摘要:

A brief account for the renal renin‐angiotensin system (RAS), its inhibitors and receptors, as for the presence of an intrinsic cerebral RAS is initially provided. The review is then focused upon the circumventricular organs as cerebral targets for blood‐borne angiotensin II (Ang II) and on centrally mediated Ang II effects. These concern influences upon the cardiovascular system, water balance, sodium balance, and ACTH‐cortisol secr

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1995.tb09956.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Neurogenic pulmonary oedema (NPO) is believed to be induced by intense activation of the sympathetic nervous system, characterized by massive secretion of catecholamines into the blood stream. There is a possibility that NPO is partly the result of increased vascular permeability. However, the mechanism for an increase in pulmonary vascular permeability is not known. The present study was designed to test the hypothesis that large doses of catecholamines increase pulmonary microvascular permeability directly. Adrenaline or noradrenaline (100 and 300 pug) was injected as a bolus into isolated dog lungs perfused with heparinized autologous blood at constant pressure. Adrenaline or noradrenaline produced sustained lung weight loss although both catecholamines increased pulmonary capillary pressure, assessed by double occlusion pressure, by 2–5 mmHg above baseline. Vascular permeability, as measured by the capillary filtration coefficient and the isogravimetric capillary pressure, did not change significantly frombaseline at 30 and 60 min after catecholamine. Finally, the final‐to‐initial wet lung weight ratio of the catecholamine‐treated lungs did not differ from that of saline‐injected control lungs. Thus, we conclude that circulating catecholamines, even at supra‐physiological doses, do not increase vascular permeability in isolated blood‐perfu

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1995.tb09957.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Salt depleted rabbits and humans excrete an oral sodium load more quickly via the kidneys than an intravenous one. This has been ascribed to the presence of a sodium sensor in the gastrointestinal tract which in some way can influence renal function. The purpose of this study was to investigate this response in the Dahl rats. Renal and faecal sodium excretion was followed in the two strains of rats (normotensive, saltresistant (SR/Jr) and hypertensive, saltsensitive (SS/Jr) rats). After 4 days on a low salt diet they were given NaCl(l.5 mmol kg‐1body wt) either by gavage or intravenously. SR/Jr rats showed an increased renal sodium excretion both after oral and intravenous sodium repletion. The excretion was 2–3 times greater after the oral than after the intravenous administration. The SS/Jr rats augmented their renal sodium excretion only after the oral load, although the sodium excretion was significantly less than in SR/Jr rats. In fact, during the first 8 h after giving sodium orally the renal excretion of sodium was on an average eight times larger in the SR/Jr than in the SS/Jr rats. Renal excretion of sodium was similar in the two strains after intravenous administration. We conclude that the hypertensive SS/Jr rats have great difficulties in excreting an oral sodium load, a phenomenon that may be of importance in the pathophysiology of arterial hypertension in this strain of r

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1995.tb09958.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Using microdialysis, extracellular 3,4‐dihydroxyphenylalanine (DOPA), noradrenaline (NA) and adrenaline (AD) concentrations in the adrenal gland were monitored in conscious rats during and after 60 min of immobilization (IMM) as well as after injection of 500 mg kg‐12‐deoxyglucose (2‐DG). IMM produced a rapid and transient increase in secretion of AD (20‐fold), NA (13‐fold) and DOPA (3.6‐fold). This was accompanied by an increase in blood pressure (+ 18 mmHg) and heart rate (‐ 146 b. p.m.). Repeated exposure to IMM (daily 60 min, for 5 days) had no influence on either catecholamine secretion of haemodynamic profiles, indicating the lack of habituation to stressful conditions. Unlike IMM, the stress of 2‐DG‐induced centralneuroglucopenia stimulated the release of AD without affecting NA secretion. AD levels peaked (5.1‐fold increase) 4&60 min after 2‐DG injection and then slowly declined. 2‐DG induced no changes in blood pressure but reduced the heart rate (‐48 b. p.m.). In separate experiments, steady‐state dialysate DOPA levels, reached during continuous infusion of decarboxylase inhibitor NSD 1015 into adrenal gland tissue through the dialysis probe, served as an index of adrenomedullary tyrosine hydroxylase (TH) activity. IMM evoked a marked increase in TH activity (DOPA formation increased 2.7‐fold), which remained elevated 60 min after the cessation of stress when AD and NA secretion had already fallen to baseline. After 2‐DG, despite significant hormonal response, adrenal TH activity was unchanged. These results give clear evidence that IMM and 2‐DG‐induced neuroglucopenia may be considered as two

