after being referred to us the patient developed pneumonia, anaemia, oedema and respiratory distress, and died on the 24th day after admission. Autopsy and histology revealed that he had a rare type of multiple endocrine neoplasia (type 1 + paraganglioma) with a mediastinal paraganglioma, parathyroidal hyperplasia, pancreatic islet cell adenoma, duodenal multiple carcinoid tumours and adrenocortical nodular hyperplasia.

Effect of immobilization stress on neuropeptides and their receptors in rat central nervous system.

The effect of immobilization stress (IM-stress) on the concentration and the receptor binding of substance P (SP), methionine-enkephalin (ME) and thyrotropin-releasing hormone (TRH) was determined in eight brain regions and the spinal cord. The concentration of SP was decreased in the septum, striatum and hippocampus, and SP receptor binding was decreased in the septum, amygdala + pyriform cortex and hypothalamus. Scatchard analysis indicated that the decrease in the SP binding is mainly due to the decrease in the number of receptors.

Starvation-induced changes in rat brain corticotropin-releasing factor (CRF) and pituitary-adrenocortical response.

Starvation-induced changes in CRF concentration in major brain regions and abnormalities in the pituitary-adrenal axis were examined in rats using rat CRF radioimmunoassay. The CRF concentrations in the hypothalamus and cerebellum were significantly reduced in the completely starved rats, while those in the midbrain, thalamus and neurointermediate lobe of the pituitary were significantly increased in the semi-starved or completely starved rats. No significant changes in the CRF concentrations were found in the pons, medulla oblongata and cerebral cortex.

Cortisol responsiveness to insulin-induced hypoglycemia in Cushing's syndrome with huge nodular adrenocortical hyperplasia.

A 51-yr-old male patient with a 3 yr history of Cushing's syndrome is described. The baseline plasma cortisol level was elevated, while the plasma ACTH levels remained at an undetectable level. Dynamic testing of pituitary-adrenal function revealed no suppression after 8 mg of dexamethasone, and there was no response to metyrapone or CRF, while plasma cortisol showed a hyperresponse to synthetic ACTH.

Effect of morphine on hypothalamic corticotropin-releasing factor (CRF) and pituitary-adrenocortical activity.

The effects of intraperitoneal and intra-third ventricular administration of morphine on the hypothalamic corticotropin-releasing factor (CRF) and the pituitary-adrenocortical activity were examined in unanesthetized, freely moving rats. Hypothalamic CRF was measured by rat CRF radioimmunoassay. Intraperitoneal or intra-third ventricular administration of morphine increased blood concentrations of ACTH and corticosterone while intraperitoneal administration tended to increase CRF concentration in the whole hypothalamus including the median eminence and intra-third ventricular administration increased CRF concentration in the hypothalamus excluding the median eminence.

Adrenocorticotropin responses to corticotropin releasing factor and vasopressin in spontaneously hypertensive rats.

The effects of exogenous corticotropin releasing factor and arginine vasopressin were evaluated in 6- and 11-week-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Basal adrenocorticotropic hormone (ACTH) and vasopressin levels did not differ between SHR and WKY, but basal corticosterone level was higher in 6-week-old SHR (p less than 0.01).

Corticotropin-releasing factor (CRF) and vasopressin concentration in major brain regions after adrenalectomy and their involvement in adrenalectomy-induced ACTH elevation.

CRF and vasopressin concentrations in major brain regions after bilateral adrenalectomy and their involvement in adrenalectomy-induced ACTH secretion were investigated. At 5, 14 and 28 days after bilateral adrenalectomy, the plasma ACTH level was greatly elevated, whereas hypothalamic CRF content was reduced at 5 days and was not changed at 14 and 28 days after adrenalectomy. The CRF concentration in the medulla oblongata was reduced at 2-4 weeks after adrenalectomy.

Effect of clonidine on insulin secretion: a case report.

