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Biomedical subjects

J L Imbs

Publications and source records attributed to J L Imbs.

At least 37 records · Page 2Linked to original sources
PubMed2000

[Sodium intake and hypertension].

The guidelines for hypertension treatment recommend a reduction of dietary sodium intake. There is still a controversy, few studies showing an inverse correlation between cardiovascular morbidity and salt intake, about the benefit expected from a reduction of sodium intake on the blood pressure level. This controversy is explained by the great variability of the pressure response when individuals are exposed to different sodium intakes, diet and environmental factors playing an additional role of variability. Salt sensitivity is more frequent in hypertensive, obese and in elderly patients. There is no harm to reduce salt overtake moreover normalisation of the dietary sodium intake has clearly demonstrated its ability to reduce hypertension complications in patients at high cardiovascular risks.

Cardiovascular Diseases↗
PubMed1999

Cardiovascular and renal effects of central administration of a mineralocorticoid receptor antagonist in conscious female rats.

In a previous study we showed that in normotensive male rats brain mineralocorticoid receptor blockade induced a long lasting decrease in blood pressure associated with increased urinary excretion of water and electrolytes. Here, we report the effect of intracerebroventricular injection of a mineralocorticoid receptor antagonist (RU28318; 3,3-oxo-7 propyl-17-hydroxy-androstan-4-en-17yl-propionic acid lactone) on cardiovascular and renal function in female rats. Compared with male rats, females are less sensitive to brain mineralocorticoid receptor blockade. Administration of RU28318 (10 ng, 100 ng) caused a significant decrease in systolic blood pressure (10-12.5%) only at 8 h after injection. An increased urinary excretion of water (about 160%) and electrolytes (about 175%) during the first 8 h after the injection was observed in the 100 ng RU28318 treated group. Heart rate, food intake and water consumption were not affected at either dose. In conclusion, in conscious female rats, brain mineralocorticoid receptors participate in blood pressure and renal function control.

Animals↗
PubMed1999

[Development of pharmaco-epidemiology in France].

A new scientific discipline: Progress in scientific knowledge, advances in therapeutic innovation, the development of new drugs and the continuing need for optimal drug use impose a new approach to the rational assessment of public health needs and the risks and benefits of therapeutic intervention. In the near future, a new scientific discipline, pharmaceutical epidemiology, will play a leading role. France seems to be a bit behind other western countries in this area. Goal setting: The objectives of industrial firms do not necessarily cover all aspects of the overall goals of society. If the scientific community leaves the development and implementation of pharmaceutical epidemiology in the hands of industrial firms alone, they risk seeing its field of action limited to industrial objectives. The goals of this new discipline must be defined within an unbiased framework aimed at meeting the needs of society in general. Organization: The development of pharmaceutical epidemiology as an integral part of medical research requires a clear definition of its objectives, methods, working hypotheses and time and human allocations. In this context, pharmaceutical epidemiology should be organized within the University and scientific settings currently contributing to scientific research in France (INSERM, CNRS, ORSTOM, etc.). Creating favorable conditions: A pharmaceutical epidemiology network with adequate human and material resources is needed. The wide range of needs expressed by existing institutions (Drug Agency, Prescription and Drug Use Observatory, industrial firms, the national health insurance system, physician and pharmacist associations) pleads for a nationally organized project working in the public domain.

Drug Prescriptions↗
PubMed1999

Vascular kinin B(1) and B(2) receptor-mediated effects in the rat isolated perfused kidney - differential regulations.

