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Biomedical subjects

K Fujii

Publications and source records attributed to K Fujii.

At least 325 records · Page 18Linked to original sources
PubMed1997

Beneficial effect of intracoronary verapamil on microvascular and myocardial salvage in patients with acute myocardial infarction.

OBJECTIVES: We assessed the acute effect of intracoronary injection of verapamil on microvascular function after primary percutaneous translumanal coronary angioplasty (PTCA) for acute myocardial infarction (AMI) with myocardial contrast echocardiography (MCE) in relation to functional outcomes. BACKGROUND: Recent clinical studies have documented the potential of verapamil for possible increase in coronary blood flow after primary PTCA. METHODS: Forty patients with a first AMI were randomly assigned to the verapamil group (n = 20) or the control group (n = 20). In the verapamil group, verapamil (0.5 mg) was injected into the infarct-related artery shortly after PTCA, followed by the oral administration. We performed MCE with an intracoronary injection of sonicated microbubbles before and after verapamil. To assess microvascular integrity, we determined the baseline-subtracted peak intensity in the risk area and the ratio of the no reflow zone plus the low reflow zone to the risk area (low reflow ratio). We determined the average wall motion score (dyskinesia/akinesia = 3; normal = 0) in the risk area on the day of AMI and a mean of 24 days later. RESULTS: The low reflow zone was observed shortly after PTCA in 14 verapamil group patients, and the low reflow ratio decreased after verapamil (0.39 +/- 0.23 vs. 0.29 +/- 0.17 [mean +/- SD], p < 0.05). Peak intensity significantly (p < 0.05) increased from 6 +/- 5 to 12 +/- 6 after verapamil. The reduction in wall motion score from the acute (day -1) to the late stage (day -24) was significantly greater in the verapamil group than in the control group (0.7 +/- 0.8 vs. 0.2 +/- 1.3, respectively, p < 0.05). CONCLUSIONS: Intracoronary administration of verapamil after primary PTCA can attenuate microvascular dysfunction and thereby augment myocardial blood flow in patients with AMI, leading to better functional outcome than with PTCA alone.

Adult↗
PubMed1997

Roles of E- and P-cadherin in the human skin.

The Ca(2+)-dependent cell-cell adhesion molecules, termed cadherins, are subdivided into several subclasses. E (epithelial)- and P (placental)-cadherins are involved in the selective adhesion of epidermal cells. E-cadherin is expressed on the cell surfaces of all epidermal layers and P-cadherin is expressed only on the surfaces of basal cells. Ultrastructural studies have shown that E-cadherin is distributed on the plasma membranes of keratinocytes with a condensation in the intercellular space of the desmosomes. During human skin development P-cadherin expression is spatiotemporally controlled and closely related to the segregation of basal layers as well as to the arrangement of epidermal cells into eccrine ducts. In human skin diseases E-cadherin expression is markedly reduced on the acantholytic cells of tissues in pemphigus and Darier's disease. Cell adhesion molecules are now considered to play a significant role in the cellular connections of cancer and metastatic cells. Reduced expression of E-cadherin on invasive neoplastic cells has been demonstrated for cancers of the stomach, liver, breast, and several other organs. This reduced or unstable expression of E- and P-cadherin is observed in squamous cell carcinoma, malignant melanoma, and Paget's disease, but cadherin expression is conserved in basal cell carcinoma. Keratinocytes cultured in high calcium produce much more intense immunofluorescence of intercellular E- and P-cadherin than those cells grown in low calcium. E-cadherins on the plasma membrane of the keratinocytes are shifted to desmosomes under physiological conditions, and therein may express an adhesion function in association with other desmosomal cadherins. Soluble E-cadherins in sera are elevated in various skin diseases including bullous pemphigoid, pemphigus vulgaris, and psoriasis, but not in patients with burns. Markedly high levels in soluble E-cadherin are demonstrated in patients with metastatic cancers.

Cadherins↗
PubMed1997

Resistance to IL-1 anti-proliferative effect, accompanied by characteristics of advanced melanoma, permits invasion of human melanoma cells in vitro, but not metastasis in the nude mouse.

