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This study evaluates the direct effects of verapamil and furosemide infused into the unilateral renal artery on renal function and the renin secretion rate in renal vein-catheterized rabbits. Catheterization did not alter the renal function parameters of the kidney. Verapamil and furosemide increased renal blood flow, urine flow, and urinary sodium, potassium and chloride excretions confined to the infused kidney. Verapamil increased the glomerular filtration rate and free water clearance. The renin secretion rate was increased by furosemide but not by verapamil. The present study shows that the technique is applicable to renal function studies in which unilateral renal arterial infusion of the agents studied is required. The contralateral kidney can be a reliable control for the infused kidney. It also provides a useful technique for the study of renin release in rabbits.

Male Wistar neonatal rats at age 1.5 days (Streptozotocin [STZ] group 1) and 5 days (STZ group 2) received a subcutaneous injection of 90 mg/kg STZ. After 10 weeks, the rats were subjected to an oral glucose tolerance test (OGTT) (2 g/kg) in a conscious state. The pancreas perfusion experiments were conducted 2 weeks after the OGTT. There was no statistical difference in insulin response between the STZ group 1 and the control group. On the contrary, in the STZ group 2, the plasma glucose response to OGTT showed a typical diabetic pattern, and the plasma insulin response was markedly blunted. In the isolated perfused rat pancreas, the infusion of glucose evoked a biphasic insulin secretion, but the peak insulin levels induced by 16.7 mmol/L glucose in the STZ group 1 were significantly lower than in the controls. We further investigated characteristics of insulin secretion in response to different secretagogues in these animal models using isolated islets. The insulin content of the islets of the STZ group 1 were about one half that of the control group. Insulin secretion in the STZ group 1 was impaired in response to glucose stimulation, but remained normal in response to arginine and forskolin. These results suggest that insulin secretion of non-insulin-dependent diabetes mellitus (NIDDM) rat model is selectively impaired in response to glucose stimulation, possibly due to a disorder of signaling mechanism other than adenylate cyclase.

Immunoreactive atrial natriuretic peptide (ir-ANP) was measured in the follicular fluid of pig ovarian follicle, and rabbit ovarian homogenates and perfusates using a specific radioimmunoassay (RIA). Serial dilution curves made with the extracts of follicular fluid, ovarian homogenates and perfusates using SepPak C18 cartridges were parallel with the RIA standard curve. On gel filtration chromatography and reverse phase HPLC, all extracted materials showed high and low molecular weight forms of ir-ANP. The amount of ir-ANP in rabbit ovary was 40.70 +/- 0.39 pg/mg and that in follicular fluid of pig ovarian follicle was 18.88 +/- 2.49 pg/ml.

Polymorphism of 5' portion of the human insulin gene was examined in 188 unrelated Japanese subjects (49 normal, 71 with IDDM, and 68 with NIDDM) using restriction endonuclease analysis. Restriction fragments were classified according to the insertion size: Class 1 (600 base pairs), Class 2 (1300 base pairs), and Class 3 (2000 base pairs). We found a very high frequency of Class 1 alleles (96.8%) and a low frequency of both Class 2 (0.8%) and Class 3 alleles (2.4%) and that approximately 94% of the genotypes were Class 1/Class 1 homozygote. In addition, there was no correlation of allelic or genotypic frequency with NIDDM or IDDM. We conclude that length polymorphism of the human insulin gene cannot be a useful marker for diabetes in Japanese.

Atrial pressure- or distension-induced release of atrial natriuretic peptide (ANP) has been considered as an important regulatory mechanism of ANP release in cardiac atria. A new technique to permit graded continuous atrial distension has been developed in an isolated perfused single rabbit atrium. Graded atrial distension was induced by changing the elevation of the outflow catheter tip. Intra-atrial volume expansion resulted in an increase in immunoreactive ANP release. The graded increase in atrial distension from 43.9 +/- 10.2 to 207.7 +/- 29.1 microliter resulted in 6.2-27.1-fold increases in volume-dependent immunoreactive ANP release. A rise in immunoreactive ANP release induced by increasing atrial distension did not occur in the state of atrial distension but occurred only after return to the reduced distension. However, in the case of atrial distension with pacing, an increase in immunoreactive ANP release was observed during atrial distension with pacing and after return to the basal level. The present study shows that the new technique is applicable to the study of the 'stretch-secretion coupling' mechanism of ANP release in vitro, and that the more important factor involved in the release of immunoreactive ANP induced by atrial distension may be the atrial reduction to basal level after distension rather than the stretch itself.