Hypertension, Vol 5, 321-327, Copyright © 1983 by American Heart Association
CA Sueta, PM Hutchins and JW Dusseau
We have studied microvascular reactivity to vasopressin alone and in
combination with norepinephrine in young (6- to 8-week-old) spontaneously
hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) controls.
Closed-circuit TV microscopy was used to quantify the in vivo diameter
responses of small arterioles (17 to 26 mu) to vasopressin (1.25 X 10(-8)
to 3.75 X 10(-7) M) injected intraarterially alone and with simultaneous
topical suffusion of a subthreshold concentration of norepinephrine in the
cremaster muscle microcirculation. Percent decrease in luminal diameter was
integrated over a 30-second period to obtain log concentration response
curves. The vasoconstrictor response to vasopressin was
concentration-dependent in both groups (p less than 0.001). A significant
increase in reactivity to vasopressin alone was exhibited by the SHR
arterioles compared to the WKY vessels (p less than 0.02). Maximum
constriction was 55% higher in the SHR (p less than 0.04). The SHR also
demonstrated a greater sensitivity to vasopressin (p less than 0.02).
Vasopressin- induced vasoconstriction was potentiated by norepinephrine in
the SHR, demonstrated by the significant shift of the curve up and to the
left of the SHR response curve to vasopressin alone (p less than 0.01). The
maximum response was 38% greater (p less than 0.02). Sensitivity was
significantly enhanced (p less than 0.01). Additionally, the presence of
norepinephrine stimulated a three-fold greater incidence of complete
closure. In contrast to SHR results, topical suffusion of norepinephrine
did not significantly alter the reactivity of the WKY arterioles to
vasopressin-induced constriction. Our results support a role for
vasopressin as a potential vasoconstrictor in the developing stage of SHR
hypertension which may be modulated by norepinephrine and thus contribute
to the elevated total peripheral resistance observed.
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