Abstract

1. Isolated kidneys from normotensive and spontaneously hypertensive rats were perfused at normothermia with Krebs-Henseleit solutions under conditions of constant flow. 2. Vascular responses to various concentrations of norepinephrine were measured by constant recording of perfusion pressure during drug administration. 3. These studies demonstrated the presence of a vascular escape mechanism in both types of kidneys, as is present in the rabbit kidney. While there was no difference in the frequency at which this escape from vasoconstriction occurred in the two experimental groups, there was a significant difference in the degree to which vascular escape occurred, the kidneys from spontaneously hypertensive rats showing a reduced level of escape from the vasoconstricting effect of norepinephrine when compared with kidneys from normotensive rats. 4. In view of the potential importance of the kidney in determining alterations in systemic blood pressure, it appears that a diminished effectiveness in the renal vascular escape mechanism may play a role in the genesis of hypertension, perhaps by preventing compensatory increases in glomerular filtration rate or salt excretion in the face of increased levels of circulating vasoconstrictors, e.g. catecholamines.

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