SUMMARYCockroach salivary glands are innervated by dopaminergic and serotonergic neurons. Both transmitters elicit saliva secretion. We studied the distribution pattern of neurons containing ␥-aminobutyric acid (GABA) and their physiological role . Immunofluorescence revealed a GABA-immunoreactive axon that originates within the subesophageal ganglion at the salivary neuron 2 (SN2) and this extends within the salivary duct nerve towards the salivary gland. GABA-positive fibers form a network on most acinar lobules and a dense plexus in the interior of a minor fraction of acinar lobules. Co-staining with anti-synapsin revealed that some putative GABAergic terminals seem to make pre-synaptic contacts with GABA-negative release sites. Many putative GABAergic release sites are at some distance from other synapses and at distance from the acinar tissue. Intracellular recordings from isolated salivary glands have revealed that GABA does not affect the basolateral membrane potential of the acinar cells directly. When applied during salivary duct nerve stimulation, GABA enhances the electrical response of the acinar cells and increases the rates of fluid and protein secretion. The effect on electrical cell responses is mimicked by the GABA B receptor agonists baclofen and SKF97541, and blocked by the GABA B receptor antagonists CGP52432 and CGP54626. These findings indicate that GABA has a modulatory role in the control of salivation, acting presynaptically on serotonergic and/or dopaminergic neurotransmission.

Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp (LV) dilation. 1 This subgroup (ie, those with dilated cardiomyopathy: DCM) constitutes the third most common type of heart failure and is the most frequent indication for heart transplantation. 2 Etiological aspects of LV dilation in DCM are under intense current investigation. 3-5 Among other factors, imbalance in the cardiac extracellular matrix (ECM) is believed to be a key pathogenic factor of ventricular chamber dilation in heart failure. This includes increased accumulation of collagens, disturbance in ECM-regulating factors such as metalloecent-onset cardiomyopathy (ROCM), described as nonischemic and nonvalvular ventricular dysfunction with cardiac symptoms of less than 6 months' duration, is a relevant cause of heart failure and includes increased morbidity and mortality. 1 Patients with ROCM show great variation in the clinical course, which ranges from sufficient myocardial recovery to end-stage heart failure and increased mortality. Background: Ventricular dilation is known as a pivotal predictor in recent-onset cardiomyopathy (ROCM), but its pathophysiology is not fully understood. In the present study we investigated whether single-cell stiffness of right and left ventricular-derived fibroblasts has an effect on cardiac phenotype in patients with ROCM.

ENaC-dependent and thiazide-sensitive sodium-retaining mechanisms are not overactive in sunitinib-induced hypertension but ENaC blockers and in particular thiazides may be suitable for its treatment.

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