bluuebunny/crossref_metadata_2025_split huggingface dataset:
Raised Intracellular Sodium Consequent to Sodium-Potassium-Dependent ATPase Inhibition Does Not Cause Myogenic Contractions of 150 μm Arteries from Rat and Guinea Pig
Authors: Mulvany M. J. , Aalkjær C. , Nilsson H. , Korsgaard N. , Petersen T. 
Published: August 2015

1. We have examined effects of inhibition of Na+,K+-dependent ATPase in large and small arterial ring preparations from rats and guinea pigs.
2. Ouabain (1 mmol/l) caused myogenic contraction of rat aorta and tail artery, but had no long-lasting effect on 150 μm mesenteric and 150 μm femoral resistance vessels over a 3 h period. Much lower concentrations of ouabain (1 μmol/l) caused contraction of guinea pig aorta, but had no effect on the mesenteric and femoral resistance vessels.
3. In the mesenteric resistance vessels, ouabain (1 mmol/l, rat vessels; 1 μmol/l, guinea pig vessels) caused the intracellular sodium content to rise over 2 h from approx. 13 mmol/l to approx. 60 mmol/l, and in the rat mesenteric resistance vessels this was associated with membrane depolarization from approx. −54 mV to approx. −30 mV after 3 h.
4. The results suggest that whereas Na+,K+-ATPase inhibition and consequent raised intracellular sodium may cause contraction of large vessels, this does not seem to be the case for small vessels. It therefore seems that further investigation is required before it is accepted that raised intracellular sodium is in itself a factor of importance in the etiology of hypertension.
Evidence for a Plasma Factor Affecting Na+ Cellular Transport in Genetic Normotensive Subjects and in Borderline Hypertensive Subjects
Authors: Costa F. V. , Montebugnoli L. , Giordani M. F. , Vasconi L. , Ambrosioni E. 
Published: August 2015

1. Lymphocytes from normotensive subjects with normal intralymphocytic sodium content were incubated for 1 h in plasma from subjects with essential hypertension, secondary hypertension or borderline hypertension, and from normotensive subjects with (genetic) and without (non-genetic) family history of hypertension.
2. Lymphocytes from non-genetic normotensive subjects greatly increase their intralymphocytic sodium content after incubation in plasma (diluted 1:4) of patients with essential hypertension (but not with secondary hypertension), of borderline subjects and of genetic normotensive subjects with abnormally high intralymphocytic sodium content (&lt;26 mmol/kg).
3. When plasma is diluted 1:8, an increase in intralymphocytic sodium content is detectable only after incubation in plasma of borderline subjects and of genetic normotensive subjects with high intralymphocytic sodium content.
4. These data suggest that a plasma factor altering Na+ transport is detectable in all the subjects in whom intralymphocytic sodium content is high, independently of their blood pressure values. The concentration (or the activity) of this substance is greater in borderline and genetic normotensive subjects than in patients with sustained essential hypertension. This suggests that these subjects are in a dynamic phase of the development of hypertension.
Studies of Sodium Transport in Thymocytes of Rats with DOC/Salt Hypertension
Authors: Jones R. B. , Patrick J. , Hilton P. J. 
Published: August 2015

1. Sodium transport and intracellular sodium content were studied in thymocytes of rats made hypertensive by treatment for 4 or 8 weeks with deoxycorticosterone (DOC) and salt (DOC/salt).
2. The systolic blood pressure in the DOC/salt animals was 152 ± sem 3 and 189 ± 3 mmHg after 4 and 8 weeks' treatment respectively. This was significantly higher than pressures in their respective controls (124 ± 4 and 126 ± 5 mmHg), which had been given 1% sodium chloride solution (171 mmol/l) only.
3. The total sodium efflux rate constant in the DOC/salt rats was lower than that in the control group after 8 weeks of treatment (5.56 ± sem 0.21 vs 6.12 ± 0.11 h−1; P &lt; 0.05) but not after 4 weeks of treatment (5.93 ± 0.13 vs 6.32 ± 0.13 h−1;0.1 &gt; P &gt; 0.05).
4. Intracellular sodium content in the DOC/salt rats was significantly higher than that of the control animals after 8 weeks' treatment (49.6 ± 2.5 vs 42.1 ± 1.0 mmol/kg dry weight; P &lt; 0.05).
5. No significant changes were observed in intracellular potassium content, sodium influx or ouabain-insensitive sodium efflux rate constant.
Intravital Studies on Cerebral Arteries in Hypertensive and Normotensive Rats
Authors: Johansson Barbro B. , Auer Ludwig M. , Sayama Ichiro 
Published: August 2015

