What is the clinical evidence from this study?

Study design: Other. Intervention: Intracerebroventricular angiotensin II (ANG II) vs. Control. Primary outcome: Efferent renal sympathetic nerve activity (RSNA).

August 1, 1997

Baroreceptor-independent renal nerve inhibition by intracerebroventricular angiotensin II in conscious sheep

Key Result

Intracerebroventricular infusion of angiotensin II in conscious sheep reduced renal sympathetic nerve activity to 38% of control at 1 nmol/h, and to 9-11% at higher doses, independent of baroreceptors.

Structured PICO

Does intracerebroventricular angiotensin II alter renal sympathetic nerve activity in conscious sheep?

Population

5 conscious sheep studied to evaluate the effect of central administration of angiotensin II on efferent renal sympathetic nerve activity.

Intervention

Intracerebroventricular infusion of angiotensin II (1, 3, and 10 nmol/h) for 30 min, with or without intracerebroventricular losartan (1 mg/h)

Comparator

Control (baseline/pre-infusion)

Outcome

Efferent renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP)surrogate

Intracerebroventricular angiotensin II has a direct central inhibitory action on renal sympathetic nerve activity mediated by AT-1 receptors, independent of baroreceptors.

Abstract

The effect of central administration of angiotensin II (ANG II) on efferent renal sympathetic nerve activity (RSNA) was studied in conscious sheep. ANG II (1 nmol/h), infused for 30 min into the lateral cerebral ventricles in five sheep, did not alter mean arterial pressure (MAP) but reduced RSNA to 38 +/- 5% of control. Intracerebroventricular infusion of higher doses of ANG II (3 and 10 nmol/h), which increased MAP by 12 +/- 2 and 14 +/- 3 mmHg, respectively, reduced RSNA to 9 +/- 5 and 11 +/- 7% of control. MAP and RSNA gradually returned to control over a period of 2 h after the infusions. Intracerebroventricular losartan (1 mg/h for 1 h before, and then during, angiotensin infusion) blocked all the effects of angiotensin (3 nmol/h). Baroreflex relationships constructed from the beat-to-beat relationship of RSNA to diastolic pressure showed a significant leftward shift during intracerebroventricular ANG II compared with the control relationship. The beat-to-beat relationship between central venous pressure and RSNA was abolished during intracerebroventricular infusion of ANG II. These findings demonstrate that intracerebroventricular ANG II has a direct central inhibitory action on RSNA that is independent of both arterial and low-pressure baroreceptors. This effect of angiotensin is mediated by central angiotensin AT-1 receptors.

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