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J Iversen

Publications and source records attributed to J Iversen.

At least 73 records · Page 4Linked to original sources
PubMed1973

Adrenergic receptors and the secretion of glucagon and insulin from the isolated, perfused canine pancreas.

During perfusion with a glucose concentration of 150 mg/100 ml, infusions of l-epinephrine, l-norepinephrine, and d-l-isoproterenol at physiological concentrations of 2 ng/ml for 9 min stimulated secretion of glucagon in a monophasic response pattern, in contrast to the biphasic response normally encountered after glucagon releasing stimuli as previously reported from our laboratory (1971. J. Clin. Invest.50: 2123). Glucagon was stimulated in spite of a glucose concentration which in itself effectively inhibits glucagon release. Release of insulin was strongly inhibited after epinephrine and norepinephrine, and strongly stimulated after isoproterenol. During perfusion with a glucose concentration of 25 mg/100 ml, secretion of glucagon was greatly accentuated by the catechols investigated. Secretion of insulin remained unchanged after epinephrine and norepinephrine, but was stimulated by isoproterenol. The catechol induced glucagon release was suppressed or abolished when the beta-blocking agent propanolol was simultaneously infused at a concentration of 1 muM, while the inhibition of insulin became further accentuated. The catechol induced glucagon release remained unchanged when alpha blockade was performed using either phentolamine (1 muM) or dibenzyline (10 mug/ml), while the inhibition of insulin was converted to a stimulation. Evidence is thus presented that both the alpha cells and the bet cells are under the influence of adrenergic substances, the stimulation of glucagon release being mediated through a beta receptor and the inhibition of insulin release being mediated through an alpha receptor.

Animals↗
PubMed1971

Secretion of glucagon from the isolated, perfused canine pancreas.

Using the isolated, perfused canine pancreas preparation, previously described, the interrelationship of the secretion of pancreatic glucagon and insulin was studied after stimulation with glucose, gastrointestinal hormones, and the amino acid arginine. The results confirm the concept that pancreatic glucagon is a hormone of "glucose need" and suggest that it may be important in a moment to moment control of glucoregulation. The secretion of pancreatic glucagon was stimulated after infusion of gastrin, pancreozymin, and arginine, while no increase was associated with secretin infusion. The magnitude of the increase was closely related to the glucose concentration present in the perfusion medium, being higher and more pronounced during perfusion with low concentrations of glucose (25 mg/100 ml or 50 mg/100 ml). Stimulation of insulin secretion was seen after glucose, gastrin, pancreozymin, secretin, and arginine. The magnitude of the increase was again closely related to the glucose concentration present, this time being higher and more pronounced during perfusion with high glucose concentrations (150 mg/100 ml). Secretion of both pancreatic hormones always followed a biphasic response pattern after the stimuli mentioned, similar to the characteristic release pattern previously described for insulin after an increment in glucose concentration. In order to elucidate whether endogenous pancreatic glucagon possesses an insulinogenic action, as it has been shown to be the case with the administration of exogenous pancreatic glucagon, the time interrelationship of the secretion of pancreatic glucagon and insulin was investigated by determining the initial rise of the hormones after stimulation with gastrin, pancreozymin, and arginine. The rise of glucagon and insulin occurred simultaneously, i.e. inside a 10 sec period. This does not, however, exclude with certainty an insulinogenic role of pancreatic glucagon.

Animals↗
PubMedDate not supplied

Rat liver regeneration after 90% partial hepatectomy.

In previous studies, 90% partial hepatectomy in the rat was invariably accompanied by 100% mortality within 40 hr. This paper describes a technique by which 90% of the liver mass can be removed with only 14% mortality, provided that rats have free access to glucose-containing drinking water. Measurements of total liver DNA, [3H]thymidine labeling index and mitotic index suggest rapid cell proliferation, commensurate with a powerful regenerative stimulus. In the presence of normoglycemia, peripheral insulin and glucagon concentrations were elevated to levels normally observed in the portal vein.

Animals↗
PubMedDate not supplied

Contractility and endothelium-dependent relaxation of resistance vessels in polycystic kidney disease rats.

Hypertension and vascular disease are common complications in autosomal-dominant polycystic kidney disease (ADPKD). The role of changes in morphology and reactivity of resistance vessels in this disease have not previously been studied. Mesenteric resistance arteries were dissected from 8- to 14-week-old heterozygous Han:SPRD polycystic kidney disease (PKD) rats, homozygous normal Han:SPRD littermates (HSPRD) and Sprague-Dawley rats (SD). The morphology, noradrenaline (NA) contractility, endothelium-dependent acetylcholine (ACh) relaxation before and after incubation with L(G)-nitro-L-arginine methyl ester (L-NAME), and endothelium-independent 3-morphollino-sydnonimine (SIN-1) relaxation were studied with the Mulvany-Halpern myograph. Blood pressure and morphology of vessels were the same in all groups of rats, apart from a slightly higher media/lumen ratio in heterozygous PKD rats (p < 0.05). Active wall tension and contractile sensitivity to NA were higher in both heterozygous PKD rats and HSPRD than SD rats (p < 0. 05). The maximum endothelium-dependent relaxation rate was markedly decreased in heterozygous PKD (19 +/- 9%) and HSPRD (34 +/- 12%) compared to SD rats (75 +/- 11%) (p < 0.05). After incubation with L-NAME, ACh-induced relaxation was significantly attenuated in SD rats, less attenuated in HSPRD, and not significantly changed in heterozygous PKD rats. SIN-1-induced endothelium-independent relaxation was similar in all three groups. In conclusion, hyperreactivity to NA and impaired endothelium-dependent relaxation were present in resistance vessels from Han:SPRD rats, especially in animals with PKD. These abnormalities in resistance vessels from PKD rats may be important for the development of hypertension and vascular disease.

Acetylcholine↗
PubMedDate not supplied

Effect of the serotonin receptor agonist, buspirone, on immune function in HIV-infected individuals: a six-month randomized, double-blind, placebo-controlled trial.

PURPOSE: Previous studies have shown that agents modulating the cAMP/PKA pathway have a beneficial effect on immune reconstitution in HIV-infected individuals. Here we evaluate the effect of buspirone on immune function as measured by CD4 and CD8 T-cell counts, CD4/CD8 T-cell ratio, HIV viral load, and response to pokeweed mitogen (PWM) in antiretroviral naive HIV-1-infected individuals. METHOD: Twenty-three HIV-infected patients with CD4 T-cell counts above 300 per microL were enrolled in a 6-month double-blinded placebo controlled trial. No patients received antiretroviral therapy during the study. Blood samples were drawn prior to treatment, after 1 week, 1 month, 3 months, and 6 months, and as a follow-up sample 1 month after completion of study. RESULTS: A significant decrease in CD8+ T-cell counts (p =.02) and an increase in CD4/CD8 ratio (p =.0003) in buspirone-treated patients compared to placebo-treated patients was observed. There were no significant differences in CD4 T-cell counts, HIV viral load, or proliferative response to PWM between those receiving placebo and those receiving buspirone. CONCLUSION: Buspirone treatment leads to significant changes in CD8 T-cell count and in CD4/CD8 ratio. Thus, agents affecting the adenosine 3', 5'-cyclic monophosphate/protein kinase A type 1 (cAMP/PKA-1) pathway may be candidates for positive immune modulation in patients with HIV-1 infection.

Adult↗