bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inter-Relationship between Autoregulation of Glomerular Filtration Rate, Tubuloglomerular Feedback and Juxtaglomerular Renin Activity in Normotensive and Hypertensive Rats
Authors: Schnermann J. , Ploth D. W. , Dahlheim H. 
Published: August 2015

1. Reduction of renal perfusion pressure from 133 mmHg to 117 mmHg in control rats did not induce a significant change of kidney glomerular filtration rate (GFR) or nephron GFR determined in distal tubules. In contrast, nephron GFR measured in proximal tubular segments (NGFR-P) fell significantly.
2. Qualitatively the same response of filtration rate to changes of arterial blood pressure was found in the chronically clipped kidneys of Goldblatt hypertensive rats after acute removal of the clip.
3. In contrast, autoregulation of kidney GFR, NGFR-D and NGFR-P was abolished in the contralateral kidneys of Goldblatt hypertensive rats.
4. Microperfusion studies showed that tubuloglomerular feedback regulation of NGFR was present in the renin-rich ischaemic kidneys of Goldblatt rats after removal of the constricting clip, but greatly attenuated in the renin-depleted contralateral kidneys.
5. These data indicate that tubuloglomerular feedback participates in establishing renal autoregulation, possibly by mediation of the renin-angiotensin system.
The Role of Sodium Retention in Goldblatt 2-Kidney Hypertension in the Rat
Authors: Thurston H. , Swales J. D. 
Published: August 2015

1. Infusion of angiotensin II antagonist failed to restore the blood pressure of short-term Goldblatt 2-kidney hypertensive rats to normal levels before and after sodium restriction.
2. The blood pressure of both normal and sodium-restricted Goldblatt 2-hypertensive rats remained elevated 6 h after bilateral nephrectomy.
3. The residual hypertension found during antagonist infusion and after bilateral nephrectomy is not maintained by the renin—angiotensin system or sodium retention.
Cardiac Output Changes during Experimental Renal Hypertension in the Rabbit
Authors: Fletcher P. J. , Korner P. I. , Angus J. A. , Oliver J. R. 
Published: August 2015

1. The haemodynamic changes during the development of hypertension in rabbits have been studied for 1 week before and 4–5 weeks after sham-operation (thirteen rabbits) or bilateral renal cellophan wrapping (thirteen rabbits), Doppler flowmeters being used to measure cardiac output.
2. There was a significant but transient rise in cardiac output on post-operative day 4 in six of thirteen sham-operated rabbits and six of thirteen renal-wrap rabbits before development of hypertension. Both groups showed the same rise in mean cardiac output of 10%. The rise in cardiac output was more transient than in other species, and was not essential for subsequent development of hypertension.
Delayed Onset and Reduced Severity of Adrenal-Compression Hypertension in Rats Treated with Digitoxin
Authors: Hall C. E. , Ayachi S. , Hall O. 
Published: August 2015

1. Bilateral compression of adrenal glands combined with unilateral nephrectomy and followed by imposition of a high sodium chloride intake caused severe hypertension in all rats, accompanied by enlargement of the heart, kidneys and adrenal glands, atrophy of the thymus and severe nephrosclerosis.
2. Digitoxin treatment delayed the onset, reduced the incidence and ameliorated the magnitude of the hypertensive response in such rats; it also reduced the degree of cardiac hypertrophy, the severity of nephrosclerosis and completely prevented enlargement of the adrenals and kidneys or atrophy of the thymus.
Follow-up of Renin in Essential Hypertension
Authors: Birkenhäger W. H. , Kho T. L. , Schalekamp M. A. , Zaal G. A. , Wester A. , De Leeuw P.W. , Vandongen R. , Fawzi-Meninger T. D. 
Published: August 2015

1. Twenty-three subjects with essential hypertension were followed for a period of up to 7 years. They were untreated during the investigations.
2. Plasma renin concentration was found to decrease temporarily in some subjects. The ultimate change was a gradual rise. In those subjects who suffered myocardial infarction renin tended to rise more sharply.
3. A relationship was established with the rise in renal vascular resistance, which almost invariably occurred over the years.
Renin—angiotensin and Kallikrein—kinin Systems in Sodium Homeostasis and Hypertension in Rats
Authors: Johnston C. I. , Matthews P. G. , Dax E. 
Published: August 2015

