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Am J Physiol Heart Circ Physiol. 2001 Apr;280(4):H1821-9.
Assembly and activation of HK-PK complex on endothelial cells results in bradykinin liberation and NO formation.

Zhao Y, Qiu Q, Mahdi F, Shariat-Madar Z, Rojkjaer R, Schmaier AH.

Division of Hematology and Oncology, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109-5669, USA.

Prekallikrein (PK) activation on human umbilical endothelial cells (HUVEC) presumably leads to bradykinin liberation. On HUVEC, PK activation requires the presence of cell-bound high-molecular-weight kininogen (HK) and Zn(2+). We examined the Zn(2+) requirement for HK binding to and the consequences of PK activation on endothelial cells. Optimal HK binding (14 pmol/10(6) HUVEC) is seen with no added Zn(2+) in HEPES-Tyrode buffer containing gelatin versus 16--32 microM added Zn(2+) in the same buffer containing bovine serum albumin. The affinity and number of HK binding sites on HUVEC are a dissociation constant of 9.6 +/- 1.8 nM and a maximal binding of 1.08 +/- 0.26 x 10(7) sites/cell (means +/- SD). PK is activated to kallikrein by an antipain-sensitive mechanism in the presence of HK and Zn(2+) on HUVEC, human microvascular endothelial cells, umbilical artery smooth muscle cells, and bovine pulmonary artery endothelial cells. Simultaneous with kallikrein formation, bradykinin (5.0 or 10.3 pmol/10(6) HUVEC in the absence or presence of lisinopril, respectively) is liberated from cell-bound HK. Liberated bradykinin stimulates the endothelial cell bradykinin B2 receptor to form nitric oxide. Assembly and activation of PK on endothelial cells modulates their physiological activities.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11247797&dopt=Abstract

art.osaka-med.ac.jp

We studied the angiotensin II-forming pathways in extracts from human and rat vascular tissues. In the extract from human artery, angiotensin I mainly converted to two products, angiotensin-(1-9) and angiotensin II, while in the extract from rat artery, the major angiotensin I products were angiotensin II and angiotensin-(5-10). The concentrations of angiotensin II and angiotensin-(1-9) generated in the human extract (1 mg protein/ml) after incubation for 30 min were 3.2 and 2.5 nmol, respectively, and that of angiotensin II and angiotensin-(5-10) generated in the rat extract (1 mg protein/ml) were 0.28 and 2.3 nmol, respectively. In the extract from human vascular tissues, the angiotensin II formation was inhibited by 8% with lisinopril and by 95% with chymostatin. The other product, angiotensin-(1-9) was inhibited completely by carboxypeptidase inhibitor. In the extract from rat vascular tissues, the angiotensin II formation was suppressed to 4% by lisinopril, but not by chymostatin. The angiotensin-(5-10) formation was completely inhibited by chymostatin. These findings suggest clearly that human vascular tissues contain two angiotensin II-forming enzymes, angiotensin-converting enzyme and chymase, but rat vascular tissues have no chymase-dependent angiotensin II-forming pathway.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11249939&dopt=Abstract




J Assoc Physicians India. 1998 May;46(5):448-51.
Angiotensin converting enzyme inhibitors and cough--a north Indian study.

Singh NP, Uppal M, Anuradha S, Agarwal A, Rizvi SN.

Department of Medicine, Maulana Azad Medical College and Associated Lok Nayak Hospital, New Delhi-110 002, India.

Cough is an important side effect of Angiotensin Converting Enzyme Inhibitor (ACEI) therapy. The incidence of cough was investigated in a prospective 8 week study in 250 hypertensive patients receiving ACEI alone or in combination with other agents. Enalapril (5-20 mg/day), Lisinopril (5-20 mg/day), Captopril (25-75 mg/day) or Ramipril (5-15 mg/day) was prescribed to patients, who were followed up at weekly visits. Cough developed in 73 of the 250 patients i.e. an incidence of 29.2%. Females had a higher incidence of cough as compared to males--37.9% versus 15.5% (p < 0.001) and there was no significant difference in the cough incidence in the various age groups. A dry, non-productive cough developed in all patients within 4 weeks of ACEI initiation. Increased nocturnal intensity of cough was reported by 79.4% patients. Cough incidence was 34.4%, 24.3% and 18.1% in patients on Enalapril, Ramipril and Lisinopril, respectively. Cough was not dose related and was not related to smoking. There was no statistically significant difference among patients on ACEI alone or in combination with beta blockers, calcium channel blockers or diuretics. Of the 18 patients with ACEI induced cough who received Indomethacin, 50 mg bid, 8 reported complete cure and cough was reduced in intensity in the remaining ten.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11273288&dopt=Abstract












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