1. The diameters of main cortical surface branches of the middle cerebral artery were continuously monitored through a closed cranial window in spontaneously hypertensive rats (SHR) and in normotensive Wistar Kyoto (WKY) rats by aid of a multichannel video-angiometer under resting conditions and under maximal vasodilatation induced by hypercapnia.
2. Initial mean arterial pressure was 172 ± sem 9 mmHg in SHR and 103 ± 5 mmHg in WKY rats; during hypercapnia the corresponding values were 183 ± 9 and 127 ± 7 mmHg.
3. The resting diameter of the arteries was 55 ± 1 μm in SHR (n = 53) and 87 ± 1 μm in WKY rats (n = 53; P &lt; 0.001). The percentage increase in diameter during vasodilatation (Paco2 70 mmHg) was larger in SHR (54%) than in WKY rats (36%). However, the maximum lumen diameter remained significantly smaller in SHR (84 ± 2 μm compared with 117 ± 5 μm in WKY rats; P &lt; 0.001). No significant further dilatation was seen in either group after α-adrenoceptor blockade.
4. The smaller diameter of cortical arteries during vasodilatation is consistent with the concept that hypertensive vascular hypertrophy encroaches on the lumen in vivo. The larger percentage increase in diameter of cortical arteries in hypertensive rats corroborates Folkow's hypothesis on the haemodynamic consequences of an altered media/lumen ratio in hypertension.
5. There is no evidence that an enhanced sympatho-adrenergic tone prevents maximum vasodilatation during hypercapnia in SHR.
Estimation of Forearm Arterial Compliance in Essential Hypertension: A Preliminary Report
Authors: Simon A. CH. , Levenson J. A. , Laurent S. P. , Safar M. E. 
Published: August 2015

1. Simultaneous brachial artery pressure and blood flow measurements were made in 21 men, including six normal subjects and 15 patients with essential hypertension of the same age and diastolic pressure at the time of investigation.
2. Blood flow was evaluated by means of a pulsed Doppler device with a double transducer probe, enabling a precise evaluation of the calibre of the brachial artery. From analysis of the pressure-flow curves during diastole, forearm arterial compliance was estimated by using an original first-order model of the forearm arterial system.
3. Forearm arterial compliance was significantly decreased in hypertensive subjects.
4. Since patients and hypertensive subjects had similar blood pressures, the results indicate that the reduced forearm compliance was independent of blood pressure per se but may reflect in hypertensive subjects adaptive changes in the walls of peripheral large arteries.
The Relation of Arterial Pressure with Plasma and Body Electrolytes is Similar in Conn's Syndrome and Essential Hypertension
Authors: Beretta-Piccoli C. , Davies D. L. , Brown J. J. , Ferriss J. B. , Fraser R. , Lever A. F. , Morton J. J. , Robertson J. I. S. 
Published: August 2015

1. Arterial pressure, exchangeable sodium (NaE), exchangeable potassium (KE) and plasma concentrations of sodium, potassium, urea, angiotension II and aldosterone were measured in 34 patients with untreated Conn's syndrome before surgical removal of their adenoma. The study was repeated in 23 patients between 3 and 12 months after the operation.
2. Plasma aldosterone, NaE and plasma sodium concentration were higher and KE and plasma potassium concentration were lower than predicted normal. Surgery corrected these abnormalities, also reducing blood pressure from an average of 183/112 to 138/86 mmHg.
3. Systolic blood pressure was positively correlated with plasma and exchangeable sodium and negatively correlated with plasma potassium concentration. The relation of NaE and arterial pressure was closer in old than in young patients. None of these correlations was significant after operation. Before operation plasma urea was insignificantly related to arterial pressure but after operation a significant and positive correlation emerged.
4. A relation between arterial pressure and NaE is to be expected in a state of mineralocorticoid excess but the different correlation in old and young patients was not expected. A similar difference exists in patients with essential hypertension.
A Role for β-Melanotropin in the Regulation of Aldosterone Secretion during Sodium Deficiency in the Rat
Authors: Yamakado Minoru , Franco-Saenz Roberto , Mulrow Patrick J. 
Published: August 2015

