bluuebunny/crossref_metadata_2025_split huggingface dataset:
POSITIVE INTERACTION OF ETHANOL AND KAVA RESIN IN MICE
Authors: Jamieson D. D. , Duffield P. H. 
Published: June 2007

SUMMARY1. The lipid soluble extract of the psychoactive beverage kava has hypnosedative properties which can be measured by the length of time that the righting reflex is lost.2. Ethanol and the lipid soluble extract (kava resin) have been shown greatly to increase each others hypnotic action in mice. Ethanol also increases the toxicity of kava markedly.3. This interaction of kava and alcohol has important clinical and social consequences since, in contrast to traditional usage, kava is now often taken in conjunction with alcoholic drinks.
NORADRENALINE SENSITIVITY AND CALCIUM FLUXES IN ARTERIES FROM RABBITS WITH PERINEPHRITIS HYPERTENSION
Authors: Hall M. T. , Wadsworth R. M. , Kane K. A. , Hamilton C. A. , Reid J. L. , Rodger I. W. 
Published: June 2007

SUMMARY1. Contractions of isolated vascular and cardiac preparations taken from rabbits with perinephritis (one kidney, one wrapped) hypertension were compared with those of preparations from control operated animals.2. Significantly increased sensitivity to noradrenaline, which acts on α1‐adrenoceptors, was found in mesenteric arterial rings but not in aortic rings. The degree of hypersensitivity was the same in the presence and absence of cocaine, suggesting that there is no increase in uptake of noradrenaline into adrenergic nerves in this model of hypertension. In contrast to these agonist‐induced contractions, no increased sensitivity was found to potassium chloride, suggesting that hypersensitivity is specific for receptor mediated rather than membrane potential mediated effects.3. No hypersensitivity to noradrenaline was found in the isolated left or right atria, which suggests that the hypertension is associated with changes in excitation–contraction coupling in blood vessels but not in cardiac muscle.4. Hypertension increased basal 45Ca uptake in the mesenteric artery but not in the aorta. However, there was no significant difference between preparations from normotensive and hypertensive rabbits in 45Ca uptake or efflux stimulated by noradrenaline or KCl.5. Increased basal 45Ca uptake could contribute to the increased sensitivity to noradrenaline found in the mesenteric artery in rabbit perinephritis hypertension.
CHANGES IN PREJUNCTIONAL POTENCY OF B‐HT 933 DURING AGING IN THE RAT VAS DEFERENS
Authors: Pagenkopf C. W. , Bourreau J‐P. , Challice C. E. 
Published: June 2007

SUMMARY1. Age‐related changes in prejunctional α2‐adrenoceptors were examined in the rat vas deferens using pharmacological techniques.2. B‐HT 933 (1 × 10‐8–1 × 10‐6 mol/L) caused a concentration‐dependent inhibition of isometric contractions (tetrodotoxin‐sensitive) induced by stimulation with single field‐stimulus pulses, in both the epididymal and prostatic regions of rat vas deferens. The concentration–response curve to B‐HT 933 was shifted to the right with age in the prostatic regions of the vas deferens.3. In high concentrations (10‐6–3 × 10‐4 mol/L), B‐HT 933 caused concentration‐dependent enhancement of the contractile response to stimulation and evoked spontaneous contractile activity. No significant difference in this postjunctional activity occurred with age in either the prostatic or epididymal regions of the vas deferens.4. Schild analysis revealed no significant differences in pA2 values for the antagonisms of the prejunctional inhibitory effect of B‐HT 933 by rauwolscine in either the prostatic or epididymal regions of vas deferens between young and old rats.5. These results could be interpreted as a decrease in α2‐adrenoceptor number with age. The more marked decrease in the prejunctional inhibitory potency of B‐HT 933 in prostatic regions of vas deferens with aging may be due to a smaller receptor reserve in this region of the vas deferens.
SELECTIVE INHIBITION OF RESPONSES TO CARBACHOL AND McN‐A‐343 IN THE RABBIT VAS DEFERENS
Authors: Choo L. K. , Mitchelson F. 
Published: June 2007

