Regulation of cardiac output during aldosterone-induced hypertension.
The classical haemodynamic transients of volume-loading hypertension have been difficult to demonstrate in aldosterone-induced hypertension. Because recent studies have shown that continuous whole-day measurements of cardiac output are superior to short-term recordings, we studied the transient haemodynamic effects of aldosterone-induced hypertension while monitoring arterial pressure and cardiac output (electromagnetic flow probe) continuously for 20 h a day. In six dogs maintained on a fixed sodium intake of 150 mmol/day, we infused aldosterone (12 micrograms/kg per day, intravenously) for 10 days. The aldosterone induced a progressive increase in mean arterial pressure, from a control value of 88 +/- 1 to 107 +/- 2 mmHg. Cardiac output increased progressively, reaching a peak average value on the 4th day of infusion of +14 +/- 5% above control, and remained slightly elevated throughout the infusion period. Total peripheral resistance increased slowly to a value averaging +13 +/- 4% above control. Therefore, our experiments show that aldosterone induces a primary increase in cardiac output followed by a secondary vasoconstriction, which is consistent with the classical transient haemodynamic effects of volume-loading hypertension.
Montani
J P
JP
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505.
Mizelle
H L
HL
Adair
T H
TH
Guyton
A C
AC
D000450:Aldosterone / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D015924:Blood Pressure Monitors; D002302:Cardiac Output / Q000187:drug effects* / Q000502:physiology; D004285:Dogs; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology*; D007262:Infusions, Intravenous; D013997:Time Factors
D000450:Aldosterone