1. The effect of sodium deficiency on adrenal sensitivity to β-melanotropin (β-melanocyte stimulating hormone; β-MSH) and the effect of β-MSH on a late step of aldosterone biosynthesis were studied using collagenase-dispersed rat adrenal cells.
2. Sodium depletion enhanced the sensitivity of the adrenal glomerulosa cells to β-MSH, resulting in a shift of the dose-response curve to the left, so that doses of β-MSH within the physiological range caused significant stimulation of aldosterone production.
3. The aldosterone level obtained by maximum doses of β-MSH was similar to that obtained after angiotensin (‘angiotensin II’; ANGII) during sodium depletion.
4. Sodium depletion did not change the corticosterone response to β-MSH by decapsular cells.
5. Similarly to ANGII, β-MSH significantly stimulated the conversion of exogenous corticosterone into aldosterone in the presence of an inhibitor of 3β-hydroxysteroid dehydrogenase, WIN 19,578.
6. These data suggest that β-MSH or peptides containing β-MSH may play a role in the regulation of aldosterone secretion during sodium depletion in the rat and that β-MSH increases aldosterone production partly by stimulating the late step in aldosterone biosynthesis, the conversion of corticosterone into aldosterone.
Generation of Inactive Renin in Vitro and in Vivo: Reversible Inactivation of the Active Plasma Enzyme in Rats
Authors: Barrett Jack D. , Eggena Peter , Sambhi Mohinder P. 
Published: August 2015

1. Active and total (trypsin treatment) plasma renins were measured in normal Wistar rats and in rats in which the renin-angiotensin system was stimulated by ether anaesthesia.
2. After incubation of normal plasma in vitro in the absence of angiotensinase inhibitors, active renin declined. This decline was shown to be due to the conversion of active renin into an inactive form, which could be re-activated by trypsin.
3. In plasma from renin-stimulated rats, the rate of decline of active renin in vitro was accelerated; however, the relative amount of inactive renin generated was decreased.
4. Ligation of the kidneys of the ether-anaesthetized animal resulted in a build-up in vivo of inactive renin concomitant with the decline of active renin.
5. These data demonstrate the conversion of active into inactive renin in vitro and indicate that inactive renin can also be generated in vivo from the active form of the enzyme.
6. Multiple forms of inactive renin may exist; some may be true ‘prorenins’ (renin zymogens) produced in the kidney, and others may result from post-biosynthetic modifications of the active plasma enzyme.
Changes in Nuclear Initiation Sites after the Treatment of Isolated Nuclei with Angiotensin II
Authors: Re Richard N. 
Published: August 2015

1. Angiotensin II (ANG II) increases hepatic RNA synthesis. Because the hormone apparently can be found in the cytoplasm of at least some target cells and because intracellular receptors have been demonstrated for this hormone, we investigated the direct effect of angiotensin II on isolated nuclei.
2. Nuclei were purified from rat liver and then treated for 2 h at 37°C with various concentrations of angiotensin II. Chromatin was then isolated and initiation-site number was estimated by utilizing exogenous Escherichia coli RNA polymerase.
3. Statistically significant increases in initiation-site number were noted in nuclei treated with angiotensin II suggesting that at least part of the hormone's stimulatory effect on RNA synthesis results by this mechanism. Furthermore, these observations suggest a direct nuclear effect of this peptide hormone.
Response of Blood Pressure and the Renin—Angiotensin—Aldosterone System to Chronic Ambulatory Peritoneal Dialysis in Hypertensive End-Stage Renal Failure
Authors: Glasson Ph. , Favre H. , Vallotton M. B. 
Published: August 2015

1. Chronic ambulatory peritoneal dialysis allows good control of blood pressure in patients with hypertensive end-stage renal disease. The role of the renin-angiotensin-aldosterone system has therefore been studied in seven patients during the first 6 months of chronic ambulatory peritoneal dialysis treatment.
2. Steady increases in plasma renin activity and aldosterone were observed with a good correlation between these two variables. Plasma electrolytes, renin substrate and body weight did not change significantly.
3. Angiotensin II perfusion tests, performed at the end of the study, showed a relative vascular resistance to angiotensin II.
4. Stimulation of the renin-angiotensin-aldosterone system may be partially explained by this last observation or by removal of an unknown vasopressor substance responsible for the inhibition of the plasma renin activity.
Effect of Ureteral Ligation of the Contralateral Kidney on Angiotensin Dependency in One-Clip, Two-Kidney Renal Hypertensive Rats
Authors: Takata Yutaka , Doyle Austin E. , Veroni Margherita , Duffy Stuart G. 
Published: August 2015