SUMMARY1. The effect of several selective muscarine receptor antagonists were evaluated on the responses of carbachol (CCh) and McN‐A‐343 (McN) during sympathetic nerve stimulation in the rabbit vas deferens.2. The muscarine M1 receptor antagonist pirenzepine exhibited similar apparent pKB values for antagonism of the prejunctional inhibitory response of either CCh (pKB, 8.2) or McN (pKB, 8.5) on sympathetic nerve stimulation.3. The muscarine M2 receptor antagonists, pancuronium and the bisalkyl ammonium compound ‘C7/3‐phth’ were selective inhibitors of the postjunctional facilitatory response produced by CCh on sympathetic nerve stimulation. They were also 17‐and three‐fold, respectively, less potent against the inhibitory responses of McN on sympathetic nerve stimulation. The apparent pKB value of pancuronium on the inhibitory response produced by CCh did not differ significantly (P>0.05) from that using McN. A similar finding was made for C7/3‐phth.4. Selective blockade of the inhibitory response to CCh with pirenzepine (0.03 or 0.5 μmol/L) did not significantly (P>0.05) modify the apparent pKB value for pancuronium on the facilitatory response of CCh.5. Selective blockade of the facilitatory response to CCh with a low concentration of pancuronium (0.5 μmol/L) did not significantly (P>0.05) modify the apparent pKB value for pancuronium (30 μmol/L) on the inhibitory response of CCh.6. It is suggested that CCh and McN activate the same prejunctional M1 muscarine receptor and that pancuronium is the most selective of the muscarine M2 receptor antagonists presently tested in this preparation for distinguishing between muscarine M1 and M2 receptors.
GIRAFFES, RATS AND MAN – WHAT IS THE IMPORTANCE OF THE ‘STRUCTURAL FACTOR’ IN NORMO‐ AND HYPERTENSIVE STATES?
Authors: Folkow Björn 
Published: June 2007

SUMMARY1. The normal structural adaptation of heart and vessels to regional changes in load or/and tissue demands is surveyed with respect to its importance for cardiovascular function in normotension as well as in physiological (giraffes) and pathophysiological (e.g. human and rat primary hypertension) variants of high pressure states.2. At the local level it implies an entirely appropriate adjustment of cardiovascular geometric design according to principles inherent in the LaPlace and Poiseuille laws. However, when generalized to all systemic circuits, as in primary hypertension, it invites to a potentially dangerous positive feedback interaction with even ordinary functional pressor influences.3. It is further emphasized how resistance vessels, besides the obvious influence of changes in: (i) vascular smooth muscle activity, are greatly affected also by changes of their (ii) geometric design, (iii) wall distensibility, and (iv) transmural pressure, how each of these four parameters can be independently altered and how they interact. Genetic reinforcements and various trophic influences may facilitate the extent and rate of ‘structural upward resetting’ in primary hypertension, and this resetting also encompasses the barostat mechanisms.4. Against such a background it is, in fact, from a physiological point of view, more difficult to explain how 85–90% of the population manage to maintain lifelong normotension than to explain why hypertension gradually afflicts the remaining 10–15%. It points to the presence of potentially powerful and durable, negative feedbacks that are still poorly understood (e.g. Muirhead's renomedullary depressor system).5. Considering the dominant haemodynamic influence of the structural factor in primary hypertension, it is finally stressed how the long‐range goal of antihypertensive treatment should be to cause full regression of the structural upward resetting, or perhaps even to prevent its early development in subjects predisposed for hypertension.
EVIDENCE FOR A ROLE FOR THE CARDIOVASCULAR AMPLIFIERS IN HUMAN PRIMARY HYPERTENSION
Authors: Jennings Garry , Korner Paul I. , Sudhir Krishnankutty , Esler Murray , Angus James A. , Laufer Eljas 
Published: June 2007

