The study suggests that reduced central dopaminergic activity in Japanese strains of hypertensive rats may be responsible for their exaggerated hypotensive responses to central dopamine.
Central dopamine effects on BP in rat models are hypothesis-generating; clinical translation to human hypertension remains untested.
The effects of intracerebroventricularly (icv) and intravenously (iv) administered dopamine (DA) on mean arterial pressure (MAP) and heart rate were investigated in conscious spontaneously hypertensive rat (SHR), stroke-prone SHR (spSHR) and normotensive Wistar-Kyoto (WKY) rat of Japanese strains, genetically hypertensive (GHR) and normotensive (NT-NZ) rat of New Zealand strains, Sprague-Dawley (SD) rat, and left renal artery stenosed hypertensive WKY (WKYLRAS) and SD (SDLRAS) rats. Icv DA (0.0125-0.4 mg/kg) caused a linear dose-related decrease in MAP, accompanied by bradycardia in all animals. By contrast, the same doses of DA given iv caused a linear dose-related increase in MAP, accompanied by reflex bradycardia in most groups (except the spSHR, SHR and WKYLRAS where tachycardia occurred to most of the doses employed), indicating that the decrease in MAP following icv DA is centrally-mediated. A "greater" relative hypotensive effect to icv DA was seen in the Japanese hypertensive strains SHR and spSHR compared to the WKY, but not between the New Zealand strains or the renal hypertensive animals. Our data also show that this marked hypotensive responsiveness is not related to the basal MAP, but appears to be strain-specific. It is thus possible that the alleged reduced central dopaminergic activity in the Japanese strains of hypertensive rats may be responsible for exaggerated hypotensive responses observed in these strains.
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Mok et al. (1987) studied this question.
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