Masato Kuchii

Differences of cardiac reactivity between spontaneously hypertensive and normotensive rats

Abstract The reactivity of the isolated atria of spontaneously hypertensive rats (SHR) in hypertensive and pre-hypertensive state (30–35 days after birth) was compared to those of two control groups of normotensive Wistar rats (NWR). SHR atria, but not pre-hypertensive atria, showed a greater amount of spontaneously developed tension than NWR atria, which may reflect compensatory changes due to the high peripheral vascular resistance in SHR. The inotropic and chronotropic responses of SHR and pre-hypertensive atria to isoproterenol were less than those of NWR atria. In SHR atria (hypertensive and pre-hypertensive), a high concentration of epinephrine and norepinephrine elicited a decreased inotropic effect in comparison to the NWR response. An abnormal negative inotropic response to potassium was observed in SHR atria (both hypertensive and pre-hypertensive). These results may indicate a difference in the nature of the β-receptor of SHR and NWR atria and an intrinsic, contractile abnormality of SHR atria. The low reactivity of SHR atria to the β-receptor stimulant may be attributed to the original changes in musculature rather than secondary changes resulting from compensatory mechanisms of hypertension.

Effects of a central stimulant substance isolated from the sea anemone Stoichactis kenti on brain monoamines of the mouse

An active substance, polypeptide in chemical nature, causing central stimulant activity in mice has been isolated from a sea anemone. Signs of central nervous stimulatory activity produced by this substance included fighting episodes, increased motor activity and clonic convulsions. The active substance produced significant decreases in brain norepinephrine concentration both at the ED50 (6.4 mg/kg) and the maximum effective dose (9.3 mg/kg) during the stimulation period. Brain dopamine concentration was significantly decreased by the active substance at the ED50 dose whereas brain serotonin concentration was not affected. The ED50 dose of the active substance significantly inhibited the re-uptake of norepinephrine during the stimulation period and elevated hormetanephrine levels. These results suggest that the active substance causes central stimulation by releasing active norepinephrine from functional pools and inhibiting its re-uptake, thus making more norepinephrine available at a adrenoceptors. It is probable that brain dopamine plays a minor role in this stimulant action of the active substance.