We reported earlier that IL-1 inhibits the growth of human melanoma cells (A375-6), and that these cells become resistant to IL-1 after prolonged periods of culture. The resistant cells constitutively produce IL-alpha and IL-6 with IL-6 production was induced by endogenous IL-1 in an autocrine manner. The cells are also resistant to IL-6 anti-proliferative effects. In the present study, we show that the resistant clones exhibited up-regulated expression of intercellular-adhesion molecule 1 (ICAM-1) and vitronectin receptor (integrin alpha(v)beta3) when compared with the IL-1-sensitive clone, A375-6. Moreover, these IL-1-resistant clones exhibited many other metastatic characteristics, such as expression of IL-8 mRNA, production of matrix metalloproteinases (MMP-2 and MMP-9), and augmented invasion activity. However, contrary to our expectations, the IL-1-resistant cells did not exhibit experimental metastasis in a nude-mouse model, similarly to the IL-1-sensitive parental A375-6 cell line. In contrast, the highly metastatic clone A375-SM exhibited alpha(v)beta3 expression at a level comparable to that of the IL-1-resistant cells, but expressed low or no ICAM-1, metalloproteinase and displayed little in vitro invasion activity. These results show that the metastatic characteristics of IL-1-resistant cells are not sufficient to produce metastasis in vivo and suggest that these resistant clones may provide a good model system for characterizing the molecular mechanisms of metastasis.

Animals↗
PubMed1997

L-arginine ameliorates recirculation and metabolic derangement in brain ischemia in hypertensive rats.

The effects of L-arginine (a precursor of nitric oxide, NO) on cerebral blood flow (CBF), cerebrovascular resistance (CVR) and metabolites in the ischemic brain were examined in spontaneously hypertensive rats with bilateral carotid artery occlusion for 30 min followed by 60 min-recirculation. The administration of L-arginine (300 mg/kg, i.v.) increased the CBF by an average of 11 ml x 100 g-1 x min-1 (P < 0.05 vs. at rest), and N(omega)-nitro-L-arginine (L-NNA, an inhibitor of NO synthase, 5 mg/kg, i.v.) reduced the CBF by 5-6 ml x 100 g-1.min-1 with increase in the mean arterial pressure by 26 mmHg. During ischemia the CBF significantly decreased to below 8% of the resting values in all rats. The largest blood flow in postischemic hyperemia was 171 +/- 9% of the resting CBF in the rats with L-arginine (P < 0.05 vs. L-NNA and saline), followed by 126 +/- 5 with saline and 109 +/- 3 with L-NNA. The CVR at 60 min of recirculation was 3.291 +/- 0.144 mmHg . ml-1. 100 g-1 .min-1 in the rats with saline, remained low level of 2.711 +/- 0.124 with L-arginine (P < 0.01 vs. L-NNA and P < 0.05 vs. saline) and in contrast, significantly increased to 5.732 +/- 0.184 with L-NNA (P < 0.01 vs. L-arginine and saline, respectively). Tissue lactate with saline increased 2.3-fold at 60 min of recirculation, whereas the increase was inhibited to 1.4-fold after L-arginine treatment (P < 0.01 vs. L-NNA) and in contrast, significantly increased 5.7-fold with L-NNA. The ATP and glucose levels were better preserved in the rats with L-arginine than in those with L-NNA or saline. These findings support that the enhanced postischemic hyperemia is beneficial to the ischemic brain and the administration of L-arginine may be potentially useful for the treatment of acute stroke.

Animals↗
PubMed1997

Surgery for gastric cancer in patients with cirrhosis.

To clarify the therapeutic strategies for gastric cancer surgery in the presence of cirrhosis, 39 patients with gastric cancer accompanied by liver cirrhosis were reviewed. Severe postoperative complications developed in 10 patients (25.6%), and there were 4 (10.3%) hospital deaths. 1 (2.6%) of which occurred within 1 month. Although extended lymph node dissection of D2 or more was adopted for low-risk patients, 3 of 19 patients who underwent such extensive operations, most of which involved complete lymph node dissection in the hepatoduodenal ligament, died. Conversely, only 1 of 20 patients who underwent limited lymph node dissection of D1 or less died. Postoperative massive ascites developed in 6 patients, 3 of whom died. The cumulative 5-year survival rate following curative resection was 63.7% for patients with early gastric cancer, and 13.9% for those with advanced gastric cancer. The most frequent cause of death was cirrhosis-related, such as hepatic failure or hepatoma. In conclusion, extensive lymph node dissection for patients with gastric cancer accompanied by cirrhosis carried a risk of postoperative fatal massive ascites as lymphorrhea. Thus, lymph node dissection in the hepatoduodenal ligament should be avoided, except in patients with evident metastases, and as a rule, aggressive surgery should not be performed in cirrhotic patients.

