Effect on Blood Pressure
Experimentally produced renal hypertension is usually attributed to the release into the blood stream of a humoral substance (renin) elaborated by the ischemic kidney. Renin is a proteolytic enzyme which acts upon a protein substrate synthetized in the liver1 to form angiotensin I, an inactive decapeptide. From this decapeptide histadylleucine is hydrolyzed, leaving an octapeptide known as angiotensin II,2 the active vasoconstrictor substance whose pressor activity is said to be ten times that of norepinephrine.3 The actual time sequence of this reaction in vivo is unknown. The elevation in mean arterial pressure following constriction of the renal artery may occur within hours, but usually a period of two to three weeks transpires before significant elevation is seen. If the reaction described above is other than instantaneous, then an opportunity is presented for metabolic attack on the development of experimental hypertension.Cerqua and Samaan
PALMER JM. Portacaval Transposition in Experimental Hypertension. Arch Surg. 1963;87(3):500–506. doi:10.1001/archsurg.1963.01310150136031
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