MYOGENIC CONTRIBUTION TO AGONIST-INDUCED RENAL VASOCONSTRICTION DURING NORMOXIA AND HYPOXIA

Acute hypoxia attenuates agonist-induced constrictor and presser respo nses in conscious rats, and a recent report suggests that hypoxia may also diminish myogenic reactivity in isolated, perfused rat kidneys. T hus we hypothesized that the diminished responsiveness to presser agen ts during hypoxia is caused by an impairment of myogenic reactivity. M ale Sprague-Dawley rats were instrumented with a pulsed Doppler flow p robe on the left renal artery, an aortic vascular occluder cuff immedi ately above the left renal artery to control renal perfusion pressure, and catheters were inserted to measure systemic arterial blood pressu re and renal arterial pressure (RAP) and for administration of agents. Animals were studied under normoxic or acute hypoxic (fractional conc entration of O-2 in inspired gials = 0.12) conditions and were adminis tered phenylephrine, arginine vasopressin, or angiotensin II. To deter mine the myogenic (pressure-dependent) component of agonist-induced va soconstriction, renal vascular resistance was calculated during agonis t infusion with RAP uncontrolled and with RAP controlled to preinfusio n levels. Significant myogenic components of agonist-induced renal vas oconstriction were evident with all presser agents used. However, hypo xia did not attenuate agonist-induced, pressure-dependent increases in renal vascular resistance. We conclude that the reduced vasoreactivit y associated with acute hypoxia is not caused by diminished myogenic r eactivity.