Neuroeffector function of isolated portal vein from spontaneously hypertensive and wistar-kyoto rats: dependence on external calcium concentration.
The calcium dependence of the vascular neuroeffector function has been studied in the portal vein of spontaneously hypertensive Okamoto rats (SHR) and Wistar-Kyoto rats (WKY). The noradrenaline (NA) sensitivity of veins of both species, expressed in terms of ED50, was decreased to the same extent in relation to the reduction in Ca2+ ion concentration below 2.5 mM. The responses to individual NA concentrations at subnormal Ca2+ concentrations were better maintained, however, in portal veins from SHR than from WKY, indicating that the excitation contraction coupling mechanism is less dependent on external Ca2+ concentrations in the portal vein from SHR than from WKY. In both strains of rats the spontaneous myogenic activity of the vessel was depressed in low Ca2+ concentrations to a greater extent than responses to nerve stimulation, which, in turn, were more reduced than the excitatory responses to exogenous NA or acetylcholine (ACh). Transmitter release (fractional overflow of 3H-NA/impulse) was less dependent on Ca2+ concentrations than the contractile nerve stimulation response. The persistence of all responses in reduced Ca2+ concentrations was significantly greater in the portal vein of SHR. It is concluded that the phasic, spontaneously active smooth muscle of the rat portal vein is highly dependent on the external calcium concentration and that various induced responses persist to a varying degree in reduced Ca2+ concentrations. It is suggested that this is due to interference with electromechanical coupling as well as myogenic spread of activation. Induced responses of the portal vein from SHR are, in general, less affected by decreased Ca2+ concentrations than the WKY portal vein, indicating an altered vascular smooth muscle excitation-contraction coupling mechanism in spontaneous hypertension. Possibly an increased efficiency of the coupling mechanism may contribute to augment vascular responses in the development of hypertension and promote structural vascular changes.
D000818:Animals; D002118:Calcium / Q000502:physiology*; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D009431:Neural Conduction / Q000187:drug effects; D009451:Neuroeffector Junction / Q000502:physiology*; D011169:Portal Vein / Q000294:innervation*; D051381:Rats; D012964:Sodium / Q000037:antagonists & inhibitors / Q000494:pharmacology
D012964:Sodium; D002118:Calcium