We have recently seen a case of non-insulin-dependent diabetes mellitus with hypertension in which chronic treatment with oral clonidine gave rise to elevation of blood glucose and decreased insulin secretion. When the response of insulin secretion to glucose administration during clonidine therapy was compared with that after 12 days of wash-out for clonidine in this patient (who was then receiving phentolamine mesylate), there was a marked suppression of insulin secretion to stimulation by intravenous glucose during oral clonidine therapy. This result indicates that the decreased insulin secretion associated with oral clonidine therapy is very unlikely to be due to any direct action of clonidine on beta cells of the pancreatic islets and may be due to suppression of catecholamine release via central alpha-adrenergic receptor stimulation.

Mechanism of hematuria. I. Electron microscopic demonstration of the passage of a red blood cell through a glomerular capillary wall in rat masugi nephritis.

Masugi nephritis was induced in Sprague-Dawley rats by an intravenous injection of rabbit anti-rat kidney serum. In the autologous phase of the disease, three of 18 rats manifested continuous hematuria. Ultrastructural examination of renal glomeruli by transmission and scanning microscopy revealed gaps in the basement membranes, and the transcapillary passage of red blood cells through the discontinuous regions in the hematuric rats.

Purification of insulin-binding antibody by affinity chromatography using monocomponent insulin as ligand.

Insulin-binding antibody (IBA) was purified by affinity chromatography using porcine monocomponent (MC) insulin as the ligand. The purity of the antibody was compared with that of the antibody extracted using porcine crystalline (Cr) insulin. Comparing the antibody solutions obtained with MC insulin (MC-lig-sol) or Cr insulin (Cr-lig-sol), the content of IBA in Cr-lig-sol was higher than in MC-lig-sol, but the content of proinsulin-binding antibody (PBA) in MC-lig-sol was very small and statistically lower than that in Cr-lig-sol (P less than 0.

Effects of morphine on hypothalamic corticotropin-releasing factor (CRF), norepinephrine and dopamine in non-stressed and stressed rats.

The effects of morphine on the hypothalamic corticotropin-releasing factor (CRF), norepinephrine (NE) and dopamine (DA) concentrations were investigated in non-stressed and stressed rats. Acutely administered morphine stimulated both the synthesis and release of CRF in the hypothalamus, thereby activating the pituitary-adrenocortical system in non-stressed rats, but inhibited the stress-induced CRF synthesis and ACTH-corticosterone secretion. Either a morphine or ether-laparotomy stress reduced NE and DA concentrations in the hypothalamus.

Reduction of specific arginine-vasopressin binding sites of renal medulla membranes in lithium treated rats.

To elucidate the early effects of lithium treatment on the kidney, arginine-vasopressin (AVP) binding sites in the renal medulla were measured by radiolabeled receptor assay (RRA) in rats injected intraperitoneally with lithium chloride (4 mmol/kg body weight) for 7 days. After the 8th day, urine volume of rats injected lithium (Li group) increased and was significantly larger than that of the control rats that were injected physiological saline (control group). On the same day, the AVP binding capacities of renal medulla membranes of the Li group (Bmax = 28.

Brain corticotropin-releasing factor (CRF) and catecholamine responses in acutely stressed rats.

Ether-laparotomy stress produced a rapid increase in rat hypothalamic CRF concentration, followed by a rapid reduction and subsequent increase. Cold-restraint stress significantly reduced hypothalamic CRF concentration at 15 min after stress onset. Serum ACTH and corticosterone levels were significantly elevated at 15 min after the onset of both stresses.

Reticuloendothelial cell function in autoimmune hemolytic anemia (AIHA): studies on the mechanism of peripheral monocyte activation.

We examined the activity of peripheral blood monocytes in patients with autoimmune hemolytic anemia (AIHA) using an in vitro assay of monocyte-macrophage interaction with erythrocytes and an antibody-dependent cell-mediated cytotoxicity (ADCC) assay. The monocytes of AIHA patients in the hemolyzing period phagocytized autologous sensitized red cells and anti-D coated red cells more avidly than normal control monocytes. There was no significant relationship between phagocytic activity and ADCC activity.