What question did this study set out to answer?

To determine whether the direct intrarenal sodium-retaining actions of low-dose angiotensin II can cause chronic hypertension.

February 1, 1979Circulation Research71 citationsOpen Access

Hypertensive and renal effects of chronic low level intrarenal angiotensin infusion in the dog.

View Full Paper

TLThomas E. Lohmeier ACAllen W. Cowley

Key Points

To determine whether the direct intrarenal sodium-retaining actions of low-dose angiotensin II can cause chronic hypertension.
Infused angiotensin II directly into the renal artery of 5 uninephrectomized dogs at 1 ng/kg/min for 10 days.
Administered intravenous angiotensin II infusions (0.5 ng/kg/min) to 4 uninephrectomized control dogs for 10 days.
Continuously monitored 24-hour mean arterial pressure alongside GFR, effective renal plasma flow, and urinary sodium excretion.
Intrarenal infusion immediately reduced GFR, ERPF, and urinary sodium excretion; mean arterial pressure rose by 9 mm Hg on day 2 and peaked at +15 mm Hg by day 10.
Intravenous infusion caused no initial sodium retention or hypertension during the first 48 hours, producing a smaller pressure increase of 7 mm Hg over days 3 to 10.
Stopping intrarenal infusion on day 10 caused rapid rebound increases in GFR, ERPF, and sodium excretion, returning arterial pressure to baseline within hours.

Abstract

SUMMARY To determine whether the intrarenal sodium-retaining effects of angiotensin II (A II) can produce chronic hypertension, we infused A II at a rate (1 ng/kg per min) that did not cause a measurable immediate rise in mean arterial pressure (MAP) for 10 days directly into the renal artery of five dogs with unilateral nephrectomy. Four additional control dogs with unilateral nephrectomy were infused intravenously with A II for 10 days at 0.5 ng/kg per min. This intravenous infusion rate of A n was calculated to produce an increase in peripheral blood levels of AII at least as great as those achieved with the intrarenal infusion of AII. MAP was recorded continuously, 24 hours/day, and daily values for MAP based on approximately 720 sample points per day were determined by computerized data analysis. Intrarenal A II infusion produced an immediate fall in glomerular filtration rate (GFR), effective renal plasma flow (ERPF), and urinary sodium (UN.V) and potassium (UKV) excretion. MAP was unchanged during the first day of the infusion period. Both GFR and ERPF remained depressed for at least 6 days of the infusion. However, sodium balance was achieved on day 2 when MAP had increased by 9 mm Hg. Subsequently, MAP continued to increase, reaching + 15 mm Hg at the end of 10 days. In contrast, there was no sodium retention or hypertension during the first 48 hours of intravenous AII infusion; yet, during days 3-10, MAP did rise by 7 mm Hg. After the intrarenal infusion of A II was stopped on day 10, there were immediate increases in GFR, ERPF, UKV, and especially UN.V, and MAP returned to control levels after a few hours. The data indicate that the intrarenal effects of A II can produce chronic sodium retention and a sustained elevation in MAP and also prevent pressure natriuresis during the hypertension. Ore Res 44:154-160, 1979 IT IS well established that chronic infusion of an-giotensin II (A II) at a rate that causes only a small increase in arterial pressure initially, will in time produce prominent hypertension (McCubbin et al.,

Ask AI

Helpful

Bookmark

View Full Paper

Ask AI

Helpful

Bookmark

View Full Paper

Hypertensive and renal effects of chronic low level intrarenal angiotensin infusion in the dog.

Key Points

Abstract

Cite This Study