1. The aim of this study was to determine whether the urinary excretory function of the contralateral kidney is essential for angiotensin dependency in two-kidney, one-clip renal hypertensive rats. Ureteric ligation was used to abolish excretion from the contralateral kidney.
2. Plasma renin activity (PRA), renal renin content (RRC) and the response of blood pressure to captopril were examined.
3. The increase of blood pressure produced by the application of a clip to one renal artery was slightly accelerated by the ureteral ligation of the contralateral kidney.
4. Ureteral ligation of the contralateral kidney did not alter the response to a single oral administration of captopril. PRA and RRC of both kidneys were not different between the ureteral ligated group and the group without ureteric ligation. The falls in blood pressure produced by captopril correlated with PRA in the two groups.
5. These results suggest that the excretory function of the contralateral kidney is not essential for angiotensin dependency in the two-kidney, one-clip hypertensive rat model.
Effects of Moderate Salt Restriction and High Potassium Intake on Intralymphocytic Sodium Content and Pressor Response to Stress in Borderline Hypertension
Authors: Ambrosioni E. , Costa F. V. , Borghi C. , Montebugnoli L. , Giordani M. F. , Vasconi L. 
Published: August 2015

1. Twenty young subjects with borderline hypertension were studied to evaluate the effects of moderate salt restriction and/or of a high potassium intake on intralymphocytic sodium content and blood pressure. Blood pressure was measured after 1 min (casual) and after 5 min (baseline) of rest and during handgrip.
2. Moderate sodium restriction (from 170 to 100 mmol of sodium/day) decreased both intralymphocytic sodium content and diastolic blood pressure at rest and during handgrip. During a high potassium diet (130 mmol of potassium/day) both intralymphocytic sodium content and baseline diastolic blood pressure rose significantly whereas casual diastolic blood pressure remained unchanged and pressor response to handgrip was reduced by 50%.
3. The increase in intralymphocytic sodium content induced by the high potassium diet was dose-dependent. A daily dose of 0.8 mmol of potassium/kg body weight produced the maximal protective effect on blood pressure during exercise with minimal effects on intralymphocytic sodium content and baseline blood pressure.
4. In borderline subjects a low sodium/high potassium diet seems to produce the most favourable effect, since intralymphocytic sodium content and baseline blood pressure remain unchanged whereas the pressor response to handgrip is reduced.
‘Vascular Kallikrein’: A Kallikrein-Like Enzyme Present in Vascular Tissue of the Rat
Authors: Nolly Héctor , Lama M. Cristina 
Published: August 2015

1. The present study was undertaken to examine whether there is a kallikrein-like enzyme in vascular tissue. Isolated saline-perfused rat mesenteric arteries were used and arterial homogenate was incubated with heat-treated dog plasma and citrate/phosphate buffer (pH 8.5) in the presence of peptidase inhibitors for 60 min.
2. The kallikrein-like enzyme showed optimum activity in the range pH 7.0-9.0. The rate at which it releases kinin is similar to the release of kinin by kallikrein and trypsin. The release is unaffected by incubation of the enzyme with trypsin-inhibitors, but completely inhibited by aprotinin.
3. The kinin released by arterial homogenate resembles bradykinin in its chemical and pharmacological properties, and by using antibodies that specifically inhibit kinins, the biological action was completely abolished.
4. These results indicate that arterial tissue contains an enzyme with physicochemical characteristics quite similar to those of kallikreins of glandular origin.
Elevated Plasma Vasopressin Contributes to Fulminating Hypertension Produced by Functional Impairment of A1 Catecholamine Neurons in Rabbit Medulla
Authors: Blessing W. W. , Sved A. F. , Reis D. J. 
Published: August 2015

1. Injection of the neurotoxin kainic acid into the region of the A1 noradrenergic neurons in the caudal ventrolateral medulla of rabbit increases blood pressure by 35 mmHg and plasma vasopressin five fold.
2. After cervical spinal cord transection or intravenous injection of phentolamine, kainic acid injected into the A1 area still elevates arterial pressure.
3. The increase in blood pressure produced by injection of kainic acid into the A1 area of the intact rabbit is almost completely reversed by the administration of a vasopressin antagonist.
4. A1 noradrenergic neurons tonically inhibit the release of vasopressin and the amount of vasopressin released by destruction of these cells is sufficient to elevate arterial pressure.
5. Imbalance within the central nervous system can produce hypertension by means of vasopressin release.
Increased Presynaptic α-Adrenoceptor-Mediated Regulation of Noradrenaline Release in the Isolated Perfused Kidney of Spontaneously Hypertensive Rats
Authors: Ekas R. D. , Steenberg M. L. , Lokhandwala M. F. 
Published: August 2015

