Hypertension I: Structure of Small Arteries in Hypertension

Re^3: Dr. Hale (0778)

Taben Hale

On Thu Dec 10, Robert M.K.W. Lee wrote
>On Thu Dec 10, Taben Hale wrote
>>On Wed Dec 9, Robert M.K.W. Lee wrote
>>>Is your "structurally-based vascular resistance" regression after 2 weeks of treatment a function of the lumen size change?

>>Although morphometric analysis has not been performed, I do not believe that there has been any change in the lumen size after two weeks of treatment.  This is because maximum dilation occurs at the same perfusion pressure in the treated animals as the untreated.  Treated animals however achieve maximum vasoconstriction at a perfusion pressure that is lower than the untreated animals, suggesting a reduction in the bulk of vascular smooth muscle tissue.  

>Do you have any evidence that there was a reduction in the bulk of vascular smooth muscle tissue?  Could the change in the sentivity of the tissue to the agonist account for this?

We use a constrictor cocktail consisting of Ang II, vasopressin, and
methoxamine.  At the point of maximal vasoconstriction the tissue "yields"
and the perfusion pressure suddenly drops.  At this point all of the
contractile elements in the bed are contracting until they finally give.
Untreated animals are able to withstand much higher perfusion pressures
because of increased bulk of vascular smooth muscle.  There is substantial
evidence (as well as in my own experiments) that there is no shift in
sensitivity to alpha 1 adrenoceptor stimulation.  Since max constriction
is induced by targetting a variety of receptors, I don't think that there
is any change in sensitivity.

Taben Hale

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