R. Corder, Effect of lisinopril on tissue levels of neuropeptide Y in normotensive and spontaneously hypertensive rats, J HUM HYPER, 14(6), 2000, pp. 381-384
Angiotensin-converting enzyme (ACE) inhibitors reduce systemic and coronary
vasoconstriction by modulating sympathetic neuroeffector function and by d
ecreasing sympathetic activation. Here, blood pressure, and tissue concentr
ations of noradrenaline and neuropeptide Y (NPY) were studied in normotensi
ve and spontaneously hypertensive rats (SHR) after 2 weeks treatment with l
isinopril (0.3 mg/day; osmotic mini-pump). MAP was reduced in both normoten
sive rats and SHR after lisinopril by 32 mm Hg and 66 mm Hg respectively (P
< 0.001 compared to corresponding control rats). NPY levels were significa
ntly higher in extracts of atria, kidney, spleen and adrenal of normotensiv
e rats compared to SHR. Lisinopril treatment increased NPY levels in atria
and skeletal muscle extracts of SHR by 15% and 70% respectively (P < 0.05).
Lisinopril also significantly increased noradrenaline content of the atria
by 16% in SHR (P < 0.05). The decrease in MAP and increase in tissue level
s of sympathetic neurotransmitters provide further evidence that inhibition
of ACE decreases sympathetic neurotransmission leading to accumulation of
stored neurotransmitters.