The aim of this study was to determine the antihypertensive effects of enzymatic hemp seed protein hydrolysate (HPH) and its peptide fractions. Hemp seed protein isolate was digested by the sequential action of pepsin and pancreatin to mimic gastrointestinal digestion in human beings. The resultant HPH was separated by membrane ultrafiltration into peptide fractions with different sizes (\1 and 1-3 kDa). The HPH led to significantly higher (P \ 0.05) in vitro inhibition of the activities of angiotensin I-converting enzyme (ACE) and renin, the two main enzymes involved in abnormal blood pressure elevation (hypertension). Kinetic studies showed that HPH and peptide fractions inhibited renin and ACE activities in a mixed-type pattern, indicating binding to areas other than the active site. Oral administration of HPH (200 mg/kg body weight) to spontaneously hypertensive rats led to significant reductions (P \ 0.05) in systolic blood pressure (SBP) that reached a maximum of -30 mmHg after 8 h. In contrast, the hypotensive effects of peptide fractions (\1 and 1-3 kDa) had a maximum value of about -15 mmHg after 6-8 h post oral administration. The results suggest a synergistic antihypertensive effect of the peptides present within HPH; this effect was reduced significantly (P \ 0.05) upon separation into peptide fractions.

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The blood pressure lowering effect of a pea protein hydrolysate (PPH) that contained <3 kDa peptides, isolated by membrane ultrafiltration from the thermolysin digest of pea protein isolate (PPI), was examined using different rat models of hypertension as well as hypertensive human subjects. The PPH showed weak in vitro activities against renin and angiotensin converting enzyme (ACE) with inhibitory activities of 17 and 19%, respectively, at 1 mg/mL test concentration. Oral administration of the PPH to spontaneously hypertensive rats (SHR) at doses of 100 and 200 mg/kg body weight led to a lowering of hourly systolic blood pressure (SBP), with a maximum reduction of 19 mmHg at 4 h. In contrast, orally administered unhydrolyzed PPI had no blood pressure reducing effect in SHR, suggesting that thermolysin hydrolysis may have been responsible for releasing bioactive peptides from the native protein. Oral administration of the PPH to the Han:SPRD-cy rat (a model of chronic kidney disease) over an 8-week period led to 29 and 25 mmHg reductions in SBP and diastolic blood pressure, respectively. The PPH-fed rats had lower plasma levels of angiotensin II, the major vasopressor involved in development of hypertension, but there was no effect on plasma activity or renal mRNA levels of ACE. However, renal expression of renin mRNA levels was reduced by approximately 50% in the PPH-fed rats, suggesting that reduced renin may be responsible for the reduced levels of angiotensin II. In a 3-week randomized double blind placebo-controlled crossover human intervention trial (7 volunteers), significant (p<0.05) reductions (over placebo) in SBP of 5 and 6 mmHg were obtained in the second and third weeks, respectively, for the PPH group. Therefore, thermolysin derived bioactive peptides from PPH reduced blood pressure in hypertensive rats and human subjects, likely via effects on the renal angiotensin system.

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