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  • Title: Cardiovascular effects of alpha-trinositol in spontaneously hypertensive and normotensive Wistar-Kyoto rats.
    Author: Sun X, Edvinsson L, Hedner T.
    Journal: J Hypertens; 1993 Sep; 11(9):935-43. PubMed ID: 8254175.
    Abstract:
    OBJECTIVE: To investigate the cardiovascular effect of alpha-trinositol (D-myo-inositol-1,2,6-trisphosphate; PP56) in spontaneously hypertensive rats (SHR) and in normotensive Wistar-Kyoto (WKY) rats. alpha-Trinositol, a representative of a new group of pharmacological agents, is an inositol phosphate which seems to bind to a single population of binding sites, inhibiting, for example, agonist-induced vasoconstriction. In particular, alpha-trinositol seems to inhibit agonist-induced (e.g. neuropeptide Y-induced) elevations in intracellular Ca2+ levels in vascular smooth muscle cells. METHODS: alpha-Trinositol was administered as a bolus injection (2-40 mg/kg body weight), followed by a continuous infusion (20-400 mg/kg body weight per h) for 40 min in freely moving SHR and WKY rats. RESULTS: Acute intravenous bolus administration of alpha-trinositol reduced systolic and diastolic blood pressure, as well as heart rate, in a dose-dependent manner in SHR and WKY rats. After completion of the 40-min infusion the reduction in blood pressure was more pronounced in the SHR than in the WKY control rats. Heart rate did not change in the SHR, whereas it was significantly increased at the highest dosage (400 mg/kg) in the WKY rats. At this dosage, three out of eight SHR died from cardiac arrhythmias after completing the infusion. The lowest dose of alpha-trinositol administered (2 mg/kg bolus followed by 20 mg/kg per h infusion over 40 min) significantly inhibited the increase in mean arterial pressure induced by neuropeptide Y (2 micrograms/kg per min for 10 min) by approximately 30% in both the SHR and WKY rats. Furthermore, alpha-trinositol treatment completely inhibited the potentiation induced by neuropeptide Y (0.1 micrograms/min for 30 min) of the blood pressure responses to intravenous bolus injections of noradrenaline (20 ng), tyramine (40 micrograms) or angiotensin II (10 ng). CONCLUSIONS: Our results demonstrate that alpha-trinositol antagonizes the direct postsynaptic pressor response to exogenous neuropeptide Y, as well as the potentiating effects of neuropeptide Y on other vasoconstrictors in SHR and WKY rats. However, in the SHR alpha-trinositol lowered basal blood pressure only in the dose range which was non-specific for neuropeptide Y inhibition. Thus, the present study indicates that neuropeptide Y is involved only slightly in the maintenance of high blood pressure in SHR.
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