1. Urinary kallikrein excretion was measured in rats by an enzyme kinetic method employing radioimmunoassay of generated bradykinin.
2. Rats given a sodium load (NaCl solution, 20 g/l, to drink) for 28 days showed acute and prolonged significant falls in urinary kallikrein excretion associated with suppression of plasma renin and angiotensin.
3. Conversely sodium-depleted rats showed increases in urinary kallikrein excretion, associated with rises in plasma renin and angiotensin.
4. A close and significant direct relation between plasma renin activity and urinary kallikrein excretion was demonstrated.
5. The diuresis and natriuresis induced by frusemide in rats was associated with increased urinary kallikrein excretion and acute rises in plasma renin.
6. In chronic renal hypertensive rats urinary kallikrein excretion was increased only in the animals with two-kidney Goldblatt hypertension. This group was also the only group that demonstrated a significant rise in plasma renin activity.
Anti-hypertensive Lipid from Tissue Culture of Renomedullary Interstitial Cells of the Rat
Authors: Muirhead E. E. , Rightsel W. A. , Leach B. E. , Byers L. W. , Pitcock J. A. , Brooks B. 
Published: August 2015

1. Allogenic transplants of cultured renomedullary interstitial cells exert a powerful anti-hypertensive action. The blood pressure of hypertensive animals usually drops slowly over 8–12 h whereas the pulse is unchanged or reduced.
2. Lipids derived from the cultured cells exert a similar anti-hypertensive action.
3. The anti-hypertensive action of transplanted cultured cells almost certainly results from the secretion of a substance(s) that acts in the manner of a hormone. The tissue culture lipid is a prime candidate hormone.
4. The relationship of the kidney to the hypertensive state is considered to entail pro- and antihypertensive actions. The pro-hypertensive actions include (a) activation of the renal pressor system (mainly renin—angiotensin), (b) failure to prevent sodium and fluid overloading because of either an injured or absent kidney or the excessive action of mineralocorticoids (mainly aldosterone). The antihypertensive actions of the kidney include (a) the relief of sodium and fluid overloading through diuresis—natriuresis and (b) the action of the renomedullary interstitial cell hormone (the antihypertensive renomedullary hormone).
Deoxycorticosterone Hypertension in the Pig
Authors: Terris J. M. , Berecek K. H. , Cohen E. L. , Stanley J. C. , Whitehouse W. M. , Bohr D. F. 
Published: August 2015

1. Deoxycorticosterone acetate (DOCA) implantation (100 mg/kg) caused mean arterial pressure to rise in 5–10 days from control pressures of 100–115 mmHg to stable hypertensive valnes of 140–160 mmHg in approximately 1 month. In six of seven pigs elevations of mean arterial pressure were entirely the result of increased total peripheral resistance.
2. Single implants maintained serum DOCA at approximately ten times normal concentration for up to 90 days.
3. Moderate but variable decreases in serum aldosterone followed implantation.
4. Hypokalaemia, polydipsia and suppressed plasma renin activity were evident by the fifth post-implantation day and persisted thereafter. No consistent change occurred in serum sodium.
5. Noradrenaline or angiotensin caused increases in total peripheral resistance at lower threshold infusion rates in hypertensive pigs compared with control animals.
6. In isolated, perfused hind-limb preparations, hypertensive vascular beds were characterized by both functional (increased vascular smooth muscle sensitivity) and structural (elevated resistance of maximally dilated vascular bed) changes. ‘Protection’ from increased arterial wall stresses in hypertensive pigs prevented structural, but not functional, alterations.
Increased Renal Sensitivity to Aldosterone in the Potassium-Loaded Rat
Authors: Adam W. R. , Funder J. W. 
Published: August 2015

1. The renal response to aldosterone (urinary sodium and potassium excretion) was determined in adrenalectomized rats previously fed either a high potassium diet or a control diet. High K+ rats showed an enhanced response to aldosterone at all doses tested.
2. This enhanced response to aldosterone required the presence of the adrenal glands during the induction period, could be suppressed by a high sodium intake, but could not be induced by a low sodium diet.
3. No difference between high K+ and control rats could be detected in renal mineralocorticoid receptors, assessed by both in vivo and in vitro binding of tritiated aldosterone.
4. The method of the induction, and the mechanism of the enhanced response, remain to be defined.
Cardiac Reflexes Conducted by Vagal Afferents in Normotensive and Renal Hypertensive Dogs
Authors: Kezdi P. 
Published: August 2015