SUMMARY1. Hypertrophy of vascular and cardiac smooth muscle is present in human primary hypertension. The amplifier properties associated with hypertrophy play a major role in maintaining hypertension.2. Long‐term antihypertensive drug therapy causes substantial regression of the structural changes, assessed by the non‐autonomic component of vascular resistance, and by left ventricular mass. The latter occurs more slowly.3. The more complete the reversal of left ventricular hypertrophy, the more slowly hypertension redevelops if long‐term antihypertensive therapy is discontinued.4. Subjects who redevelop hypertension more rapidly tend to have higher cardiac output, suggesting that the cardiac amplifier may play a role in the pathogenesis.5. Studies of small arteries and of veins from patients with primary hypertension suggest that there may be a general disturbance of vascular smooth muscle function, independent of the mechanical effects of elevated systemic blood pressure.
NEUROPEPTIDE Y AND CARDIOVASCULAR REGULATION
Authors: McCloskey D. I. , Potter Erica K. 
Published: June 2007

SUMMARY1. The effects of neuropeptide Y (NPY) and related peptide fragments on blood pressure and vagal action at the heart were compared in the anaesthetized rat.2. A change in vagal action was taken as a measure of presynaptic activity and a change in blood pressure was taken as a measure of postsynaptic activity.3. NPY, NPY‐(13‐36) and a stabilized 13‐36 analogue of NPY (ANA NPY) all exerted pressor actions and attenuated vagal action at the heart.4. On the basis of different potencies demonstrated for the pressor and vagal inhibitory actions of these peptides, the results are consistent with the proposal that there are two populations of NPY receptors.
CARDIOVASCULAR FUNCTIONS OF CENTRAL NORADRENERGIC NEURONS IN RABBITS
Authors: Head Geoffrey A. 
Published: June 2007

SUMMARY1. The cardiovascular actions of central noradrenergic (NA) neurons was examined using the acute neurotransmitter releasing actions of intracisternal 6‐hydroxydopamine in conscious rabbits.2. The predominant actions of NA pathways in the brain‐stem are to inhibit vasomotor and cardiac sympathetic activity and to facilitate cardiac vagal responses.3. NA projections to the spinal cord tonically inhibit vasoconstrictor tone and form part of a high gain control system for responding to changes in specific afferent information.4. The forebrain NA projections influence heart rate through modulation of the baroreflex gain of the cardiac vagus.5. Central antihypertensive drugs such as clonidine and α‐methyldopa mimic most of the brain‐stem actions of the central NA neurons. They also utilize the ascending NA pathways influencing the baroreflex vagal gain to minimize the baroreflex effects of reducing mean arterial pressure.6. Thus, NA neurons influence the circulatory system through actions at all levels of the central nervous system and provide a comprehensive framework for integrating cardiovascular information from multiple inputs. This provides a number of targets for future development of useful pharmacological agents.
THE USE OF NON‐INVASIVE BLOOD PRESSURE MEASUREMENTS TO MEASURE PRESSOR RESPONSES IN RATS DURING AIR STRESS
Authors: Spanos H. G. , DiNicolantonio R. , Morgan T. O. 
Published: June 2007

SUMMARY1. A non‐invasive tail cuff method was validated against direct intra‐arterial blood pressure measurements (r2 >0.9) and then used to measure the systolic blood pressure (SBP) responses to air‐jet stimulation in mature conscious Sprague‐Dawley (SD) and spontaneously hypertensive rats (SHR). The experiments with the SHR were conducted in parallel with age matched SD rats.2. All rats were trained to remain in perspex holders and when their SBP had stabilized, a jet of air of 10 min duration was directed at the rat's nose via rubber tubing. The blood pressure was measured during the first, fifth and tenth minute.3. The maximum SBP response normally occurred during the first min of air‐jet stimulation and averaged + 30 mmHg in the SHR and +21 mmHg in the SD. Although of higher magnitude in the SHR, when expressed as a percentage of the control SBP, the rise was similar for both strains, 13% and 14%, respectively.4. The pressor response of three SD rats stimulated daily for up to 12 days did not show any evidence of habituation to the stimulus.5. The pressor responses to air‐jet stimulation were abolished in anaesthetized rats, suggesting that they are primarily higher centre responses.
NORMOTENSIVE WISTAR RATS DIFFER FROM SPONTANEOUSLY HYPERTENSIVE AND RENAL HYPERTENSIVE RATS IN THEIR CARDIOVASCULAR RESPONSES TO OPIOID AGONISTS
Authors: Tyszkiewicz Ewa Widy‐ , Czlonkowski Andrzej 
Published: June 2007