Adult↗
PubMed1997

The effects of proteoglycan on GALT in rats treated with TPN.

It is well known that total parenteral nutrition (TPN) causes atrophy of the intestinal mucosa, resulting in degeneration and atrophy of the gut-associated lymphoid tissues (GALT). This study was conducted to examine the suppressive effect of TPN on GALT in rats. Rats that received TPN alone for 2 weeks, i.e., the TPN group, showed a decreased number of Peyer's patches and thoracic duct lymphocytes (TDL), as well as atrophy. Conversely, those treated with TPN in combination with polysaccharide K (PSK) at a daily dose of 1000 mg/kg for 2 weeks, i.e., the PSK group, showed increases in the number of Peyer's patches and TDL and improvement in the TDL subsets compared with the TPN group. Immunohistological examination of the changes in immunocytes in GALT using monoclonal antibodies revealed increases in the production of the major histocompatibility complex (MHC)-I and (MHC)-II, helper T cells, and interleukin 2 (IL-2). These findings indicate that PSK improves GALT suppression induced by TPN.

Animals↗
PubMed1997

Distant lymph node metastasis of early gastric cancer.

Among 601 patients with early gastric cancer (EGC), the clinicopathological findings of 5 patients (invasion of the mucosal layer in 2 and of the submucosal layer in 3) with distant lymph node metastasis according to TNM classification (third- or fourth-tier lymph node metastasis according to the Japanese classification) were investigated. The proliferating-cell nuclear antigen (PCNA) expression of EGC was also examined immunohistologically. The sites of distant metastasis were the nodes at the root of the mesentery, in the hepatoduodenal ligament, and the paraaortic nodes. While the PCNA-positive rate of EGC with distant lymph node metastasis (35.4%) was significantly higher than that of EGC without lymph node metastasis (14.7% P = 0.01), it was similar to that of EGC with perigastric lymph node metastasis. The cumulative survival rate of the EGC patients with distant lymph node metastasis (5-year survival rate 20.0%) was significantly lower than that without lymph node metastasis (88.2%, P < 0.0001), first-tier lymph node metastasis (76.9%, P < 0.04), or second-tier lymph node metastasis (77.1%, P < 0.04). Thus, although the prognosis of EGC patients with distant lymph node metastasis was poor, a dissection of the distant lymph nodes should be performed when metastasis is suspected.

Adenocarcinoma↗
PubMed1997

The efficacy of bypass surgery for the patients with hemorrhagic moyamoya disease.

The efficacy of bypass surgery for the patients with hemorrhagic Moyamoya disease were studied by multi-center retrospective questionnaire study. The rebleeding rate was 28.3% (39/138 patients) in conservative treatment group and 19.1% (29/152 patients) in bypass surgery group with no significant statistical difference. It is still difficult to clarify the efficacy of bypass surgery for prevention of hemorrhagic attack.

Adolescent↗
PubMed1997

Percutaneous transluminal angioplasty attenuates day-night difference in ambulatory blood pressure in renovascular hypertension.

To evaluate whether the circadian rhythm of blood pressure (BP) was altered in renovascular hypertension (RVH), ambulatory BP was monitored using a noninvasive recorder in nine patients with RVH attributable to fibromuscular dysplasia before and after percutaneous transluminal angioplasty (PCTA). The circadian rhythm of BP was assessed by the day-night difference in BP and by the single cosinor method. The day-night difference in BP before PCTA was significantly greater than in age- and sex-matched normotensive subjects (n = 9, P < .01) and patients with essential hypertension (n = 9, P < .05). PCTA decreased significantly the 24-h BP as well as plasma renin activity (P < .01). In the chronogram, the BP reduction after PCTA was evident especially during the day. Accordingly, the day-night difference in BP decreased significantly after PCTA (P < .01). In the cosinor analysis, the mesor and the percent amplitude of BP decreased significantly after PCTA (P < .01). In summary, circadian rhythm of BP was preserved or rather exaggerated in RVH. The stimulated renin angiotensin system in RVH possibly contributes to the altered circadian rhythm of BP primarily by elevating the daytime BP.

