What is the clinical evidence from this study?

Study design: Other. Population: Hypertension. Intervention: Endothelin vs. Wistar-Kyoto normotensive rats (WKY). Primary outcome: Release of immunoreactive atrial natriuretic factor (irANF) (1.5-4.5-fold increase).

July 1, 1989Open Access

Enhanced release of atrial natriuretic factor by endothelin in atria from hypertensive rats.

Key Result

Endothelin caused a 1.5- to 4.5-fold concentration-dependent increase in the release of atrial natriuretic factor from isolated rat right atria, which was significantly greater in hypertensive rats.

Structured PICO

Does endothelin increase the release of atrial natriuretic factor in isolated atria from hypertensive rats compared to normotensive rats?

Population

Isolated right atria from spontaneously hypertensive rats (SHR) and Wistar-Kyoto normotensive rats (WKY)

Intervention

Endothelin (10(-8) and 10(-7) M)

Comparator

Wistar-Kyoto normotensive rats (WKY) and baseline (pre-exposure)

Outcome

Release of immunoreactive atrial natriuretic factor (irANF)surrogate

Endothelin directly stimulates the release of atrial natriuretic factor from rat atria in vitro, with an accentuated response in hypertensive rats, suggesting a potential mechanism for its in vivo depressor effect.

Main Result

Effect estimate: 1.5-4.5-fold increase

Abstract

Intravenous (bolus) administration of endothelin results in a transient fall in blood pressure that is accentuated in spontaneously hypertensive rats (SHR) compared with Wistar-Kyoto normotensive rats (WKY). In attempting to discern possible mechanisms underlying this depressor response, we examined the ability of endothelin to release atrial natriuretic factor (ANF) from isolated, spontaneously contracting atria from SHR and WKY. Isolated right atria were suspended under 3.0 g of resting force in tissue baths with the amount of immunoreactive ANF (irANF) released after exposure to endothelin assessed by radioimmunoassay. Endothelin (10(-8) and 10(-7) M) caused a concentration-dependent increase (1.5-4.5-fold) in the release of irANF, which was significantly greater in atria of SHR compared with WKY. The greater release of irANF in atria of SHR versus WKY was not related to tissue weight or changes in contractile rate or force induced by endothelin. Therefore, endothelin appears to cause a direct release of irANF from rat right atria in vitro. As found for the depressor response in vivo, endothelin is more efficacious in the hypertensive compared with the normotensive atrial preparation. Release of ANF may be important in the hypotensive response to endothelin in vivo.