1. The renal sympathetic reflex responses to transient balloon occlusion of the descending aorta (systemic baroreceptor activation) and the ascending aorta (cardiac stretch-receptor activation) have been studied together with blood pressure increases after successive cutting of carotid sinus, aortic and vagus nerves in acute experiments in the dog.
2. Results from these experiments provide evidence for cardiac vagal afferent participation in the tonic regulation of systemic blood pressure.
3. In other experiments the reflex pressure-response curve of the isolated gracilis muscle at constant flow to transient ascending aorta occlusion was measured. This curve was moved to the right in renal hypertensive dogs as compared with normotensive dogs. The threshold response of left ventricular vagal afferent nerves was shifted to higher left ventricular pressure in the former.
3. These findings indicate resetting of ventricular receptors in hypertensive animals.
Baroreflex Control of Coronary Conductance in Normotensive and Renal Hypertensive Conscious Dogs with Complete Heart Block
Authors: White S. W. , Porges W. L. , Reid J. V. O. , Bhagat C. I. 
Published: August 2015

1. The autonomic and local control of the circumflex coronary bed evoked through acute rises in aortic pressure (aortic balloon inflation) was analysed in conscious, normotensive and hypertensive dogs in complete heart block with ventricles paced at 100 beats/min.
2. In normotensive dogs there was an initial rise (6–12 s) in circumflex conductance preceding a fall in conductance as aortic pressure increased and was sustained. The initial rise, but not the later fall, in circumflex conductance was partly due to a cholino-receptor and partly due to α-adrenoreceptor mechanisms. Local constrictor mechanisms were responsible for the later fall in conductance.
3. The initial cholinoreceptor component of the rise in circumflex conductance is initiated through arterial baroreflex mechanisms.
4. The initial autonomic mechanisms regulating circumflex conductance appear to be absent in renal hypertension.
5. The absence of the transient autonomic rise in circumflex flow and conductance in response to rapid elevations in aortic pressure in certain forms of hypertension, e.g. during tachyarrhythmias and behavioural disturbances, may result in myocardial ischaemia when it is least appropriate.
Valsalva Vasoconstrictor Reflex in Human Hypertension and after β-Adrenoreceptor Blockade in Conscious Rabbits
Authors: Korner P. I. , Blombery P. A. , Bobik A. , Tonkin A. M. , Uther J. B. 
Published: August 2015

1. A Valsalva-like manoeuvre was used to elicit graded rises in total peripheral resistance (TPR) in conscious rabbits. The rises were reflex and mediated through sympathetic constrictors. Propranolol infused at different rates reaching plasma concentrations up to 240 (sem 33) ng/ml had no effect on this reflex but reduced mean arterial pressure. However, the response was attenuated by clonidine in a dose-dependent manner.
2. Valsalva manoeuvres were used to elicit graded sympathetically mediated rises in TPR index in twenty-nine subjects with mean arterial pressure ranging from 75 to 165 mmHg. Absolute sensitivity of the constrictor response increased with rising resting TPR index, resulting in some enhancement of constrictor responses in the hypertensive subjects. It seems likely that non-autonomic factors (e.g. vessel structure) rather than hyperactive neural constrictor effects are involved in the enhanced constrictor responses in essential hypertension.
Effect of Angiotensin II on Noradrenaline Content in the Rat Hypothalamus
Authors: Iijima M. , Kitamura Y. , Yamamoto N. , Kawamura H. , Yasugi T. , Hatano M. 
Published: August 2015

1. Intravenous administration of angiotensin II reduced the adrenaline content, increased the catechol-O-methyltransferase activity, and decreased the monoamine oxidase activity of the rat hypothalamus.
2. Intraventricularly administered angiotensin II reduced the noradrenaline content to a smaller extent.
3. The change produced by intravenous administration of angiotensin might be indirectly caused by a response to angiotensin.
Neural and Non-Neural Mechanisms in Spontaneous Hypertension
Authors: Yamori Y. 
Published: August 2015

1. The pathogenesis of hypertension in spontaneously hypertensive rats (SHR) is considered to consist of neurogenic and non-neurogenic factors, both of which contribute to initiation and maintenance mechanisms.
2. Neurogenic factors have been demonstrated by the destruction of the central nervous system, sympathectomy, recording of sympathetic discharge, hind-limb perfusion and study of noradrenaline. These factors are mainly involved in the initiation of hypertension, and they appear to diminish in importance after the establishment of hypertension, as indicated by the noradrenaline-turnover study.
3. The non-neurogenic factors have been demonstrated haemodynamically by increased peripheral vascular resistance remaining even after sympathectomy. They have also been demonstrated histologically by the narrowing of resistance arteries with medial hyperplasia or hypertrophy. These factors appear to participate in maintenance mechanisms.
4. Increased incorporation of labelled amino acid into non-collagenous and collagenous protein of the arterial walls precedes medial hypertrophy and hypertensive arteriosclerosis. It seems to play a role therefore both during neurogenic initiation and later non-neurogenic maintenance of blood pressure.
5. Non-collagenous protein metabolism of arterial walls is increased in young SHR, and it is partly dependent on neural innervation as detected by surgical or pharmacological sympathectomy. It indicates a close linkage between neurological and structural changes in the initiation of spontaneous hypertension.
Sympathotonia in Primary Hypertension and in a Caricature Resembling Dysautonomia
Authors: Dequattro V. , Campese V. , Miura Y. , Esler M. 
Published: August 2015

