[The influence of coronary flow on atrio-ventricular transmission and ventricular contraction in the isolated guinea pig heart].
It has been demonstrated that coronary flow, through hemodynamic forces, stimulates ventricular contraction and atrio-ventricular transmission; however, the mechanisms involved in these effects remain unknown. A possibility to explain the transduction mechanism, from a mechanical stimulus into a physiological response, could be the stretch-activated ion channels. Additionally we explored the role of nitric oxide as mediator of these actions.


METHODS
We used the isolated perfused guinea pig heart according to the method of Langendorff, perfused with Krebs solution. We recorded the ventricular contraction by development of left ventricular pressure and the atrio-ventricular transmission. We studied the effects of the stretch activated ion channel blocker; gadolinium. Synthesis of nitric oxide was inhibited by L-NAME and induced with L-arginine.


RESULTS
Gadolinium inhibited the stimulating effect of flow on atrio-ventricular transmission and ventricular contraction. Verapamil, a specific blocker of calcium channels, had no effect in the stimulatory effect of flow indicating that this type of calcium channel, do not play significant role in the effects of flow. L-NAME and L-arginine did not have effects on the effects of flow.


CONCLUSIONS
The stimulating effect of coronary flow in these parameters is regulated by stretch-activated ionic channels. This effect is independent of nitric oxide.
Torres
J C
JC
Escuela Superior de Medicina del I.P.N., México, D.F.
Pastelín
G
G
Suárez
J
J
D000818:Animals; D001120:Arginine / Q000494:pharmacology; D001283:Atrioventricular Node / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D003326:Coronary Circulation / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005682:Gadolinium / Q000494:pharmacology; D006168:Guinea Pigs; D066298:In Vitro Techniques; D007473:Ion Channels / Q000037:antagonists & inhibitors / Q000502:physiology; D008297:Male; D008465:Mechanoreceptors / Q000502:physiology; D009200:Myocardial Contraction / Q000502:physiology*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000096:biosynthesis; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D052250:Nitric Oxide Synthase Type III; D015398:Signal Transduction / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology*; D016276:Ventricular Function; D014700:Verapamil / Q000494:pharmacology
D002121:Calcium Channel Blockers; D004791:Enzyme Inhibitors; D007473:Ion Channels; D009569:Nitric Oxide; D001120:Arginine; D005682:Gadolinium; D014700:Verapamil; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; D019331:NG-Nitroarginine Methyl Ester