AJP - Regulatory, Integrative and Comparative Physiology, Vol 241, Issue 5 379-R384, Copyright © 1981 by American Physiological Society
Sympathetic nerve function and vascular reactivity in spontaneously hypertensive rats
R. D. Ekas Jr and M. F. Lokhandwala
Increased neurotransmitter release during sympathetic nerve stimulation may
contribute importantly to the maintenance of spontaneous hypertension.
Therefore, transmitter release and vascular reactivity were measured in
perfused mesenteric vasculature of spontaneously hypertensive (SHR) and
normotensive Wistar-Kyoto rats (WKY). Increase in norepinephrine release,
measured as total tritium overflow, during periarterial nerve stimulation
was significantly greater in SHR than in WKY, as was the vasoconstrictor
response. Even after blockade of neuronal uptake with cocaine (10 microM),
or of neuronal as well as extraneuronal uptake with cocaine plus
metanephrine (20 microM), norepinephrine overflow was still greater in SHR
than in WKY. The greater vasoconstrictor response in SHR still persisted
following uptake blockade. Phentolamine (5.3 microM) increased transmitter
overflow markedly but equally in both SHR and WKY thereby suggesting that
increased transmitter release in SHR was not due to alterations in
presynaptic alpha-adrenoceptor mechanism. Vascular reactivity not only to
periarterial nerve stimulation but also to norepinephrine, vasopressin, and
barium chloride was increased in SHR. These results suggest that, in SHR,
increases in norepinephrine release as well as vasoconstrictor reactivity
contribute to the maintenance of hypertension.
