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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Kohlmann, O. et al.

Role of substance P in blood pressure regulation in salt-dependent experimental hypertension.

The participation of substance P in the pathogenesis of five models of experimental hypertension, ie, DOCA-salt, subtotal nephrectomy, one-kidney-one clip renovascular, two-kidney-one clip renovascular, and spontaneous hypertension, was evaluated via an acute infusion of a newly synthesized potent, specific nonpeptide antagonist of substance P at the NK-1 receptor, the agent CP 96,345. In conscious unrestrained rats, CP 96,345 induced significant and sustained increases in mean arterial pressure of DOCA-salt, subtotal nephrectomy, and one-kidney-one clip renovascular hypertensive rats but only small and nonsignificant changes in blood pressure of two-kidney-one clip renovascular and spontaneously hypertensive rats. CP 96,345 had no effect on the blood pressure of sham-treated controls and Wistar-Kyoto rats. This NK-1 receptor antagonist did not significantly affect the heart rate of any experimental model studied. The data suggest that endogenous substance P may act as a partial counterregulatory mechanism against vasoconstriction in models of salt-dependent hypertension.[1]

References

Role of substance P in blood pressure regulation in salt-dependent experimental hypertension. Kohlmann, O., Cesaretti, M.L., Ginoza, M., Tavares, A., Zanella, M.T., Ribeiro, A.B., Ramos, O.L., Leeman, S.E., Gavras, I., Gavras, H. Hypertension (1997) [Pubmed]

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