Adolescent↗
PubMed1997

Clinical and biochemical aspects of thiamine treatment for metabolic acidosis during total parenteral nutrition.

We encountered six cases of total parenteral nutrition (TPN)-associated lactic acidosis during the 6-y period of 1988-1993. The patients were characterized by severe disease of the digestive organs, minimal food intake before surgery, and postoperative TPN with no food intake and with no vitamin supplements. Within 4 wk of TPN, they developed hypotension (< or = 80/60 mmHg), Kussmaul's respiration, and clouding of consciousness, as well as abdominal pain not directly related to the underlying disease. Routine laboratory examinations revealed no acute aggravation in hepatic, renal, or pancreatic functions. Arterial blood gas analysis showed pH < or = 7.134 and base excess < or = -17.5 mmol/L. Additional laboratory examinations revealed serum lactate > or = 10.9 mmol/L, serum pyruvate > or = 159 mumol/L, and lactate/pyruvate ratio > or = 0.029. None of the patients responded to sodium bicarbonate or other conventional emergency treatments for shock and lactic acidosis. After the first case, we suspected that thiamine deficiency might be responsible for this pathologic condition, Serum thiamine was proved to be < or = 196 nmol/L in 5 patients. Thiamine replenishment at intravenous doses of 100 mg every 12 h resolved lactic acidosis and improved the clinical condition in 3 patients. This article includes a review of 11 relevant reports published from 1982-1992 and a discussion of the biochemical mechanism of onset of thiamine deficiency-associated lactic acidosis. We emphasize the needs (1) to supplement TPN with thiamine-containing vitamins for the patients whose food intake does not meet nutritional requirements; (2) to monitor the patients routinely measuring serum thiamine concentration and erythrocyte transketolase activity during TPN; and (3) to intravenously replenish using high-dose thiamine simultaneously with the manifestation of signs and symptoms of lactic acidosis.

Acidosis, Lactic↗
PubMed1997

TP53 mutations in stage I gallbladder carcinoma with special attention to growth patterns.

32 stage I cases of gallbladder carcinoma (GC) were examined to evaluate TP53 mutations with special attention to growth patterns. Their growth patterns were classified into two types: polypoid (P-type) and flat (F-type). 16 cases of GC were classified as P-type and 16 as F-type. p53 immunohistochemistry was performed using a mouse monoclonal anti-p53 antibody. Mutations in exons 5-8 were examined by polymerase chain reaction single strand conformation polymorphism (PCR-SSCP) and direct sequencing. The incidence of p53 immunoreactivity was greater in the cases of F-type (11/16, 69%) than those in P-type (14/16, 25%) (P < 0.05). PCR-SSCP or direct sequencing revealed that TP53 mutations were detected in all cases positive for p53 protein. These results suggest that TP53 mutations may contribute to the carcinogenesis of the F-type GC, and than this pathway in the F-type may differ from that in the P-type GC.

Adenocarcinoma↗
PubMed1997

Alteration of pharmacokinetics and nephrotoxicity of cisplatin by alginates.

This study was undertaken to demonstrate that alginates could form a complex with cisplatin and that the pharmacokinetics and nephrotoxicity of cisplatin could be altered by this complexation. The complexes were prepared with alginates of mean molecular weights of 10000 (AL-1) and 40000 (AL-2). The plasma clearances of cisplatin-alginate complexes were significantly reduced when compared with the drug alone. Urinary excretion of platinum (Pt) was increased when animals were dosed with the cisplatin-AL-1 complex, but not with the cisplatin-AL-2 complex. Renal clearance of cisplatin, when administered alone, was more rapid during the first 2 h than the rest of the study period (96 h) and was higher than its plasma clearance, which is consistent with irreversible binding of cisplatin to plasma protein. On the other hand, renal clearance of cisplatin-alginate complexes was not highly time dependent, and the values were more similar to those of plasma clearance. Complexation of cisplatin with alginates, especially AL-1, inhibited the accumulation of Pt in the kidneys and reduced blood urea nitrogen elevation by cisplatin. The in vitro antitumor activities against U937, P388, and cisplatin-resistant P388 (P388/cisplatin) cells were similar among cisplatin and its alginate complexes. These studies indicated that the pharmacokinetics and nephrotoxicity of cisplatin could be altered through complexation with alginate by (1) reducing cisplatin clearance, (2) inhibition of Pt accumulation of in the kidneys, and (3) reduction of apparent nephrotoxicity without decrease in in vitro antitumor activity.

