bluuebunny/crossref_metadata_2025_split huggingface dataset:
Renal Kallikrein Activity and Urinary Kallikrein Excretion in Rats with Experimental Renal Hypertension
Authors: Marin-Grez M. , Schaechtelin G. , Bönner G. , Speck G. , Ganten D. , Gross F. 
Published: August 2015

1. Rats were made hypertensive by ligating the aorta between the origins of both renal arteries. Sham-operated animals served as controls. Urinary and renal kallikrein activities, as well as plasma and renal renin activities, were measured 8 and 90 days after surgery.
2. Blood pressure was 155 ± 6 mmHg on day 8 after aortic ligature and 142 ± 6 mmHg on day 90; in controls pressures were 107 ± 3 and 110 ± 5 mmHg respectively.
3. Eight days after aortic ligature, kallikrein activity in the ischaemic kidneys was about 6·5 times, and in the non-ischaemic kidneys almost 2 times, that in controls. After 90 days the kallikrein activity was reduced to one-half of that in the controls in the ischaemic kidneys and it was normal in the contralateral.
4. The urinary kallikrein excretion of hypertensive rats was about one-third of that of the controls at both 8 and 90 days after aortic ligature.
5. The plasma renin activity in hypertensive rats was approximately seven times that in control animals 8 days after aortic ligature and did not differ from the control value after 90 days. Renin activity in the kidneys showed the same pattern as in other models of renovascular hypertension: elevation in the ischaemic kidney and reduction in the non-ischaemic one.
Effects of Frusemide on the Renal Kallikrein–Kinin System of the Rat
Authors: Bönner G. , Beck D. , Deeg M. , Marin-Grez M. , Gross F. 
Published: August 2015

1. In male Wistar rats, three doses of frusemide (0·5, 5·0 and 50·0 mg/kg) were injected subcutaneously. A dose-related increase in urine flow and natriuresis occurred, whereas there was a biphasic response in kallikrein excretion with an initial, dose-related transient increase and a secondary reduction. When the urine losses were replaced by the infusion of 0·9% NaCl solution, the biphasic response of urinary kallikrein excretion was maintained.
2. In all experiments, urinary excretion of kallikrein correlated with the excretion of potassium. Frusemide enhanced the excretion of kinins, which correlated with the urine volume and the natriuresis, but not with kallikrein excretion.
3. In contrast to the initially increased excretion of kallikrein, kallikrein activity in the renal cortex remained unchanged or was even reduced. Kininogen content of the perfused tissue of the renal cortex did not vary throughout the experiment, but decreased markedly in the non-perfused tissue of the cortex 30 min after the injection of frusemide.
4. It is concluded that forced diuresis induced by frusemide causes a ‘wash out’ of renal kallikrein in urine, probably not indicating the true changes in the activity of the renal kallikrein-kinin system within the kidney. Kinin excretion in urine was not correlated with kallikrein excretion but with changes in diuresis. Thus it might be suggested that the renal kallikrein-kinin system could be involved by kinins in the regulation of renal water and sodium excretion as well as of renal plasma flow.
Diffuse Structural Abnormalities in Cell Membranes from Genetically Hypertensive Rats: A Fluorescence Polarization Study
Authors: Aragon Inès , Montenay-Garestier Thérèse , Nunez Marie-Aude , Pernollet Marie-Gabrielle , Nunez Anne-Marie , Ben-Ishay Drori , Meyer Philippe , Helene Claude 
Published: August 2015

1. Diphenylhexatriene was used as a fluorescence probe to detect structural differences between membranes from genetically hypertensive rats and those from their normotensive controls. Both isolated membranes (erythrocyte ghosts) and whole cells (platelets) were studied.
2. In the Okamoto-Aoki strain, the fluorescence polarization of diphenylhexatriene and consequently the ‘equivalent microviscosities' were altered in all membranes, even in those of young normotensive SHR. These abnormalities varied with age (in whole cells) and were not detected in females.
3. These alterations were not restricted to the SHR strain and were also observed in the Sabra hypertensive strain (SBH). The ‘equivalent microviscosity’ of hypertensive Sabra erythrocyte ghosts was higher than that of the original Sabra rats. Salt loading of the Sabra rats promoted an increase in the ‘equivalent microviscosity’ of their erythrocyte membranes, which nearly reached the Sabra hypertensive level.
4. These results support the hypothesis of a genetic change in hypertensive rats leading, directly or indirectly, to diffuse alterations of cell membrane structure, which seem to be similar to those caused by high salt intake.
Augmentation of Prostaglandin Production by Linoleic Acid in Man
Authors: Epstein Murray , Lifschitz Meyer , Rappaport Kenneth 
Published: August 2015

