Neuronal carbonic anhydrase VII provides GABAergic excitatory drive to exacerbate febrile seizures

Peer reviewe

Neuronal effects of locally formed angiotensin II in human atria

Es wurde gezeigt, dass in vitalen menschlichen Herzvorhofpräparaten eine lokale Konversion von Angiotensin I in Angiotensin II sowohl durch ACE, als auch durch alternative Mechanismen stattfindet. Die präsynaptische, steigernde Wirkung von Angiotensin II auf die stimulationsinduzierte Freisetzung von Noradrenalin aus den sympathischen Fasern in diesem Modell wird durch Blockade jeweils einer der beiden Rezeptorsubtypen AT1 und AT2 inhibiert. Es wird anhand der erhobenen Daten eine Interaktion zwischen beiden Rezeptorsubtypen vermutet.In a model of vital tissue preparations of human atria the existance of a local conversion of angiotensin I to angiotensin II by ACE as well as by alternative mechanisms was shown. In this model the presynaptic enhancing effect of angiotensin II on stimulation induced release of epinephrine from sympathic fibers was diminished by blockade of either the AT1 or the AT2 receptor subtype. From the found data an interaction between both receptor subtypes is hypothesized

Pancreatic Islets Accumulate Cadmium in a Rodent Model of Cadmium-Induced Hyperglycemia

Cadmium (Cd) is an anthropogenic as well as a naturally occurring toxicant associated with prediabetes and T2DM in humans and experimental models of Cd exposure. However, relatively few studies have examined the mechanism(s) of Cd-induced hyperglycemia. The purpose of this study was to examine the role of pancreatic islets in Cd-induced hyperglycemia. Male Sprague–Dawley rats were given daily subcutaneous doses of Cd at 0.6 mg/kg over 12 weeks. There was a resulting time-dependent increase in fasting blood glucose and altered insulin release in vitro. Islets isolated from control (saline-treated) and Cd-treated animals were incubated in low (0.5 mg/mL) or high (3 mg/mL) glucose conditions. Islets from 12 week Cd-treated animals had significantly less glucose-stimulated insulin release compared to islets from saline-treated control animals. The actual Cd content of isolated islets was 5 fold higher than the whole pancreas (endocrine + exocrine) and roughly 70% of that present in the renal cortex. Interestingly, islets isolated from Cd-treated animals and incubated in high glucose conditions contained significantly less Cd and zinc than those incubated in low glucose. These results show that within whole pancreatic tissue, Cd selectively accumulates in pancreatic islets and causes altered islet function that likely contributes to dysglycemia.</jats:p