1. Plasma catecholamines and adrenergic correlates of cardiac function were compared in young men with borderline hypertension, classified according to renin status (group 1). Plasma catecholamines were increased and cardiac pre-ejection periods were shortened in ‘high’-renin patients.
2. Plasma catecholamines were raised in 70% of ‘high’-renin patients with primary hypertension (group 2), were related directly with age in normotensive females and were related inversely with catecholamine responses to postural stress in both normotensive and hypertensive subjects (P < 0·01).
3. The raised catecholamines of four ‘high’-renin patients with pronounced features of sympathetic nerve activity-caricatures were elevated further during hypertensive periods. Mean arterial blood pressures were reduced 20–30% after either α- or β-receptor blockade. Catecholamines were reduced after β-receptor blockade.
4. There appears to be a spectrum of neurogenic ‘gain’ in primary hypertension; it is suppressed in ‘low’-renin hypertension, directly related to blood pressure in ‘normal’-renin hypertension, increased in ‘high’-renin hypertension and achieves a maximum in caricatures. Neurogenic factors seem to be important in the cause and maintenance of ‘high’- and ‘normal’-renin hypertension respectively. The caricatures may be examples of a severe form of hypothalamic stimulation.
Plasma Noradrenaline and Renovascular Hypertension in the Rat
Authors: Reid J. L. , Dargie H. J. , Franklin S. S. , Fraser Beverly 
Published: August 2015

1. Plasma noradrenaline was measured in groups of rats up to 4 weeks after application of a renal artery clip.
2. When renal artery clipping was accompanied by contralateral nephrectomy (one-kidney model) plasma noradrenaline was significantly higher in hypertensive rats than in sham-operated control rats at 7, 14 and 28 days.
3. Plasma noradrenaline was not altered at any time examined in the two-kidney model (unilateral clip and contralateral kidney left in situ).
4. Neurogenic mechanisms mediated by the peripheral sympathetic nervous system appear to participate in the development of one-kidney renovascular hypertension, but do not play a significant role in the two-kidney model.
Interaction of Angiotensin II with Catecholamines in the Circulation of the Dog and Cat
Authors: Ng K. K. F. , Duffy S. , Louis W. J. , Doyle A. E. 
Published: August 2015

1. The blood-bathed organ technique was employed to study the effects of angiotensin II and catecholamines on an isolated everted rat aorta bathed in the extracorporeal circulating blood of adult dogs and cats.
2. When the injections were made into the bathing blood close to the everted rat aorta, angiotensin II was half as potent as adrenaline or noradrenaline on a molar basis.
3. After intravenous injections, the vasoconstrictor potency of angiotensin was twenty times that of adrenaline or noradrenaline on the everted rat aorta. The increase in potency was due to the interaction of angiotensin II with catecholamines on the preparation.
4. Intravenous phenoxybenzamine abolished the potentiated vasoconstrictor effect of angiotensin II on the blood-bathed everted rat aorta, but it did not abolish the pressor effect of angiotensin II on the cardiovascular system of the animals. The results suggest that catecholamines released into the circulating blood by intravenous angiotensin II do not play an important role in the pressor effect of angiotensin II.
Catecholamines, Blood Pressure, Renin and Myocardial Function in the Spontaneously Hypertensive Rat
Authors: Oparil Suzanne , Erinoff Lynda , Cutilletta A. 
Published: August 2015

1. Neither nerve-growth-factor antiserum (NGFAS) administered subcutaneously nor 6-hydroxydopamine administered intraventricularly to immature spontaneously hypertensive rats (SHR) inhibited the development of the hypertensive syndrome. In contrast, NGFAS did not affect blood pressure in normotensive Kyoto/Wistar rats.
2. Peripheral vascular resistance was increased and cardiac index decreased in both NGFAS and 6-hydroxydopamine-treated SHR despite preservation of normal blood pressure.
3. NGFAS treatment did not influence the development of left ventricular hypertrophy in SHR, despite the lowering of blood pressure. In contrast, 6-hydroxydopamine caused an attenuation in the development of left ventricular hypertrophy.
4. Indices of left ventricular contractility were depressed by NGFAS treatment but not by 6-hydroxydopamine.
5. Plasma renin activity was unaffected by NGFAS treatment and increased by 6-hydroxydopamine.
Haemodynamic Long-Term Effects of β-Receptor-Blocking Agents in Hypertension: A Comparison between Alprenolol, Atenolol, Metoprolol and Timolol
Authors: Lund-Johansen P. , Ohm O. J. 
Published: August 2015