Alginates↗
PubMed1997

Correlation between relative number of circulating low-density hepatitis C virus particles and disease activity in patients with chronic hepatitis C.

Hepatitis C virus (HCV) circulates as particles having differing buoyant densities. Changes in the relative proportions of virus particles of different densities were examined in 19 patients with chronic hepatitis C: 6 without (group A) and 13 with (group B) abnormal serum alanine aminotransferase (ALT) levels. High- and low-density virus particles were separated by differential flotation centrifugation. The numbers of high-density particles consistently exceeded that of low-density particles in all patients in group A, whereas the titers of both types of particles were the same at least once in 7 of 10 patients sampled at two time points in group B. The ALT level significantly increased <2 months later (P < 0.05) when the titers of both types of particles were the same in patients in group B. Thus, we found a correlation between the relative numbers of circulating low-density HCV particles and disease activity in chronic hepatitis C patients.

Adult↗
PubMed1997

Age-related ischemia in the brain following bilateral carotid artery occlusion--collateral blood flow and brain metabolism.

Cerebral blood flow (CBF) and cerebellar blood flow (CeBF) were measured and correlated with brain lactate, pyruvate and adenosine triphosphate concentrations from groups representing 3-week old suckling (n = 10), 18-22-week old adult (n = 9) and 70-week old aged (n = 7) Sprague-Dawley rats before and during bilateral carotid occlusion (BCO). The steal ratio, calculated as the ratio of %control CBF to %control CeBF, was 1.02 +/- 0.06 (mean +/- SEM) at 60 minutes of BCO in adult rats that exhibited normal levels of brain metabolites. By contrast, the ratios significantly decreased to 0.74 +/- 0.06 in suckling rats and 0.69 +/- 0.06 in aged rats with simultaneous increases by 2.4 to 2.9-fold of tissue lactate. Pyruvate and lactate/pyruvate ratio also increased by 1.4 to 1.8 times control in both suckling and aged rats. We conclude that there is age-related steal phenomenon occurring with blood flow during BCO. Ischemic derangement of the brain metabolism is in part related to poor blood supply from the posterior circulation in suckling and aged rats.

Adenosine Triphosphate↗
PubMed1997

Role of Ca(2+)-activated K+ channels in acetylcholine-induced dilatation of the basilar artery in vivo.

1. We tested the hypothesis that activation of large conductance calcium-activated potassium channels is involved in dilator responses of the basilar artery to acetylcholine in vivo. Using a cranial window in anaesthetized rats, we examined responses of the basilar artery to acetylcholine. 2. Topical application of acetylcholine (10(-6) and 10(-5) M) increased diameter of the basilar artery from 238 +/- 7 microns to 268 +/- 7 and 288 +/- 7 microns, respectively (P < 0.05 vs. baseline diameter). Iberiotoxin (10(-8) M), an inhibitor of large conductance calcium-activated potassium channels, did not affect baseline diameter of the basilar artery. In the presence of 10(-8) M iberiotoxin, 10(-6) and 10(-5) M acetylcholine increased diameter of the basilar artery from 239 +/- 7 microns to 246 +/- 7 and 261 +/- 7 microns, respectively. Thus, iberiotoxin attenuated acetylcholine-induced dilatation of the basilar artery (P < 0.05). 3. Sodium nitroprusside (10(-7) and 10(-6) M) increased diameter of the basilar artery from 242 +/- 9 microns to 310 +/- 12 and 374 +/- 13 microns, respectively (P < 0.05 vs. baseline diameter). In the presence of iberiotoxin (10(-8) M), sodium nitroprusside (10(-7) and 10(-6) M) increased diameter of the basilar artery from 243 +/- 6 microns to 259 +/- 9 and 311 +/- 12 microns, respectively. Thus, iberiotoxin attenuated dilator responses of the basilar artery to sodium nitroprusside (P < 0.05). 4. Iberiotoxin partly inhibited dilator responses of the basilar artery to forskolin, a direct activator of adenylate cyclase, but did not affect vasodilatation produced by levcromakalim, a potassium channel opener. 5. These results suggest that dilator responses of the basilar artery to acetylcholine and sodium nitroprusside are mediated, in part, by activation of large conductance calcium-activated potassium channels. Because both acetylcholine and sodium nitroprusside have been shown to activate guanylate cyclase via nitric oxide, activation of large conductance calcium-activated potassium channels may be one of the major mechanisms by which cyclic GMP causes dilatation of the basilar artery in vivo.

