α-lactorphin and β-lactorphin improve arterial function in spontaneously hypertensive rats

Autor: Riitta Korpela, Marja-Leena Nurminen, Heikki Vapaatalo, Marika Sipola, Anne Pihlanto-Leppälä, Hannu J. T. Korhonen, Piet Finckenberg
Rok vydání: 2002
Předmět:
Male
Nitroprusside
medicine.medical_specialty
030309 nutrition & dietetics
Vasodilator Agents
Blood Pressure
Vasodilation
In Vitro Techniques
030204 cardiovascular system & hematology
Rats
Inbred WKY
General Biochemistry
Genetics and Molecular Biology
Nitric oxide
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Rats
Inbred SHR
Internal medicine
medicine
Animals
Nitric Oxide Donors
Enzyme Inhibitors
General Pharmacology
Toxicology and Pharmaceutics
Mesenteric arteries
Antihypertensive Agents
0303 health sciences
Tetrapeptide
biology
General Medicine
Acetylcholine
Potassium channel
Mesenteric Arteries
Rats
3. Good health
NG-Nitroarginine Methyl Ester
Endocrinology
medicine.anatomical_structure
chemistry
Hypertension
biology.protein
Sodium nitroprusside
Cyclooxygenase
Nitric Oxide Synthase
Oligopeptides
medicine.drug
Zdroj: Life Sciences. 71:1245-1253
ISSN: 0024-3205
DOI: 10.1016/s0024-3205(02)01793-9
Popis: alpha-lactorphin (Tyr-Gly-Leu-Phe) lowers blood pressure in conscious adult SHR. This tetrapeptide is originally released from milk protein alpha-lactalbumin by enzymatic hydrolysis. In order to evaluate the antihypertensive mechanisms of alpha-lactorphin, the effects of the tetrapeptide on vascular function were investigated in (30-35 weeks old) spontaneously hypertensive rats (SHR) with established hypertension and age-matched normotensive Wistar-Kyoto (WKY) rats in vitro. In addition, we studied the vascular effects of another structurally related tetrapeptide, beta-lactorphin (Tyr-Leu-Leu-Phe), which originates from milk protein beta-lactoglobulin. Endothelium-dependent relaxation to acetylcholine (ACh) was reduced in mesenteric arterial preparations of SHR as compared to those of WKY. In SHR, the ACh-induced relaxation was augmented by alpha-lactorphin or beta-lactorphin. The role of nitric oxide (NO) is suggested, since this improvement was abolished by the NO synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME). Simultaneous potassium channel inhibitor tetraethylammonium (TEA) elicited no additional effect on the ACh-induced relaxation. The cyclooxygenase inhibitor diclofenac did not attenuate the augmented ACh relaxation induced by alpha-lactorphin or beta-lactorphin, suggesting that endothelial vasodilatory prostanoids were not involved in the effect of the tetrapeptides. Endothelium-independent relaxation to the NO donor sodium nitroprusside (SNP) was augmented in mesenteric arterial preparations of SHR by simultaneous beta-lactorphin. The tetrapeptides did not alter vascular responses in mesenteric arteries from WKY. In conclusion, both alpha-lactorphin and beta-lactorphin improved vascular relaxation in adult SHR in vitro. The beneficial effect of alpha-lactorphin was directed towards endothelial function, whereas beta-lactorphin also enhanced endothelium-independent relaxation.
Databáze: OpenAIRE
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