1. Since several lines of evidence have suggested that a diminution of endogenous prostaglandins (PG) may participate in the pathogenesis of a variety of disease states, it would be advantageous to develop therapeutic approaches that augment endogenous prostaglandin synthesis. Since linoleic acid is readily converted to arachidonic acid, we assessed the effects of linoleic acid administration on immunoassayable PGE and 6-oxo-PGF1α excretion as indices of PGE2 and PGI2 production.
2. Six normal subjects were studied twice: during a seated control study and during an 8 h infusion of a 10% emulsion of safflower oil (Liposyn) containing approx. 77% linoleic acid, in a dose of 1·5 g/kg body weight.
3. Liposyn induced a profound increase in immunoassayable 6-oxo-PGF1α excretion.
4. Simultaneously, immunoassayable PGE excretion increased modestly.
5. The current study raises the possibility that linoleic acid administration might constitute a new therapeutic approach in managing disorders characterized by an impairment of the ability to augment prostaglandin synthesis.
Erythrocyte Membrane Transport Systems as Possible Markers for Essential Hypertension
Authors: Barlassina D. Cusi. C. , Ferrandi M. , Brevi R. , Vazzola A. , Bianchi G. 
Published: August 2015

1. Erythrocyte Na+-K+ cotransport and Na+-Li+ countertransport were measured at the same time in 56 essential hypertensive patients, 24 of their normotensive offspring and 36 matched normotensive controls.
2. The mean value of Na+-K+ cotransport is slower and of Na+-Li+ countertransport is faster in the essential hypertensive group and in some of their normotensive offspring, but a great overlap with the value of the normotensive group was observed.
3. Na+-K+ cotransport values were bimodally distributed in the hypertensive group, with the first mode at 250 and the second at 600 μmol h−1 l−1 of erythrocytes.
4. The ratio Na+-K+ cotransport/Na+-Li+ countertransport was calculated. It was found that such a ratio distinguishes between normotensive and essential hypertensive subjects better than the individual transport systems alone.
Increased Vascular Sensitivity to Serotonin and Methysergide in Hypertension in Rats
Authors: Webb R. Clinton 
Published: August 2015

1. The effect of the hypertensive process on vascular sensitivity to serotonin and methysergide was studied.
2. Isometric contractions were recorded from arteries isolated from spontaneously hypertensive (SHR), Kyoto-Wistar normotensive (WKY), deoxycorticosterone acetate (DOCA)-hypertensive and Sprague-Dawley normotensive rats.
3. Arteries from hypertensive rats (except SHR aorta) were more sensitive (lower ED30) to noradrenaline, serotonin and methysergide relative to those from controls.
4. The magnitude of the leftward shift in ED30 was similar for the three agonists in mesenteric and tail arteries from DOCA rats, whereas the shift in ED30 for serotonin and methylsergide in aortae exceeded that to noradrenaline. In SHR, the shift in ED30 for serotonin and methylsergide in tail and mesenteric arteries was greater than that to noradrenaline; SHR aortae did not differ from WKY aortae.
5. Arteries from hypertensive rats (except SHR aorta) developed a greater maximal contraction to methysergide than those from controls; maximal contractions to noradrenaline and serotonin were either less than or similar to those of controls.
6. The agonistic action of methysergide in DOCA rats paralleled the development of high arterial pressure. Low sodium diet abated the high pressure in DOCA rats and reduced vascular sensitivity to all agonists.
7. These observations support the view that in hypertension there is a generalized increase in vasoconstrictor sensitivity. The major finding is that, in two hypertensive models, there is a uniquely greater increase in vascular responsiveness to the agonistic action of methysergide.
Glucocorticoid Hypersecretion and Hypertensive Vascular Disease in Experimental Malignant Hypertension in Rats
Authors: Chatelain R. E. , Bumpus F. M. , Dibello P. M. , Ferrario C. M. 
Published: August 2015