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1995.tb09959.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Inter‐compartmental body‐fluid distribution is contingent upon posture, exercise state and environmental temperature. This investigation aimed at quantifying the distribution of intra‐ and extravascular fluid volumes during postural manipulations. Fluid shifts were measured in eight males utilizing a simultaneous, radionuclide dilution technique, in which radioiodinated serum fibrinogen, radiochromated crythrocytes, radiobromine and tritiated water were used to measure plasma, red cell, extracellular and total body water volumes. Subjects were exposed to three postural changes [seated (control), supine and standing] for 30 min at an air temperature of 22.0 d̀C, with each posture separated by 30 min seated rest. Total body water content remained stable throughout postural changes (P= 0.842). Relative to seated volumes, BV increased by 89 mL when supine, and decreased by 406 mL while standing (P= 0.003), with such shifts being primarily a result of plasma movement (P= 0.011). Red cell volume changes were not significant. Vascular fluid lost during standing was filtered into the interstitial compartment (P= 0.014), with the extracellular and intracellular volumes remaining unaffected (P= 0.271 andP= 0.800, respectively). These observations confirmed the influence of posture on inter‐compartmental body‐fluid distribution. The intravascular fluid loss when standing was caused by the filtration of plasma into the interstitium, while, during supine rest, intravascular volume increased, reflecting fluid flux from the interstitium to the c

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1995.tb09960.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

As opposed to the salt‐resistant Dahl‐R rat the salt‐sensitive Dahl‐S has a defective renal dopamine DA1, receptor that may be involved in its susceptibility to develop hypertension during a high salt diet. To compare the ability of prehypertensive Dahl‐R and Dahl‐S to respond to a severe isotonic sodium load, renal function was monitored during a severe form of acute isotonic volume expansion (10% VE). Mean arterial blood pressure before VE was similar in Dahl‐R and Dahl‐S and decreased in both strains by 6% during VE. The accumulated sodium excretion during VE in Dahl‐R was 411 ± 64 μmol 100 min1g1kidney wt (kw) which was not different from that in Dahl‐S (420±95 μmol 100min‐1g‐1kw). The accumulated dopamine excretion (a mirror of renal dopamine synthesis) during VE was also similar in Dahl‐R (134±13 ng 100 min‐1g1kw) and Dahl‐S (126 ± 16 ng 100 min1g‐1kw). The excretion of DOPAC, the main metabolite of Dahl‐S, glomerular filtration rate and systemic haematocrit did not differ between the strains before, during or after VE. To conclude, in spite of a defective renal DA1, receptor prehypertensive Dahl‐S do not respond with an attenuated natriuretic or dopamine excretory response when subjected to a severe isotonic sodium load. The results do not support a sodium retaining role over a defective DA1, receptor in

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1995.tb09961.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Using a preparation of isolated rat kidneys perfused at constant renal artery pressure (80 mmHg) we investigated the role of endothelins in the regulation of renin release. Addition of three related endothelins (ET‐1, ET‐2, ET‐3) at a concentration of 10 pmol L‐1tended to enhance renin secretion rates. Higher doses (100 pmol L‐1, 1 nmol L‐1) of different ETs such as the selective ETB, receptor agonist sarafotoxin S6c (100 pmol L‐1, 1 nmol L‐1) inhibited renin release and increased renal vascular resistance with similar potency. These effects of ETs were blunted when calcium ions were removed from the perfusate. Renin release activated by isoproterenol (10 nmol L‐1) was also significantly reduced with ET‐1, ‐2 and ‐3 (1 nmol L‐1). BQ‐123 (500 nmol L‐1), a selective ETAreceptor antagonist, only attenuated, whilst the nonselective ET receptor blocker bosentan (Ro 47–0203, 10 μmol L‐1) almost abolished the renal vasopressor and renin inhibitory action of ET‐1 and sarafotoxin S6c. BQ‐123 and bosentan alone did not affect either perfusate flow or basal renin secretion rates in isolated perfused kidneys. These findings indicate that all three ET peptides equipotently inhibit renin secretion from the kidneys. Most of the vasopressor and renin inhibitory effect of ETs is mediated by ETb, rather than ETAreceptors involving a calcium‐dependent signal transduction mechanism. Moreover, our results suggest that intrarenally released ETs do not contribute to the regulation of renin secr