SUMMARY1. The effects of three opioid receptor agonists on the blood pressure and heart rate of anaesthetized normotensive, spontaneously hypertensive and renal hypertensive rats were measured.2. Mu agonist morphiceptin i.c.v. induced a pressor response and increase in heart rate in hypertensive rats, but hypotension in normotensive rats. After intravenous (i.v.) injection, morphiceptin produced a hypotensive response in all three groups of rats.3. In contrast, the delta agonist DTLET i.c.v. decreased blood pressure and heart rate in hypertensive rats, but increased both pressure and beat rate in normotensive rats. After i.v. injections DTLET produced a hypertensive response and increase in heart rate in all groups of rats.4. Kappa agonist U‐50, 488H given i.c.v. induced effects similar to morphiceptin: an increase in blood pressure and heart rate in hypertensive and a decrease in normotensive rats. After i.v. injections U‐50, 488H produced decreases in blood pressure and heart rate in all treated groups of rats.5. Pretreatment with naloxone antagonized the activity of morphiceptin but prevented only the stimulating effect of DTLET in normotensive rats. Cardiovascular actions of U‐50, 488H were not blocked by naloxone.6. The results suggest that opioid agonists exert similar changes in cardiovascular function at central and peripheral sites in both models of experimental hypertension and these effects are different in normotensive rats.
RENAL SODIUM EXCRETION FOLLOWING SYSTEMIC INFUSION OF VASOACTIVE INTESTINAL PEPTIDE IN THE RAT
Authors: Lonergan M. A. , Field M. J. 
Published: June 2007

SUMMARY1. The aim of this clearance study was to examine the renal effects of systemic infusion of vasoactive intestinal peptide (VIP) in the intact rat.2. Mean arterial blood pressure (MAP), plasma electrolytes and haematocrit, glomerular filtration rate (GFR), and urinary sodium and potassium excretion were measured in a baseline period and following VIP infusion (0.1–1.2 nmol/h per 200 g), as well as during a time control study.3. During infusion of low doses of VIP (0.1 and 0.4 nmol/h per 200 g), a small increase in fractional and absolute excretion of sodium occurred but this did not differ from that occurring in the time control group. In the high dose VIP group (1.2 nmol/h per 200 g), significant falls occurred in MAP and GFR, and absolute sodium excretion fell (though not significantly) from its baseline level.4. These findings suggest that systemic VIP has no net natriuretic effect in the rat, but produces haemodynamic changes associated with reduced sodium excretion at high doses. This study does not exclude the possibility of direct effects on tubular sodium transport of VIP released from renal nerves.
EFFECTS OF OPIATES ON SODIUM EXCRETION IN THE ISOLATED PERFUSED RAT KIDNEY
Authors: Ellis Andrew G. , Adam William R. 
Published: June 2007

SUMMARY1. A rat isolated perfused kidney preparation was utilized to define clearly a renal site of action. The variables measured were perfusate pressure and flow, glomerular filtration rate, urine volume, sodium excretion and potassium excretion.2. Dextromethorphan (3 nmol/L) and dextrorphan (10 nmol/L) reduced sodium excretion in kidneys from rats on either control or high K+ diet, in the absence of any other measured renal effects. Dextromethorphan (10 nmol/L) produced a decrease in glomerular filtration rate as well as a decrease in sodium excretion. Naloxone (1 μmol/L) inhibited the effect of dextromethorphan on sodium excretion but had no effect when administered alone.3. The levorotatory opiates levorphanol and levomethorphan, the kappa agonist ketocyclazocine and a range of other opiates had no effect on sodium excretion.4. The results suggest a renal action specific for dextrorotatory opiates. This renal action is consistent with earlier binding studies suggesting preferential recognition of dextrorotatory opiates.
FUTURE DIRECTIONS FOR RESEARCH INTO DIETARY AND OTHER LIFESTYLE FACTORS IN HYPERTENSION
Authors: Beilin L. J. 
Published: June 2007