1. Changes in plasma glucocorticoid levels and the alterations they imposed upon the lymphoid system and vascular hypertrophy were studied in rats developing either the benign or malignant forms of hypertension during the initial 30 days after aortic ligation.
2. A threefold increase in plasma corticosterone was observed during both the acute and chronic phases of malignant hypertension, whereas in benign hypertension, after a short-lasting twofold increase, corticosterone returned to normal within 9 days.
3. Thymus atrophy, thymocyte depletion and impaired thymocyte reactivity characterized the acute phase of benign and malignant hypertension. After 9 days these alterations receded in benign hypertension, whereas they were permanent features accompanied by severe lymphocytopenia and marked neutrophilia in malignant hypertension.
4. Syntheses and contents of collagen and elastin were impaired in the arteries of malignant hypertensive rats. In contrast, elevated synthesis and increased deposition of these proteins were observed in benign hypertensive rats. Both forms of the disease were characterized by increased deposition of arterial non-fibrous protein.
5. Although acute arterial fibrinoid deposition was observed in benign and malignant hypertension, fibrinoid disappeared in benign hypertensive rats whereas it evolved into necrotizing lesions characterized by disruption of the arterial structure and lymphoid cell infiltration in malignant hypertensive rats.
6. These studies indicate that differing patterns of altered glucocorticoid secretion accompany the development of benign and malignant hypertension. These hormones, by altering the lymphoid system and arterial connective tissue metabolism may participate in the development and perpetuation of the necrotizing arterial lesions observed in malignant hypertension.
Outpatient Screening Procedures for Primary Aldosteronism
Authors: Streeten David H. P. , Anderson Gunnar H. , Springer Jay M. 
Published: August 2015

1. The sensitivity and specificity of several individual and combined measurements for the diagnosis of primary aldosteronism have been calculated in 22 patients with established primary aldosteronism and 140 essential hypertensive controls.
2. Excellent sensitivity and specificity (93-100%) in the diagnosis of primary aldosteronism cannot be accomplished with any single test but can be achieved with combinations of (a) a low ‘stimulated’ plasma renin activity (PRA) (after frusemide and orthostasis) together with either hypokalaemia or a high ‘stimulated’ plasma aldosterone concentration (above 944 pmol/l), or (b) a low ‘stimulated’ PRA, together with either hypokalaemia or a high saline-suppressed plasma aldosterone concentration (above 236 pmol/l), or (c) a pressor response to saralasin together with elevated values of NaCl-suppressed or frusemide-stimulated plasma aldosterone concentration. Procedures (a) or (c) can be completed in 3–4 h; (b) requires 8 h.
Regional Distribution of Angiotensinogen in the Central Nervous System of the Rat: Effect of DOC-Salt Treatment
Authors: Basso Nidia , Grispon Diana , Ruiz Patricia , Taquini Alberto C. 
Published: August 2015

1. The distribution of angiotensinogen and endogenous renin-like activity were analysed in different areas of the central nervous system in normal and DOC-salt-treated hypertensive rats.
2. Angiotensinogen concentration and renin-like activity were significantly increased in the cerebral cortex, cerebellum, hypothalamus and brain stem of the DOC-salt-treated rats 30 days after the initiation of the experiment.
3. Influence of plasma contamination on the former results was evaluated by the determination of (a) plasma angiotensinogen concentration in control and treated animals and (b) blood content remaining in the different regions of the central nervous system, after saline perfusion of the brain, in a group of normal rats.
4. Plasma angiotensinogen concentration was significantly decreased in DOC-salt-treated rats, therefore blood contamination would tend to diminish the magnitude of increase in central nervous system angiotensinogen in these animals.
5. Present results have shown an increased concentration of angiotensinogen in some areas of the central nervous system in DOC-salt-treated rats. The results have also confirmed an enhanced activity of the endogenous renin-like enzyme in the same regions; this change seems to be mainly due to the increment in angiotensinogen. Increased formation of central angiotensin could be involved in the development of DOC-salt hypertension. The biosynthetic pathways of renin substrate as well as its endogenous regulation remain undetermined.
Changes in Blood Pressure in Relation to Vascular and Plasma Renin after Renin Injection in Rats
Authors: Loudon M. , Bing R. F. , Swales J. D. , Thurston H. 
Published: August 2015