1. Bradydykinin (BK) and analogs acting preferentially at kinin B(1) or B(2) receptors were tested on the rat isolated perfused kidney. Kidneys were perfused in an open circuit with Tyrode's solution. Kidneys preconstricted with prostaglandin F(2alpha) were used for the analysis of vasodilator responses. 2. BK induced a concentration-dependent renal relaxation (pD(2)=8.9+/-0.4); this vasodilator response was reproduced by a selective B(2) receptor agonist, Tyr(Me)(8)-BK (pD(2)=9.0+/-0.1) with a higher maximum effect (E(max)=78.9+/-6.6 and 55.8+/-4.3% of ACh-induced relaxation respectively, n=6 and 19, P<0.02). Icatibant (10 nM), a selective B(2) receptor antagonist, abolished BK-elicited relaxation. Tachyphylaxis of kinin B(2) receptors appeared when repeatedly stimulated at 10 min intervals. 3. Des-Arg(9)-BK, a selective B(1) receptor agonist, induced concentration-dependent vasoconstriction at micromolar concentration. Maximum response was enhanced in the presence of lisinopril (1 microM) and inhibited by R 715 (8 microM), a selective B(1) receptor antagonist. Des-Arg(9)-[Leu(8)]-BK behaved as an agonist. 4. A contractile response to des-Arg(9)-BK occurred after 1 of perfusion and increased with time by a factor of about three over a 3 h perfusion. This post-isolation sensitization to des-Arg(9)-BK was abolished by dexamethasone (DEX, 30 mg kg(-1) i.p., 3 h before the start of the experiment and 10 microM in perfusate) and actinomycin D (2 microM). Acute exposure to DEX (10 microM) had no effect on sensitized des-Arg(9)-BK response, in contrast to indomethacin (30 microM) that abolished it. DEX pretreatment however had no effect on BK-induced renal vasodilation. 5. Present results indicate that the main renal vascular response to BK consists of relaxation linked to the activation of kinin B(2) receptors which rapidly desensitize. Renal B(1) receptors are also present and are time-dependently sensitized during the in vitro perfusion of the rat kidneys.

Animals↗
PubMed1999

Brain mineralocorticoid receptor control of blood pressure and kidney function in normotensive rats.

Brain mineralocorticoid receptors appear to contribute to mineralocorticoid hypertension and may be involved in blood pressure control in normotensive rats. We examined the effect of blockade of central mineralocorticoid receptors with the use of a selective antagonist (RU28318) on cardiovascular and renal function in conscious normotensive rats. The contribution of renal innervation was evaluated in rats with bilaterally denervated kidneys. Young adult, male Wistar rats were trained for systolic blood pressure measurement by a tail sphygmographic method and accustomed to metabolic cages for collection of urine. One week before experimentation, an intracerebroventricular cannula was implanted. Systolic blood pressure was diminished 30 minutes after an intracerebroventricular dose of 10 ng of RU28318. The effect was maximal at 8 hours and was still present after 24 hours. Blood pressure returned to the basal level by 48 hours. During the period 0 to 8 hours after intracerebroventricular injection, rats treated with the antagonist showed an increase in diuresis and urinary electrolyte excretion. No significant effect on plasma renin activity, measured 8 and 30 hours after administration of RU28318, was observed. In denervated rats, the decrease in systolic blood pressure after administration of RU28318 was reduced. The difference was statistically significant compared with controls at 2 hours but not at 8 hours, and blood pressure returned to the basal value by 24 hours. The increases in diuresis and urinary electrolyte excretion induced by RU28318 were abolished in denervated rats. These results show that brain mineralocorticoid receptors are involved in blood pressure regulation and kidney function homeostasis in conscious normotensive rats. The renal nerves appear to participate in the brain mineralocorticoid receptor control of blood pressure.

Animals↗
PubMed1998

Plasma active renin, angiotensin I, and angiotensin II during pregnancy and in preeclampsia.

OBJECTIVE: To evaluate the activity of the renin-angiotensin-aldosterone system in the circulation during the three trimesters of normal pregnancy and in women with preeclampsia. METHODS: Normal pregnant volunteers (n = 7) were studied throughout pregnancy, and women with preeclampsia (n = 8) were studied in the third trimester. Plasma active renin and aldosterone were measured by radioimmunoassay. Angiotensin I and angiotensin II were determined by radioimmunoassay after separation of the peptides by high-performance liquid chromatography. RESULTS: Active renin concentration increased in the first trimester of normal pregnancy, whereas angiotensin I, angiotensin II, and aldosterone remained at a level comparable to the postpartum values. Highest activity of the renin-angiotensin-aldosterone system was observed during the third trimester with increased levels of angiotensin I, angiotensin II, and aldosterone. In contrast, in patients with preeclampsia, despite a slight increase of active renin levels, the other parameters of the renin-angiotensin-aldosterone system were low compared with the third trimester of normal pregnancy and were comparable to postpartum data. CONCLUSION: Our results suggest that during the first trimester of normal pregnancy, active renin concentration in the plasma is increased and that renin is not the factor that limits angiotensin II synthesis. These results also confirm decreased activity of the renin-angiotensin-aldosterone system in preeclampsia. This could contribute to the diminished hemodynamic control observed in pregnant women developing preeclampsia.

