The binding of insulin (IMS) and glucagon (GL) on isolated rat hepatocytes during the process of liver regeneration after partial hepatectomy was determined. Adult male rats were subjected to 65-70 % partial hepatectomy, control animals were sham-operated. The binding of radioiodine labelled IMS and GL to isolated hepatocytes was determined 1, 2, 3 and 5 days after the surgery. The plasma levels of IMS and glucose and microviscosity of liver plasma membranes were also measured. The decrease of IMS receptor binding capacity was found 1, 2, and 3 days after operation. Mo differences in sham and partially hepatectomized groups in IMS binding were noted 5 days after operation. A single insulin injection during the process of regeneration did not affect these changes of IMS binding to hepatocytes. The increase of GL binding was observed on the third day after partial hepatectomy, however, on the 5th day no changes of GL binding to its receptors were noted. The plasma insulin and glucose levels were similar in both hepatectomized and sham-operated rats. The increase of plasma membrane microviscosity of hepatocytes during the process of liver regeneration and a negative correlation between IMS binding and membrane microviscosity were found. These results demonstrated significant changes in binding parameters of both IMS and GL receptors in hepatocytes during liver regeneration induced by partial hepatectomy.
The purpose of this study was to elucidate the intestinal serotonin (5-HT) receptor subtypes involved in fluid transport in the pig jejunum in uioo. The fluid accumulating effect of intraluminally administered 5-HT, renzapride, methysergide, ketanserin, granisetron, citalopram and intravenous indomethacin, was tested in tied- off loops in uiuo. 5-HT caused a dose-dependent fluid accumulation, which was reduced by indomethacin by about 30 %. Renzapride, methysergide, ketanserin, granisetron and citalopram all caused fluid accumulation. Taking into account these fluid accumulating effects, renzapride, methysergide, ketanserin and granisetron reduced the fluid accumulating effect of 5-HT, giving a maximal reduction of 70, 46, 76, and 80 %, respectively. These data suggest the existence of intestinal 5-HT receptor subtypes involved in fluid transport in the pig jejunum. The antagonistic effects of indomethacin, ketanserin and granisetron, suggest the involvement of prostangladins, as well as the 5-HT2 and the 5-HT3 receptor subtypes in the fluid accumulating response of 5-HT.
The effect of L-glutamate, kainate and N-methyl-D-aspartate (NMDA) on membrane currents of astrocytes, oligodendrocytes and their respective precursors was studied in acute spinal cord slices of rats between the ages of postnatal days 5 and 13 using the whole-cell patch-clamp technique. L-glutamate (10~3 M), kainate (10-3 M), and NMDA (2xl0-3 M) evoked inward currents in all glial cells. Kainate evoked larger currents in precursors than in astrocytes and oligodendrocytes, while NMDA induced larger currents in astrocytes and oligodendrocytes than in precursors. Kainate-evoked currents were blocked by the AMPA/kainate receptor antagonist CNQX (10-4 M) and were, with the exception of the precursors, larger in dorsal than in ventral horns, as were NMDA-evoked currents. Currents evoked by NMDA were unaffected by CNQX and, in contrast to those seen in neurones, were not sensitive to Mg2 + . In addition, they significantly decreased during development and were present when synaptic transmission was blocked in a Ca2+-free solution. NMDA-evoked currents were not abolished during the block of K+ inward currents in glial cells by Ba2+; thus they are unlikely to be mediated by an increase in extracellular K+ during neuronal activity. We provide evidence that spinal cord glial cells are sensitive to the application of L-glutamate, kainate and transiently, during postnatal development, to NMDA.
a1_Vascular resistance in the mammalian pulmonary circulation is affected by many endogenous agents that influence vascular smooth muscle, right ventricular myocardium, endothelial function, collagen and elastin deposition, and fluid balance. When the balance of these agents is disturbed, e.g. by airway hypoxia from high altitude or pulmonary obstructive disorders, pulmonary hypertension ensues, as characterized by elevated pulmonary artery pressure (PPA). Among neuropeptides with local pulmonary artery pressor effects are endothelin-1 (ET-1), angiotensin II (AII), and substance P, and among mitigating peptides are calcitonin gene-related peptide (CGRP), adrenomedullin (ADM), atrial natriuretic peptide (ANP), vasoactive intestinal peptide (VIP) and ET-3. Moreover, somatostatin28 (SOM28) exacerbates, whereas SOM14 decreases PPA in hypoxic rats, with lowering and increasing of lung CGRP levels, respectively. Pressure can also be modulated by increasing or decreasing plasma volume (VIP and ANP, respectively), or by induction or suppression of vascular tissue remodeling (ET-1 and CGRP, respectively). Peptide bioavailability and potency can be regulated through hypoxic up- and down- regulation of synthesis or release, activation by converting enzymes (ACE for AII and ECE for ET-1), inactivation by neutral endopeptidase and proteases, or by interaction with nitric oxide (NO). Moreover, altered receptor density and affinity can account for changed peptide efficacy. For example, upregulation of ETA receptors and ET-1 synthesis occurs in the hypoxic lung concomitantly with reduced CGRP release. Also, receptor activity modifying protein 2 (RAMP2) has been shown to confer ADM affinity to the pulmonary calcitonin-receptor-like receptor (CRLR). We recently detected the mRNA encoding for RAMP2, CRLR, and the CGRP receptor RDC-1 in rat lung., a2_The search for an effective, lung selective treatment of pulmonary hypertension will likely benefit from exploring the imbalance and restoring the balance between these native modulators of intrapulmonary pressure. For example, blocking of the ET-1 receptor ETA and vasodilation by supplemental CGRP delivered i. v. or via airway gene transfer, have proven to be useful experimentally., I. M. Keith., and Obsahuje bibliografii
The ‘buccal complex’ of Pricea multae Chauhan, 1945 consists of two buccal suckers, the pharynx, a putative taste organ and the mouth cavity. The two suckers are dorsal to the mouth cavity, and the pharynx posterior to them. The septum in each sucker consists of connective tissue containing muscle filaments, lined by tegument with short irregular microvilli. The mouth cavity and the lumen of the suckers are lined by tegument with short irregular lamellae and by tegument with long bulbous, interconnected lamellae, separated from each other and from the body surface tegument by septate junctions. A ventral extension of the mouth cavity is also lined by tegument with short irregular lamellae. An anterior ‘taste organ’ is lined by ‘normal’ (body) tegument and tegument with short irregular lamellae. Glandular ducts open into it, and it contains many small uni-ciliate and multiciliate receptors, as well as two receptor complexes each consisting of a large non-ciliate receptor surrounded by small and large uniciliate receptors, with multiciliate receptors closeby. The four types of receptors are described in detail. The anterior part of the pharyngeal lumen is lined by an epithelium with dense surface lamellae and is penetrated by non-ciliate receptors. Attention is drawn to significant differences between the buccal complexes of the polyopisthocotylean monogeneans Pricea multae (Gastrocotylidae), Gotocotyla secunda (Tripartii, 1956) (Gastrocotylidae), Pulylabroides australis (Murray, 1931) (Microcotylidae), Zeuxapia serialae (Meserve, 1938) (Axinidae) and Diclidophora merlangi (Kuhn, 1832) (Diclidophoridae).