1. To assess the relative importance of vascular as opposed to plasma renin, groups of conscious rats received a single intravenous injection of partially purified rat renin 18 h after bilateral nephrectomy. Blood pressure was monitored continuously and plasma and aortic renin concentrations were determined at 1, 3, 6 or 9 h after injection. In separate groups of rats the effect of the competitive angiotensin II antagonist, saralasin, on blood pressure was measured 3 or 6 h after renin injection.
2. Blood pressure remained elevated for up to 6 h after renin injection, returning to normal by 9 h. Saralasin infusion reversed the rise in blood pressure at both 3 and 6 h after injection.
3. Aortic renin concentration followed the pattern of the pressor response whereas plasma renin concentration had returned to subnormal values by 3 h.
4. Circulating renin of renal origin is taken up by aortic tissue. The pressor response to exogenous renin in rats after bilateral nephrectomy is not related to changes in plasma renin but is similar in duration to the persistence of aortic renin-like activity and can be blocked by saralasin at both 3 and 6 h after injection.
Release and Extraction of Pressor Hormones by the Human Hypertensive Kidney
Authors: De Leeuw P. W. , Punt R. , Van Soest G. A. , Tchang P. , Birkenhäger W. H. 
Published: August 2015

1. In 11 patients with uncomplicated essential hypertension in whom renal arteriography had been carried out, arterial and venous samples were drawn for determination of active renin, angiotensin II and catecholamines, both before and after 3 min of static exercise (handgrip).
2. In five patients the experiment was continued by administration of phentolamine (5 μg min−1 kg−1) into the renal artery. During this procedure blood samples were drawn again before and after handgrip exercise. At all times renal plasma flow was measured from the clearance and extraction of [125I]hippuran.
3. At rest the kidney secreted renin and noradrenaline, and angiotensin II and adrenaline were extracted from the circulation. During static exercise secretion of renin and noradrenaline was enhanced, and extraction efficiency for angiotensin II and adrenaline was reduced. During infusion of phentolamine similar patterns were found for renin and catecholamines, but the pattern for angiotensin II was reversed.
4. It is concluded that sympathetic activity in the kidney and perhaps also the absolute level of renal blood flow determine the renal extraction efficiency for angiotensin II. Reduced uptake of angiotensin II by an α-adrenergic mechanism may protect the kidney from excessive vasoconstriction.
Significance of the Brain Renin—Angiotensin System in Spontaneously Hypertensive Rats
Authors: Tonnaer Jeroen A. D. M. , van Put Joke J. , Wiegant Victor M. , de Jong Wybren 
Published: August 2015

1. The renin inhibitor N-acetyl-pepstatin was infused for 14 days or 5 days into the cerebral ventricular system of young and adult spontaneously hypertensive rats respectively.
2. The blood pressure and heart rate of the young animals was significantly lower as a result of this treatment, whereas the pressure of the adult animals tended to decrease.
3. The mechanism involved in the hypotensive effect of N-acetyl-pepstatin appeared to be independent of the peripheral renin-angiotensin system. The possible involvement of a decreased sympathetic outflow is suggested.
4. The present data indicate that the brain renin-angiotensin system contributes to the development of hypertension in the spontaneously hypertensive rat.
Reversible Acid-Activation of Inactive Renin: Evidence Favouring a Unimolecular Reaction
Authors: Atlas Steven A. , Hesson Thomas E. , Sealey Jean E. , Laragh John H. 
Published: August 2015

1. Purified inactive renin from human kidney or plasma was activated to a similar extent by incubation with trypsin or by dialysis to pH 3.3.
2. Trypsin- or acid-activated inactive renin was like active renal renin in terms of pH optimum (pH 5.5-6.0) and inhibition by mono-specific antibody. The apparent Km of homologous angiotensinogen for acid-activated inactive renin (1.11 μmol/l) was the same as for trypsin-activated inactive renin (1.12 μmol/l) or active renal renin (1.07 μmol/l).
3. In contrast with trypsin-activated renin, acid-activated renin was reversibly inactivated in a time-dependent manner during incubation at 37°C above pH 5. The maximal rate of reversal occurred in the pH 7–8 range. Reversal was prevented by prior incubation with trypsin, plasmin, glandular kallikrein or plasma kallikrein.
4. By kinetic analysis, the reversal of activation was found to be a first-order decay process with a reaction half-time (7–8 min at 37°C, pH 7.4) that was independent of the initial concentration of activated enzyme.
5. These results indicate that reversible acid-activation of inactive renin is a unimolecular reaction, consistent with the hypothesis that acid pH induces a conformational change in a single polypeptide chain.
Antibody-Sensitive Renin of Adrenal and Resistance Vessels is Markedly Elevated in Spontaneously Hypertensive Rats
Authors: Naruse Mitsuhide , Inagami Tadashi 
Published: August 2015

1. Three-week-old spontaneously hypertensive rats (SHR) showed markedly elevated specific renin activity in the adrenal and the mesenteric vessels compared with control Wistar-Kyoto (WKY)rats.
2. In 17-week-old SHR with established hypertension, adrenal renin remained markedly elevated over that of WKY rats, whereas no significant difference was observed in renin of the mesenteric vessels.
3. The specific renin activity of the aorta showed no significant difference compared with that of WKY rats at 3 or 17 weeks of age.
4. These results suggest possible involvement of adrenal and vascular renin in the pathogenesis of hypertension in SHR.
Proximal and Distal Tubular Reabsorption during Isotonic Volume Expansion in Patients with Essential Hypertension as Estimated by Means of Combined Lithium and 51Cr-Labelled EDTA Clearance
Authors: Holstein-Rathlou N.-H. , Svendsen U. G. , Leyssac P. P. 
Published: August 2015

1. Ten patients with essential hypertension and ten normotensive control subjects were investigated before and after an isotonic volume load.
2. The increases in the clearances of lithium and of sodium were greater in the hypertensive than in the normotensive subjects (P &lt; 0.05). The fractional increases showed a positive correlation (rs = 0.68, P &lt; 0.05) in the hypertensive patients.
3. An increase in glomerular filtration rate in the hypertensive patients correlated positively with the increase in proximal output (rs = 0.70, P &lt; 0.05), but did not correlate with the change in sodium excretion.
4. The exaggerated natriuresis was accompanied by a significant rise in the absolute rate of sodium reabsorption in the distal segments, but distal fractional reabsorption decreased.
5. It is concluded that the exaggerated natriuresis can be accounted for by an increase in the proximal output of sodium and water.
Total Nephrectomy Alters Circulating Humoral Agents in Salt-Fed, Low-Renin Dahl S Rats to Favour Reduced Vasoconstriction in an Isolated, Perfused Bioassay Hindquarters
Authors: Tobian Louis , Johnson-Hanlon Susan , Zitur Mary , Iwai Junichi 
Published: August 2015

1. When all renal tissue is removed from salt-fed Dahl S rats, the excessive amounts of a circulating humoral vasoconstrictor effect (or lack of a vasodilator effect) are abolished, and Dahl S rats become the equal of Dahl R rats with regard to these circulating vasoconstrictor effects.
2. Total nephrectomy of salt-fed S rats also alters circulating humoral agents so that vasoconstrictor responses to sympathetic nerve stimulation and to noradrenaline infusions are markedly diminished in a perfused hindquarters preparation.
3. Both these effects of total nephrectomy are seen only in S rats, not in R rats, although plasma renin levels are lower in S rats. Thus total nephrectomy must remove much more renin and angiotensin II in R rats.
4. The effect of total nephrectomy in S rats need not necessarily be the direct removal of circulating vasoconstrictor humoral agents issuing from the S kidney. It is quite possible that removal of S kidneys has a strong influence upon the release of circulating vasconstrictor or vasodilator agents emerging from other parts of the body.
6. These effects of total nephrectomy occurring solely in S rats add still more evidence pointing to a pivotal role for the kidney in the mechanism of the NaCl hypertension of Dahl S rats.
Arachidonic Acid Stimulates Renal Kallikrein Release in Isolated Rat Kidney
Authors: Vio Carlos P. , Churchill Laurie , Terragno Alicia , McGiff John C. , Terragno Norberto A. 
Published: August 2015

1. The effect of arachidonic acid on kallikrein release was studied in an isolated rat kidney perfused with a modified Krebs-Henseleit solution.
2. Kallikrein activity was measured in both venous and urinary effluents, after DEAE-Sephadex chromatography with D-Val-Leu-Arg-p-nitroanilide as a substrate.
3. Arachidonic acid (AA) (30 nmol/ml) induced a threefold increase in kallikrein activity in the venous effluent (control = 131 ± 9 kallikrein amidase μ-units/ml vs AA = 411 ±49 kallikrein amidase μ-units/ml, P &lt; 0.005).
4. The stimulatory effect of arachidonic acid on kallikrein release is mediated by prostaglandins, since it can be prevented by the addition of indomethacin (1 μg/ml).
5. Our results demonstrate that kallikrein is released by the perfused kidney into the renal venous effluent, and that this release can be hormonally regulated by a mechanism involving prostaglandin synthesis.