Objective: The objectives of the present study were to determine funct
ional (i.e., heparin-releasable) and intracellular (i.e., heparin-non-
releasable) cardiac lipoprotein lipase (LPL) activity during the devel
opment of hypertension in spontaneously hypertensive (SHR) rats. Metho
ds: Male WKY and SHR rats were killed before (7-8 weeks of age) and fo
llowing (15-16 weeks of age) the development of severe hypertension in
SHR rats. LPL activity in coronary perfusates was determined by retro
gradely perfusing the hearts with heparin (5 U/ml). Cardiac myocytes w
ere also isolated from the two groups of rats by collagenase digestion
, and surface-bound and intracellular LPL activity measured. Results:
With the development of hypertension in SHR rats, there was a concomit
ant and progressive reduction in the heparin-releasable coronary endot
helial LPL activity. Neither insulin action nor cell-associated enzyme
activity could explain this low LPL activity in coronary blood vessel
s. However, acute vasodilation with nifedipine (a Ca2+ influx blocker)
or CGS-21680 (A(2)-purinergic receptor agonist) increased the peak he
parin-releasable LPL activity in hearts isolated from SHR rats. Conclu
sions: Our results indicate that hypertension per se may play a signif
icant role in regulating cardiac LPL activity, and hence fatty acid su
pply to the hypertensive SHR rat heart.