Pflügers Archiv

, Volume 343, Issue 1, pp 79–88 | Cite as

Interaction of H+ and Ca++ in the regulation of local pial vascular resistance

  • E. Betz
  • H. G. Enzenroß
  • V. Vlahov


Mock CSF of various compositions was injected into the perivascular space of different small pial arteries by means of micropipettes. Acid CSF (pH 6.5) caused local vascular dilatation, as did normal CSF with the addition of EDTA or EGTA. Systemic acidosis caused by CO2 respiration also caused pial vasodilatation. Tiny silver-chloride electrodes were placed directly on the surface of small pial arterioles. Current-constant stimulation with series of DC-impulses (2–5 mA strength, duration 1 ms/imp.; stimulation lasted 10 sec) caused local vasoconstriction of the stimulated vessel. The constricted region of the vessel was of a different shape. Most frequently spindle-shaped constrictions with an extention not exceeding the length of the indifferent electrode were seen. In some cases the constriction was unilaterally placed near the different electrode (100 μm ∅) and in a few cases the constriction was propagated along the whole vessel.

Stimulation after application of acid CSF or during CO2-respiration caused a constrictory action of about the same degree as in normal CSF. The acidotic dilatation, however, remained visible because the resulting vascular diameter after stimulation remained greater than in the controls with normal CSF. In Ca++-free CSF the stimulation elicited a small response and during EGTA no constriction appeared after stimulation.

In CSF with EDTA the constrictory response was distinctly diminished. From the experiments it cannot be excluded that the constriction of pial vessels caused by electrical stimulation is based on another mechanism than that caused by extravascular alkalosis. Ca++ is necessary for both mechanisms.

Key words

Pial Vessels Ca++-Electrical Stimulation pH Cerebral Circulation Smooth Muscles Microperfusion 


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Copyright information

© Springer-Verlag 1973

Authors and Affiliations

  • E. Betz
    • 1
  • H. G. Enzenroß
    • 1
  • V. Vlahov
    • 1
  1. 1.Physiologisches Institut, Lehrstuhl IUniversität TübingenGermany

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