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  • Inner medullary collecting duct cells  (1)
  • reperfusion arrhythmia  (1)
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  • 1
    Electronic Resource
    Electronic Resource
    Hyperosmolality rapidly reduces atrial-natriuretic-peptide-dependent cyclic guanosine monophosphate production in cultured rat inner medullary collecting duct cells (1995)
    Springer
    Pflügers Archiv 430 (1995), S. 81-87 
    Details
    ISSN: 1432-2013
    Keywords: Hyperosmolality ; ANP ; cGMP ; Inner medullary collecting duct cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study was undertaken to explore the acute effect of hyperosmolality on the response of cultured rat inner medullary collecting duct (IMCD) cells to atrial natriuretic peptide (ANP). In contrast to the stimulatory effect of chronic incubation (12 h) in hypertonic medium, it was found that short-term incubation (〈 2 h) reversibly suppressed the ANP-dependent cyclic guanosine monophosphate (cGMP) production. Urea, NaCl and mannitol were equi-potent as the osmolyte in suppressing the ANP-dependent cGMP production. Receptor binding assay revealed that hyperosmolality induced a rapid and marked reduction of the maximum binding (B max) of ANP without a significant change of the dissociation constant (K d). Pretreatment with protein kinase C inhibitors (calphostin-C, staurosporin) or with cytoskeleton modulators (cytochalasin-B, colchicine) did not affect the inhibitory effect of hyperosmolality. In conclusion, acute hypertonicity inhibited the ANP-induced cGMP production in contrast to chronic hypertonicity, and reduction of the number of ANP binding sites was considered to be a mechanism responsible for the inhibitory effect of hypertonicity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00373842
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Suppression of reperfusion arrhythmia by ischemic preconditioning in the rat: Is it mediated by the adenosine receptor, prostaglandin, or bradykinin receptor? (1995)
    Springer
    Basic research in cardiology 90 (1995), S. 240-246 
    Details
    ISSN: 1435-1803
    Keywords: Preconditioning ; reperfusion arrhythmia ; adenosine receptor ; prostaglandin ; bradykinin ; rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The mechanism for the suppression of reperfusion arrhythmia by preconditioning (PC) remains unknown. This study aimed to examine the roles of the adenosine receptor, prostaglandin (PG), and bradykinin (BK) receptor in PC. Under pentobarbital anesthesia, the coronary artery of the rat was occluded for 5 min and then reperfused. In untreated controls, this protocol induced ventricular tachycardia (VT) in 100% of the rats and ventricular fibrillation (VF) in 60%. PC with 2 min ischemia/5 min reperfusion prior to the 5 min coronary occlusion significantly reduced the incidence of reperfusion VT and VF to 30% and 0%, respectively. This antiarrhythmic effect of the PC was not blocked when rats were pretreated with 8-phenyltheophylline (8-PT, 10 mg/kg), aspirin-DL-lysin (18 mg/kg), or a specific BK receptor antagonist, Hoe 140 (20 nmol/kg). None of these agents alone significantly modified the incidence of reperfusion VT or VF. These results suggest that neither the adenosine receptor, endogenous PG, nor BK receptor play a major role in the mechanism of suppression of perfusion arrhythmias by PC in the rat heart.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00805667
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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