1. Oxygen consumption and central haemodynamics were recorded at rest and during exercise in fifty-one men with essential hypertension (W.H.O. stage I) and repeated after 1 year on a single drug: alprenolol (n = 10), atenolol (13) metoprolol (12) and timolol (16).
2. Mean arterial pressure was significantly reduced in all groups at rest (11–18%) and during exercise (5–11%). Heart rate was significantly reduced in all groups (20–28%) at rest and (17–26%) during exercise. Owing to increase in supine resting and exercise stroke volume in the alprenolol and atenolol group, cardiac index decreased less than heart rate-in contrast to the timolol group where cardiac index was decreased 26–32%. The calculated post-treatment total peripheral resistance was significantly increased at rest and during exercise in the timolol group. In the other groups the total peripheral resistance was significantly increased at rest when sitting, but not at rest when supine and during exercise.
3. It is concluded that the major haemodynamic changes induced in subjects with moderate and mild essential hypertension by these different β-receptor blockers are the same, but that minor differences exist with respect to effect upon stroke volume and total peripheral resistance.
Clinical Evaluation of Atenolol in Hypertension
Authors: Hansson L. , Karlberg B. E. , Åberg H. , Westerlund A. , Henningsen N. C. , Jameson S. 
Published: August 2015

1. Atenolol (ICI 66.082, Tenormin) is a new β-adrenoreceptor-blocking agent, devoid of intrinsic sympathomimetic and membrane-stabilizing properties. It does not cross the blood—brain barrier.
2. Atenolol given to hypertensive patients in initial open trials reduced arterial blood pressure significantly.
3. A double-blind comparison between atenolol and placebo in forty-five patients with essential hypertension demonstrated that atenolol gave a statistically significant reduction of blood pressure (Δ 28/15 mmHg, P < 0·005).
4. The optimum anti-hypertensive dose of atenolol in patients with mild to moderately severe essential hypertension was 200 mg daily.
5. Atenolol was compared with propranolol in thirty patients with essential hypertension. No statistically significant differences of anti-hypertensive effect were observed between the two drugs.
6. Long-term results (up to 2 years) in 117 hypertensive patients indicate that drug tolerance is good. No serious toxic effects were observed.
7. In four of twelve hypertensive patients with obstructive airways disease atenolol had to be withdrawn owing to deterioration of ventilatory function.
A Controlled Study on the Anti-Hypertensive Effect of a new β-Adrenoreceptor-Blocking Drug, Metoprolol, in Combination with Chlorthalidone
Authors: Jäättelä A. , Pyörälä K. 
Published: August 2015

1. A double-blind cross-over evaluation of the anti-hypertensive effect of metoprolol vs placebo was carried out in a series of twenty-three patients with mild or moderate essential hypertension who were receiving 25 mg of chlorthalidone daily as their basic treatment. An individually determined dose of metoprolol (75–300 mg) was used.
2. Metoprolol, as compared with placebo, produced a statistically significant reduction of blood pressure, both in supine and standing positions.
3. During the double-blind cross-over study mild side effects were more common at the beginning of metoprolol/chlorthalidone treatment than during placebo/chlorthalidone, but these tended to diminish or disappear with time.
4. Metoprolol in combination with chlorthalidone appears to be an effective and well-tolerated treatment for mild and moderate hypertension in patients not responding to chlorthalidone alone.
Clinical and Haemodynamic Study of Atenolol (Tenormin) in Essential Hypertension
Authors: Jensen H. Æ. , Rasmussen K. , Mosbæk N. 
Published: August 2015

1. The β1-adrenoreceptor-blocking agent atenolol was studied in the treatment of twelve out-patients with essential hypertension.
2. With a mean dose of 110 mg of atenolol daily (range 75–200 mg/day) we observed a pronounced decrease in blood pressure.
3. Only minimal side effects were seen.
4. Cardiac output decreased from 4·6 to 3·4 l/min during treatment. This decrease did not correlate with the decrease in blood pressure but correlated well with the changes in calculated total peripheral resistance.