SUMMARY1. Directions for future research into dietary and other lifestyle factors which influence blood pressure can only be signposted at this stage. It is suggested that eight parallel and interrelated paths merit attention.2. The following questions might be addressed. Which techniques measure lower blood pressure most effectively? How do different environmental factors interact with one another and what is their influence on physiological control mechanisms? How do genetic and environmental influences interrelate? How can behavioural change be more readily achieved? What role if any do stress and personality play in hypertension? What are the relative costs and benefits of drug and non‐drug measures in the management of hypertension? Finally what are the most effective ways of reducing the cardiovascular morbidity and mortality associated with hypertension?
POLYAMIDE‐OLIGONUCLEOTIDE HYBRID MOLECULES
Authors: Haralambidis Jim , Coghlan John P. 
Published: June 2007

SUMMARY1. Recent experience with polyamide–oligonucleotide hybrids shows the versility of this approach for replacement of radioactive isotopes for detection of hybridization on gels and for hybridization histochemistry.2. These molecular hybrids also show great promise as antisense inhibitors.
CARDIAC CHEMORECEPTORS: PHARMACOLOGICAL CURIOSITIES OR PHYSIOLOGICAL TOOLS?
Authors: Ludbrook John , Evans Roger G. 
Published: June 2007

SUMMARY1. We have tested in unanaesthetized rabbits two hypotheses regarding a physiological role for cardiogenic chemoreflexes in acute central hypovolaemia.2. In rabbits, the sympathoinhibitory phase of acute central hypovolaemia depends on the activation of a brain‐stem δ‐opioid receptor mechanism by a signal from the heart. Blockade of this by fourth ventricular injection of the δ‐receptor antagonist ICI 174864 had no effect on the reflex haemodynamic responses to left atrial phenylbiguanide or intrapericardial nicotine.3. Intravenous administration of the 5‐HT3 receptor antagonist MDL 72222, or intrapericardial administration of the nicotinic ganglionic cholinoceptor antagonist mecamylamine HCl, had no effect on the haemodynamic response to acute central hypovolaemia.4. We conclude that phenylbiguanide‐sensitive myocardial afferents and nicotine‐sensitive epicardial afferents play no part in the response to acute hypovolaemia in rabbits, and that the reflex effects evoked by chemically exciting these afferents do not depend on a brain‐stem δ‐opioid mechanism.
THERE ARE FEW CATECHOLAMINE‐ OR NEUROPEPTIDE Y‐CONTAINING SYNAPSES IN THE INTERMEDIOLATERAL CELL COLUMN OF RAT THORACIC SPINAL CORD
Authors: Llewellyn‐Smith Ida J. , Minson Jane B. , Pilowsky Paul M. , Chalmers John P. 
Published: June 2007

SUMMARY1. A quantitative electron microscopic immunocytochemical technique was used to assess the number of synapses immunoreactive for tyrosine hydroxylase (TH), phenylethanolamine N‐methyltransferase (PNMT) and neuropeptide Y (NPY) in the intermediolateral cell column in segments T2 and T3 of rat thoracic spinal cord.2. TH synapses comprised about 5%; PNMT synapses 1–2%; and NPY synapses 1–2% of the total number of synapses in the intermediolateral cell column. All three types of synapses were predominantly or exclusively on dendrites.3. Our results suggest that catecholamine/NPY neurons may not provide a major synaptic input to sympathetic preganglionic neurons in rat upper thoracic spinal cord.
THE ROLE OF THE MACULA DENSA IN RENIN SYNTHESIS
Authors: Morgan Trefor , Barrett Graham , Zhang Yanling , Alcorn Daine 
Published: June 2007