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1995.tb09962.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

The aim of this study was to investigate the effects of renal nerve stimulation on the humoral renal antihypertensive system. An isolated kidney (IK) was perfused at normal or high arterial pressures from a normotensive assay rat by means of a perfusion pump. Perfusion pressure (PP) to the IK was 90 mmHg for a control period of 30 min. In three of five experimental groups PP was then increased to 175 mmHg. In two of the groups the renal nerves were stimulated at 2 (P‐1752Hz) or 5 Hz (P‐1755Hz) for 60 min. The remaining group served as a control (P‐175c). In two groups IK pressure was maintained at 90 mmHg with 5Hz nerve stimulation (P‐905Hz) or without nerve stimulation (P‐90c). MAP of the assay rat decreased by 22 and 27% (P<0.001) in the P‐175cand P1752Hzgroups, respectively during the 60 min period of nerve stimulation, but remained stable in P‐1755Hz. Renal blood flow increased in the IK when PP was increased in P‐175c, but did not change significantly in P‐1752Hzor P‐1755Hz. Blood pressure remained constant in the assay rat when the IK was perfused at 90 mmHg. The renal excretory functions of the IK decreased in a frequency dependent manner by 2 and 5 Hz renal nerve stimulation compared with P‐175c. We conclude that 5 Hz renal nerve stimulation inhibits the pressure dependent release of humoral depressor substances from an IK perfused at 175 mmHg, whereas this is not seen when stimulating at 2 Hz. It is suggested that the release of antihypertensive substances from the renal medulla requires an increased ren

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1995.tb09963.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Neuropeptide Y (NPY) and noradrenaline (NA) are co‐stored in sympathetic perivascular nerves of the airway mucosa and lung. The superior laryngeal, bronchial and pulmonary vascular responses were therefore studied in anaesthetized pigs after systemic injections of NPY and NA and after stimulation (2 or 10 Hz, 15 V, 5 ms) of the cranial and caudal portions of the cervical sympathetic trunk or the stellate ganglia. NPY and NA increased vascular resistance, suggesting vasoconstriction in all three vascular beds. Stimulation of the cervical sympathetic trunk in the cranial direction caused clear‐cut vasoconstriction and a decrease in the superficial blood flow in the laryngeal and tracheal circulation supplied by the superior laryngeal artery. This vascular response may be related to release of NA at 2 Hz and possibly also NPY at 10 Hz, since a remaining vasoconstrictor response at 10 Hz was present in reserpinized preganglionically transected pigs when tissue content of NA but not NPY was depleted. The decrease in superficial blood flow in the tracheal mucosa on sympathetic stimulation was absent after reserpine, however. Stimulation of the cervical sympathetic trunk in caudal direction provoked vasoconstriction in the bronchial and pulmonary vascular beds in control pigs. The basal tone of these two vascular beds was not influenced on electrical stimulation after reserpine pretreatment, however, suggesting involvement of NA and possibly also NPY, which were both depleted by reserpine. Electrical stimulation of the stellate ganglia also evoked reserpine‐sensitive vasoconstriction in both the bronchial and pulmonary vascular beds. The left stellate ganglion dominated the vasomotor response in the bronchial circulation, whereas the right side mainly influenced the pulmonary circulation and the

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1995.tb09964.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Changes in the function of the autonomic nervous system underlying changes in heart rate variability are not fully understood. Furthermore, decreased heart rate variability has been found to be related to poor prognosis, for example, in patients with coronary artery disease. Our aim was to study how modulation in sympathetic stimulation at various frequencies is transferred into heart rate variation, and how the interaction between sympathetic and parasympathetic inputs can affect the high‐frequency component of heart rate variability. We stimulated electrically cardiac sympathetic and vagal nerves in anaesthetized, vagotomized, spinal anaesthetized dogs. We controlled the frequency and magnitude of the modulation in programmed stimulation patterns and analysed the resulting changes in heart rate variability by power spectral analysis. We found that modulations in sympathetic stimulation were reflected in the high‐frequency component of heart rate variability, as well as in the low‐ and medium‐frequency components. In addition, a novel finding was that sympathetic stimulation reduced the magnitude of the high‐frequency variations caused by vagal stimulation. This suggests that, although the high‐frequency component of heart rate variability is mainly under parasympathetic regulation, it may also be influenced by the sympathetic ner

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1995.tb09965.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY