Vascular reactivity of isolated perfused kidneys from male and female spontaneously hypertensive rats.

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Abstract
Vascular reactivity was investigated in isolated, Tyrode perfused kidneys from male (blood pressure, 222.6 mm Hg) and female (blood pressure, 178.5 mm Hg) spontaneously hypertensive rats (SHR, 4-6 mo. old) and sex and weight matched normotensive Kyoto Wistar and Wistar control rats. Optimal perfusion flows and basal pressures were similar in sex-matched SHR and control rats. Submaximal constrictor responses to renal nerve stimulation were normal in SHR kidneys, but responses to exogenous norepinephrine were greater than control. Cocaine potentiated nerve stimulation responses more in SHR than control kidneys; exogenous norepinephrine responses were potentiated to a similar extent. Dose-response curves in SHR kidneys were to the left of control with the following order of shift magnitude: 5-hydroxytryptamine > angiotensin II .gtoreq. norepinephrine > Ba. In SHR kidneys, the ED20 (dose of agonist that evoked a 20% maximal response) for norepinephrine, 5-hydroxytryptamine and angiotensin, but not for Ba, was significantly lower than control response duration was normal for norepinephrine and 5-hydroxytryptamine, but prolonged for Ba and angiotensin. SHR kidneys developed 5-hydroxytryptamine tachyphylaxis more slowly than control. Dose-response curve shifts were greater in kidneys from male than female SHR; maximal responses were always increased in the former, but only for 5-hydroxytrypptamine and angiotensin in the latter. In the SHR kidney structural vascular changes may contribute to hyperreactivity in the male; renal vessels of male and female SHR are supersensitive to receptor-stimulating agonists and exhibit impaired relaxation; normal nerve stimulation response amplitude is due to a more efficient, cocaine sensitive, neurotransmitter disposition masking increased norepinephrine sensitivity; and the large increase in 5-hydroxytryptamine reactivity is partly due to attenuated tachyphylaxis.

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