SUMMARY1. The role of the macula densa in renin synthesis was studied using mice with one hydronephrotic kidney.2. Renin synthesis was assessed by measurement of renal renin, renal mRNA for renin and plasma renin.3. Sodium depletion stimulated mRNA and renal renin to a similar extent in the hydronephrotic and contralateral kidney.4. Enalapril stimulated mRNA concentration in both kidneys but renal renin did not rise in the hydronephrotic kidney.5. Propranolol did not alter the response to sodium depletion in either kidney.6. The macula densa is not crucial for the stimulation of renin synthesis following sodium depletion. However, it may regulate renin production after mRNA synthesis, possibly by controlling the conversion of prorenin to renin.
ENDOTHELIN‐1 ENHANCES VASOCONSTRICTOR RESPONSES TO SYMPATHETIC NERVE STIMULATION AND NORADRENALINE IN THE RABBIT EAR ARTERY
Authors: Wong‐Dusting Helen K. , La Mylinh , Rand Michael J. 
Published: June 2007

SUMMARY1. In rabbit isolated perfused ear arteries denuded of endothelium, a low concentration of endothelin‐1 (0.1 nmol/L) that had no direct vasoconstrictor action produced slowly developing enhancements of vasoconstrictor responses to noradrenaline and sympathetic nerve stimulation. The enhancements reached maximal levels after 60 min of exposure to endothelin‐1.2. A higher concentration of endothelin‐1 (1 nmol/L), which produced a slow‐developing increase in perfusion pressure of 70 mmHg over the course of 1 h, significantly enhanced vasoconstrictor responses to sympathetic nerve stimulation for the first 30 min, after which there was no significant enhancement. Responses to noradrenaline were not enhanced by 1 nmol/L endothelin‐1.3. The enhancing effect of low concentrations of endothelin‐1 on vasoconstrictor responses to sympathetic nerve stimulation and noradrenaline may play a physiological role in modulating vasomotor function.
ORTHOSTATIC AND POSTPRANDIAL BLOOD PRESSURE REDUCTION IN PATIENTS WITH ESSENTIAL HYPERTENSION
Authors: Masuo Kazuko , Mikami Hiroshi , Habara Nanao , Ogihara Toshio 
Published: June 2007

SUMMARY1. The role of the sympathetic nervous system in orthostatic and postprandial blood pressure reduction in patients with essential hypertension was studied in 13 hypertensive patients and 10 age‐matched normotensive subjects.2. The blood pressure (BP), pulse rate, and plasma norepinephrine (NE) were measured: (i) every minute for 20 min in the upright position after overnight recumbency (ii) every 30 min after food intake for 3 h in the supine position.3. Orthostatic BP reduction (> 13 mmHg in mean BP) was observed in eight hypertensive patients with a maximum after 4 min. Seven of these patients showed postprandial hypotension (> 13 mmHg) with a maximum 90 min after eating, while none of the normotensives exhibited such BP reductions. Before and during the tests the plasma NE levels were higher in hypertensive patients than in the normotensives. The plasma NE level was increased from 370±80 to 790±110 pg/mL 4 min after standing (P<0.01) in hypertensive patients and from 220±40 to 530±90 pg/mL (P<0.01) in normotensive subjects. The plasma NE level was decreased 90 min after food intake from 390±90 to 260±80 pg/mL in hypertensives. Changes in plasma NE correlated with those in mean BP after standing for 4 min (r= 0.379, P<0.05) and also with those 90 min after food intake (r= 0.457, P<0.05).4. These findings suggest that patients with essential hypertension have abnormally increased basal sympathetic nerve activity at rest, and that their orthostatic and postprandial BP reductions may both be caused by impairment of the sympathetic nervous system and of cardiovascular reflexes.