Contrasting dopaminergic patterns in two forms of genetic hypertension.
Dopaminergic mechanisms in genetic hypertension were explored via the measurement of catecholamine (CA) turnover, tissue concentration and urinary excretion of dopamine (DA) and its metabolites. In salt-sensitive (S) Dahl rats, the tissue concentration and urinary excretion of DA and its metabolites were decreased in response to salt loading, while adrenal dopamine-beta-hydroxylase (D beta H) activity and aldosterone responsiveness to angiotensin II (A II) were increased. In contrast, spontaneously-hypertensive rats (SHR) showed elevated tissue levels and urinary excretion of DA and its metabolites, adrenal DA turnover and ganglionic DA generation following cholinergic stimulation, but D beta H activity and aldosterone responsiveness to A II were diminished. These two patterns, the hypodopaminergic state in Dahl S rats and the hyperdopaminergic state in SHR, account for two distinct mechanisms of hypertension and precede its development. We detected striking dopaminergic activity-related similarities between Dahl S rats and low-renin essential hypertension (EH) on the one hand, and SHR and non-modulator EH patients on the other.
D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000311:Adrenal Glands / Q000201:enzymology / Q000378:metabolism; D000818:Animals; D004298:Dopamine / Q000378:metabolism / Q000502:physiology*; D004299:Dopamine beta-Hydroxylase / Q000378:metabolism; D005727:Ganglia, Spinal / Q000378:metabolism; D006719:Homovanillic Acid / Q000378:metabolism; D006973:Hypertension / Q000201:enzymology / Q000235:genetics / Q000503:physiopathology*; D008781:Methyltyrosines / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D011919:Rats, Inbred Strains; D011921:Rats, Inbred WKY
D008781:Methyltyrosines; D015102:3,4-Dihydroxyphenylacetic Acid; D004299:Dopamine beta-Hydroxylase; D004298:Dopamine; D009638:Norepinephrine; D006719:Homovanillic Acid