Acetylcholine↗
PubMed1997

Role of eicosanoids in alteration of membrane electrical properties in isolated mesenteric arteries of salt-loaded, Dahl salt-sensitive rats.

1. The role of eicosanoids in altered membrane electrical properties of Dahl salt-sensitive (DS) rats was investigated, by use of conventional microelectrodes technique, in isolated superior mesenteric arteries of DS rats and Dahl salt-resistant (DR) rats fed either a high or low salt diet. 2. The membrane was significantly depolarized in salt-loaded DS rats compared with the other three groups. In addition, the arteries of salt-loaded DS rats exhibited spontaneous electrical activity. 3. Spontaneous electrical activity in salt-loaded DS rats was inhibited by the following: indomethacin, a cyclo-oxygenase inhibitor; ONO-3708, a prostaglandin H2/thromboxane A2 receptor antagonist; OKY-046, a thromboxane A2 synthase inhibitor; nicardipine, a Ca(2+)-channel antagonist and by Ca(2+)-free solution. In addition, spontaneous electrical activity was enhanced by a thromboxane A2 analogue and by prostaglandin H2. Spontaneous electrical activity was unaffected by phentolamine, atropine and tetrodotoxin. 4. Membrane potential in arteries of salt-loaded DS rats was not affected by either indomethacin or ONO-3708. 5. Spontaneous contraction, sensitive to indomethacin, was present, and contractile sensitivity to high potassium solution was enhanced in arteries of salt-loaded DS rats. 6. These findings suggest that eicosanoid action, together with membrane depolarization, may lead to the activation of voltage-dependent Ca(2+)-channels, thereby causing spontaneous electrical activity in mesenteric arteries of salt-loaded DS rats. In addition, tension data suggest that these changes in membrane properties are related to enhanced contractile activities in salt-loaded DS rats. Mechanisms of depolarization remain to be determined.

Animals↗
PubMed1997

Enhancement by exogenous and locally generated angiotensin II of purinergic neurotransmission via angiotensin type 1 receptor in the guinea-pig isolated mesenteric artery.

1. Angiotensin II is known to enhance sympathetic neurotransmission in the vasculature by increasing the release of noradrenaline, but little is known about the effect on the co-released transmitter, adenosine 5'-triphosphate (ATP). In the present study we have examined the effect of angiotensin II on the excitatory junction potential (e.j.p.) elicited by repetitive field stimulation in the guinea-pig isolated mesenteric artery, to establish the angiotensin II receptor subtype involved in modulating the release of ATP and the role of the endothelium in converting angiotensin I to angiotensin II. 2. Suramin (300 microM), a P2 purinoceptor antagonist, abolished both the e.j.p.s and depolarizing response to alpha,beta-methylene-ATP, a stable analogue of ATP, without affecting the resting membrane potential and noradrenaline-induced depolarization. 3. Angiotensin II (0.1 microM) affected neither the resting membrane potential nor the amplitude of the first e.j.p., but increased the amplitudes of the subsequent e.j.p.s. This enhancing effect of angiotensin II was abolished by CV-11974 (0.1 microM), an angiotensin II type 1 (AT1) receptor antagonist, but unaffected by PD 123319 (1 microM), an angiotensin II type 2 (AT2) receptor antagonist, or CGP 42112A (1 microM), AT2 receptor ligand. 4. Angiotensin I (0.1 microM) exerted a similar effect on e.j.p.s to that of angiotensin II. CV-11974 (0.1 microM) or temocaprilat (10 microM), an angiotensin converting enzyme (ACE) inhibitor, abolished the effect of angiotensin I. Removal of the endothelium did not alter the action of angiotensin I. 5. The results of the present study indicate that the release of ATP from sympathetic nerves innervating the guinea-pig isolated mesenteric artery, as determined from the magnitude of the e.j.p., can be enhanced by angiotensin II via activation of prejunctional AT1 receptors. Qualitatively similar effects were observed with angiotensin I, which appears to be converted into angiotensin II by a subendothelial process.

Adenosine Triphosphate↗