Adult↗
PubMed1998

Vascular and neuroendocrine components in altered blood pressure regulation after surgical repair of coarctation of the aorta.

STUDY OBJECTIVE: To investigate potential vascular and neuroendocrine determinants of altered blood pressure (BP) regulation in patients previously operated on for aortic coarctation. DESIGN, SETTING AND PATIENTS: We prospectively re-evaluated 45 patients operated on for aortic coarctation at Strasbourg University Hospital over a 13-year period. Four of these patients were less than 2 years old at the time of the operation and four were older than 20 years. Patient age and time since the operation were on average 21+/-13 years and 8+/-3 years, respectively. Surgery consisted of a resection with end-to-end anastomosis for 18 patients, angioplasty (8), prosthesis (4) or sub-clavian flap (15). RESULTS: Despite repair of the coarctation, about 40% of the patients showed an abnormal BP status at rest. The majority of these patients had uncomplicated borderline hypertension. The orthostasis test as well as the BP circadian rhythm were frequently abnormal. While the ankle/arm systolic pressure index measured at rest was generally within the normal range, diminished carotid-femoral pulse wave velocity was observed. Plasma adrenaline and aldosterone levels were elevated in about 50% of the patients examined. CONCLUSIONS: These new findings suggest that there are 'cause and effect' relationships between aortic structural and functional vascular abnormalities, and augmented plasma adrenaline and aldosterone in some patients after coarctation repair. These phenomena are likely to be involved in altered BP regulation and might result in recurrent hypertension.

Adolescent↗
PubMed1998

[Brain mineralocorticoid receptor and blood pressure control in the conscious normotensive rat].

Brain control of arterial blood pressure in man and in animals has been studied increasingly over the last few decades. Despite our knowledge about short term regulation (chemoreceptor and baroreceptor reflexes) there is much more uncertainty about the degree of involvement of brain mechanisms in long term control of blood pressure, and in hypertension. The last decade, a role of brain mineralocorticoid receptors (MR) has been outlined in animal experiments. Stimulation of brain MR by aldosterone or related mineralocorticoids induces an increase in blood pressure and hypertension under chronic conditions. These effects of mineralocorticoid excess can be blocked by specific MR antagonists administered centrally. Stimulation of brain glucocorticoid receptors, as compared to stimulation of brain MR, has an opposite effect, i.e. decreases blood pressure. As in the typical peripheral target organs of aldosterone, in the brain, enzymatic protection of MR against glucocorticoids appears to play an important role. We showed that in conscious normotensive rats intracerebroventricular (i.c.v.) injection of a specific MR antagonist (RU28318) in a low dose (10 ng) decreases blood pressure by about 20% without affecting heart rate. A similar but smaller effect (not statistically significant) was observed in conscious female rats. Only in the male rats an increased diuresis occurred and this may have contributed to the observed hypotension. We conclude that hypertension caused by mineralocorticoid excess may depend on a concerted action of the steroid on the kidney and on the brain. The mechanism by which brain MR increases blood pressure is unknown. It is possible that increased sympathetic outflow and renal mechanisms are involved. Interference with brain MR not only affects blood pressure but it also has effect on renal function.

Animals↗
PubMed1998

[Effects of hydroxyl radicals on purified angiotensin I converting enzyme].

Somatic angiotensin-converting enzyme (ACE) is a protein which contains two similar domains (N and C), each possessing a functional active site. The relationship between ACE, its natural substrates and oxygen free radicals is starting to be explored. On one hand, superoxide anions production is induced by angiotensin II and on the other hand, activated polynuclear neutrophils, through free radicals generation, alter endothelial ACE activity. In this study, we examined the impact of hydroxyl radicals (.OH) on purified ACE. .OH were produced using a generator: 2,2'-azo-bis 2-amidinopropane (GRH) provided by Lara-Spiral (Fr). GRH (3 mM), in a time-dependent fashion, inhibited ACE activity. When ACE was co-incubated for 4 h with GRH, its activity decreased by 70%. Addition of dimethylthiourea (DMTU: 0.03 to 1 mM) or mannitol + methionine (20/10 mM), two sets of .OH scavengers, produced a dose-dependent protection on ACE activity. To examine whether oxidation of thiol groups in the ACE molecule could be involved in the action of GRH, the effects of thiol reducing agents: mercaptoethanol and dithiotreitol (DTT) were investigated. These compounds produced a dose-dependent and significant protection; with 100% protection at 0.2 and 0.3 mM for mercaptoethanol and at 0.1 mM for DTT. The hydrolysis of two natural and domain-specific substrates were also explored. The hydrolysis of angiotensin I preferentially cleaved by the C domain was significantly (p < 0.01) inhibited by 57, 58 and 69% in contact with 0.3, 1 and 3 mM GRH [in nmol angio II formed/min/nmol of ACE, n = 4; 35.9 +/- 0.6 (control), 15.5 +/- 2.8 (GRH : 0.3 mM), 15.1 +/- 0.5 (1), 10.9 +/- 0.6 (3)]. The hydrolysis of the hemoregulatory peptide (hp), preferential substrate for the N domain was not affected by GRH at 0.3 mM and inhibited by 28% (not significant) by 1 mM GRH [in nmol ph hydrolized/min/nmol ACE, n = 4; 12.6 +/- 1.9 (control), 14.9 (GRH : 0.3 mM), 8.3 +/- 4.0 (1). These results demonstrated that .OH affect ACE activity and could suggest a privileged impact of GRH on the C domain. The precise sites of action of .OH remain unknown. The Cys residues near the active centers, by forming disulphide bridges during the oxidation could be of critical importance. Further studies will be needed to determine whether oxidative stress again ACE can be involved in the genesis of inflammatory vascular pathologies.

Enzyme Activation↗
PubMed1998

[Modulation by nitric oxide of vasopressin induced renal vasoconstriction varies with perfusate viscosity in the isolated rat kidney].

Previously we reported that AVP is a potent vasoconstrictor in the TYRODE's perfused rat kidney. In vivo however AVP elicited only minor effects on renal blood flow. We hypothetized that differences in shear stress, particularly related to differences in viscosity could be involved. In this study, we investigate the role of perfusate viscosity in the modulation of AVP-induced renal vasoconstriction by NO. Experiments were performed in kidneys isolated from male Sprague-Dawley rats (220 g). Kidneys were perfused at a constant flow of 8 mL/min, in a recirculating system, with TYRODE's solutions supplemented with 6% bovin serum albumin (BSA) or 4.7% Ficoll 400 (Ficoll). The viscosities relative to water were respectively of 1.33 (BSA), 2.32 (Ficoll) and 1.03 (TYRODE). Concentration-response curves to AVP were constructed in the absence or presence of 100 microM N omega-nitro-L-arginine (L-NA), an inhibitor of NO synthase, and compared to those obtained in kidneys perfused with TYRODE's solution. AVP elicited a concentration-dependent renal vasoconstriction, with a progressive shift of the curves to the right and a small decrease in the maximum response when the kidneys were perfused with perfusates of increasing viscosities: logEC50 = -9.9 +/- 0.1 (TYRODE, n = 14), -9.7 +/- 0.1 (BSA, n = 5), -9.0 +/- 0.1 (Ficoll, n = 5) (m +/- e.s.m. Anova, p < 0.001); Emax = 34 +/- 1, 31 +/- 2 and 26 +/- 3 mmHg/mL/min (Anova, p < 0.001). L-NA abolished the differences between kidneys perfused with solutions of different viscosities in logEC50 for vasopressin (10.3 +/- 0.1, 10.4 +/- 0.1 and 10.5 +/- 0.1, n = 5-11, Anova, NS) but did not affect Emax values. In conclusion, present results show that 1) AVP-induced renal vasoconstriction is modulated according to the viscosity of perfusate and 2) NO is involved in this effect. Viscosity, a major determinant of shear stress, should be considered in hemodynamic studies performed on isolated kidneys.

Animals↗
PubMed1998

[Diuretic resistance: mechanisms and therapeutic possibilities].

The diuretics, with the exception of spironolactone, act on the luminal (or apical) surface of the tubular cells of different segments of the nephron. In order to act, they must be secreted into the tubular lumen. This transfer of the drug to its site of action may be blocked by decreased renal blood flow, the saturation of the systems of tubular transport or fixation to the albumin present in the primary urine. All these pharmacokinetic abnormalities (observed in renal failure or the nephrotic syndrome) lead to diuretic resistance. Increasing the dosage, the repetition, intravenous administration, even as an infusion, are possible solutions. Resistance may be observed in the absence of pharmacokinetic abnormalities: in these cases, there is an abnormal response of the tubular cells to otherwise effective diuretic concentrations, or the activation of homeostatic mechanisms leading to sodium retention and preventing negativisation of the salt and water balance. These situations are often associated in cardiac failure or cirrhosis with oedema. Increasing the dosage is not a logical solution, but increasing the frequency of administration may be helpful. The importance of secondary hyperaldosteronism in cirrhotic oedema makes spironolactone the treatment of choice. In all cases, the addition of two mechanisms of inhibition of tubular reabsorption of sodium at different sites in the nephron often results in an effective diuresis: usually, this implies the addition of a thiazide (e.g. hydrochlorothiazide) to an initial prescription of a loop diuretic.

Diuretics↗
PubMed1998

[French system of drug surveillance].

The French drug surveillance system is characterized by: a network of thirty one regional drug surveillance centres, located to provide convenient proximity to health care professionals; a causality assessment method, compulsory for all persons involved in drug surveillance, to assess the causal relationship between an adverse effect and one or more drugs; if necessary, an additional evaluation of the causal relationship will be performed using pharmaco-epidemiology methods; a Technical committee and a National Commission of Drug Surveillance which centralize and assess all the data in order to provide a consensual advice to the relevant authorities on necessary measures, to prevent, or reduce a drug related adverse effect; in the case of an inquiry, the drug surveillance department of the pharmaceutical company and the network of regional drug surveillance centers will pool their data with the aim to exchange information and ideas.

Adverse Drug Reaction Reporting Systems↗
PubMed1997

[Mechanisms of drug interactions with renal elimination of lithium].

Using indomethacin (2.5 mg/kg/day, i.m.) in rats, we confirmed the well-known interaction of NSAID's and the urinary elimination of lithium. This is due to an increase in the tubular reabsorption of lithium, probably associated with an increase in the reabsorption of sodium in the ascending limb of the loop of Henle, following inhibition of the synthesis of prostaglandins. With ramipril (1 mg/kg/day, p.o.), we confirmed an interaction with lithium pharmacokinetics in rats, also associated with an increase in the tubular reabsorption of sodium. In contrast, the angiotensin receptor antagonist losartan (10 mg/kg/day, p.o.) had no effect in this paradigm. Since the effects of ramipril were partially inhibited by an i.v. infusion of an antagonist of the bradykinin B2 receptor icatibant (0.1 mg/kg/day), we suggest that bradykinin contributes to the interaction between angiotensin converting enzyme inhibitors and renal excretion of lithium.

Animals↗
PubMed1997

[Renal vascular responses of bradykinin in the isolated rat kidney].

Kinins, by an autocrine or paracrine hormonal action, are potent modulators of regional vasomotricity. Their effects on the renal circulation are not well defined. The aim of this study was to analyse the renal vascular response induced by bradykinin, to precise the type(s) of receptor involved and to evaluate the contribution of various peptidases in the local catabolism of the kinin. Experiments were performed on the isolated rat kidney, perfused in an open circuit, at a constant flow of 8 mL/min, with a Tyrode's solution. Vasodilator responses were evaluated after renal vascular tone had been restored by a continuous perfusion with prostaglandin F2 alpha. Infusion of bradykinin (0.1-30 nM) induced a concentration-dependent renal vasorelaxation. A maximal response of 39.5 +/- 2.8% (n = 32) reversion of the tone induced by prostaglandin F2 alpha (about 50% of the maximal response induced by acetylcholine on the same kidneys) was obtained at 30 nM. Bradykinin-induced vasodilatation was completely inhibited by HOE 140 (10 nM), a selective bradykinin B2 receptor antagonist. At a supramaximal concentration of 300 nM, bradykinin-induced vasorelaxation was modulated by a concomitant vasoconstriction. A concentration-dependent vasoconstriction was also obtained with desArg9 bradykinin (1-8 microM), a selective agonist of the bradykinin B1 receptor. The inhibition of neutral endopeptidase by phosphoramidon (10 microM) or the inhibition of carboxypeptidase M by MGTPA (10 microM) did not modify the bradykinin-induced renal vasorelaxation. On the other hand, the inhibition of angiotensin I converting enzyme by lisinopril (1 microM) potentiated by about 32% the vasorelaxant response induced by 30 nM bradykinin (52.3 +/- 11.8% relaxation, n = 5, p < 0.05). Present results demonstrate that 1) bradykinin primarily evokes B2 receptor-linked renal vasodilatation, 2) bradykinin B1 receptors appear also to be present on the rat renal vasculature and 3) angiotensin 1 converting enzyme contributes to the local vascular catabolism of the kinin.

Adrenergic beta-Antagonists↗
PubMed1997

[Renal tissue angiotensins during converting enzyme inhibition of angiotensin I in spontaneously hypertensive rat].

To compare the effects of an angiotensin-converting enzyme inhibitor on circulating and tissue renin-angiotensin system, we measured different renin-angiotensin system parameters during the first day of treatment (Day 1) as well as after two weeks of treatment (Day 14). Ramipril was given orally once daily to adult male spontaneously hypertensive rats. Renin activity, angiotensin-converting enzyme activity and levels of angiotensin I and angiotensin II in the plasma, renal cortex and renal medullar were assessed at Day 1 and Day 14 of the treatment. In the plasma, both renin activity and angiotensin I increased 10 to 15 fold one to four hours after acute as well as at Day 14 of ramipril treatment and then returned to basal values within 24 hours. Plasma angiotensin II levels were not significantly decreased at Day 1 or Day 14. The decrease in the angiotensin II/angiotensin I ratio suggested a sustained inhibition of plasma angiotensin-converting enzyme at Day 14. In the renal cortex and medulla, a clearly different pattern was observed: in ramipril treated rats, renin activity in the renal cortex and medulla did not change at Day 1 but at Day 14 we observed a slight and sustained increase in renin activity. Despite very high basal levels of renin activity, angiotensin I levels in the renal cortex were comparable to those in the plasma. The angiotensin I level increased only one-fold one hour after ramipril intake at Day 1 and Day 14. This suggests that angiotensinogen may have a limiting role in the synthesis of angiotensin I in the kidney. Angiotensin II levels were slightly higher in the renal cortex and medulla than in the plasma suggesting local synthesis of the peptide. In the kidney, angiotensin II levels decreased one and four hours after the acute or prolonged ramipril treatment and the angiotensin II/angiotensin I ratio was reduced at the same time. Our results show that the responses of the plasma and kidney components of the renin-angiotensin system to angiotensin-converting enzyme inhibition are different in the plasma and the kidney suggesting that the circulating and tissue renin-angiotensin system are at least in part independent.

Angiotensin I↗
PubMed1996

Vascular effects of [Arg8]vasopressin in the isolated perfused rat kidney.

The renal vascular effects of [Arg8]vasopressin (vasopressin) were investigated in the isolated perfused rat kidney. Vasopressin (0.01-3 nM) elicited a dose-dependent vasoconstriction in kidneys from Sprague Dawley rats, with a EC50 value of 0.206 +/- 0.044 nM. Inhibition of nitric oxide synthase by N omega-nitro-L-arginine (100 microM) shifted the vasopressin-induced vasoconstrictor response curve to the left. Inhibition of cyclooxygenase by indomethacin (10 or 30 microM) blunted the constriction induced by low concentrations of the peptide. Vasopressin, like angiotensin II but not noradrenaline, induced tachyphylaxis, SR 49059 ((2S)1-[(2R,3S)-5-chloro-3-(2-chlorophenyl)-1-(3,4-dimethoxybenzene- sulfonyl)-3-hydroxy-2,3-dihydro-1H-indole-2-carbonyl]-pyrrolidine-2- carboxamide) (1-30 nM), a new potent and selective non-peptide vasopressin V1A receptor antagonist, shifted the concentration-response curve for vasopressin to the right without decreasing the maximum contraction. Antagonism became competitive with a pA2 value (+/- S.D.) of 9.72 +/- 0.20 during inhibition of nitric oxide release. [Mpa1,D-Arg8]Vasopressin (desmopressin; 0.1-100 nM), or vasopressin (0.01-1 nM) after blockade of the vasopressin V1A receptor by SR 49059, induced no vasopressin V2 receptor-related renal relaxation in kidneys with vascular tone previously restored by noradrenaline or prostaglandin F2 alpha. These findings indicate that in the isolated perfused rat kidney vasopressin is a potent renal vasoconstrictor. The constriction depends on activation of smooth muscle vasopressin V1A receptors and is modulated by endothelial nitric oxide but not by prostacyclin or vasopressin V2 receptor-related vasodilation.

Angiotensin II↗