1. Release of [3H]noradrenaline during peri-arterial nerve stimulation and its inhibition by the presynaptic α-adrenoceptor mechanism were studied in the isolated perfused kidney from spontaneously hypertensive and Wistar-Kyoto rats.
2. A frequency related vasoconstriction as well as [3H]noradrenaline release were observed over the stimulating range of 0.25-32 Hz in both the Wistar-Kyoto and spontaneously hypertensive rats. The spontaneously hypertensive rat kidneys exhibited both an increased vasoconstrictor response and a greater [3H]noradrenaline release when compared with the Wistar-Kyoto rat kidneys.
3. Presynaptic inhibition of [3H]noradrenaline release was evaluated at 2 Hz by using the α-adrenoceptor agonist, tramazoline. Increasing concentrations of tramazoline from 2 × 10−9 mol/l to 2 × 10−7 mol/l caused a dose-dependent decrease in the stimulus-induced release of [3H]noradrenaline in spontaneously hypertensive rats but not in Wistar-Kyoto rats. Only 2 × 10−7 mol/l tramazoline had an inhibitory effect in the Wistar-Kyoto rats.
4. These data indicate that noradrenaline release during sympathetic nerve stimulation is greater in the spontaneously hypertensive rat. The supersensitivity of presynaptic α-adrenoceptors observed in spontaneously hypertensive rats may be a consequence of the greater noradrenaline release present in these animals.
Effect of an Anteroventral Third-Ventricle Lesion on Sodium Chloride Hypertension in Dahl S Rats
Authors: Goto Atsuo , Ganguli Mukul , Tobian Louis , Johnson Mary Ann , Iwai Junichi 
Published: August 2015

1. After a lesion had been made in the anteroventral third ventricle (AV3V), Dahl S rats received daily injections of either pitressin (500 m-units/kg) or vehicle during 10 weeks of high (8%) NaCl diet. Rats with sham lesions served as controls. The blood pressure in sham-lesion rats receiving vehicle was 189 mmHg after 10 weeks of high NaCl diet. Lesion rats given vehicle showed a 60% smaller increase in blood pressure than sham-lesion rats (P &lt; 0.001), the blood pressure averaging 161 mmHg at 10 weeks.
2. Lesion rats given pitressin also showed a smaller increase in blood pressure than sham-lesion rats (P &lt; 0.05), but the final blood pressure averaged 176 mmHg and was significantly higher than that of lesion rats given vehicle (P &lt; 0.025). Pitressin injections corrected the hypernatraemia in lesion rats.
3. In another experiment, the effect of the AV3V lesion on the renal papillary plasma flow (RPPF) in Dahl S rats was studied. Dahl S rats have a lower RPPF than Dahl salt-resistant (R) rats even on a low NaCl intake. The AV3V lesion increased the RPPF by 14% in S rats (P &lt; 0.025).
4. These findings suggest that NaCl-induced hypertension in Dahl S rats requires the integrity of the AV3V region for its full expression, and the ability of the AV3V lesion to attenuate the NaCl-induced hypertension in Dahl S rats is partly related to the attenuation of vasopressin release. Moreover, the AV3V lesion partly corrected one of the characteristic features of Dahl S rats: the reduction in RPPF compared with Dahl R rats on a low NaCl intake.
Renal Function and Sympathetic Activity during Mental Stress in Spontaneously Hypertensive Rats
Authors: Lundin S. , Thorén P. 
Published: August 2015

1. The role of the renal sympathetic nerves in the urinary sodium excretion response to ‘mental stress’ in spontaneously hypertensive rats (SHR) and in Wistar-Kyoto normotensive (WKY) rats was examined. Urinary sodium excretion was measured during ‘rest’ and during a 20 min period of ‘mental stress’ in intact rats and in renal denervated rats. Under similar conditions renal sympathetic activity was also measured in a separate group of rats.
2. Urinary sodium excretion fell more during the stress period in SHR (-64 ± 5%) than in WKY rats (-34 ± 7%), despite a greater arterial pressure increase in SHR. This greater decrease in sodium excretion appeared to result from both a more pronounced reduction in GFR and a greater increase in tubular sodium reabsorbtion.
3. Renal sympathetic nerve activity, which was higher at rest in SHR than in WKY rats, increased much more in SHR than in WKY rats during stress. This may explain the greater reduction in sodium excretion in SHR during stress, because renal denervation almost abolished this latter response.
4. The neurogenically elicited renal response might contribute in an important way to the early development of SHR hypertension. Renal denervation, as well as attenuating sodium retention, also delays the pressure rise in the young SHR.
5. The initial tachycardia after mental stress gradually subsided towards the end of the stress period in SHR, whereas renal sympathetic activity remained elevated. This indicates that the increase in heart rate, if anything, may underestimate the true extent of sympathetic activation in for example the renal and splanchnic regions during arousal.