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Pharmacological profile of valsartan, a non-peptide angiotensin II type 1 receptor antagonist. 3rd communication: hemodynamic effects of valsartan in rats and dogs.

Valsartan ((S)-N-valeryl-N-¿[2'-(1H-tetrazol-5-yl)biphenyl-4-yl)methyl¿ valine, CAS 137862-53-4, CGP 48933) at 10 and 30 mg/kg p.o. significantly inhibited angiotensin I and angiotensin II-induced pressor response at 1-8 h after administration in normotensive conscious dogs, but had no effect on blood pressure, heart rate or cardiac functions such as cardiac output, left ventricular pressure, left ventricular max. dP/dt and left ventricular end-diastolic pressure. In contrast to enalapril, this drug did not potentiate bradykinin-induced depressor response. In anesthetized dogs, valsartan at 10 mg/kg i.v. significantly increased renal blood flow, urinary sodium and chloride excretion and urine volume and significantly decreased renal vascular resistance and filtration fraction without affecting blood pressure. The preferential effects on renal hemodynamics were confirmed by the increase in blood flow into the kidneys of spontaneously hypertensive rats at 3 h following oral administration.[1]

References

  1. Pharmacological profile of valsartan, a non-peptide angiotensin II type 1 receptor antagonist. 3rd communication: hemodynamic effects of valsartan in rats and dogs. Hayashi, N., Yamamoto, S., Kometani, M., Nakao, K. Arzneimittel-Forschung. (1997) [Pubmed]
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