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Biomedical subjects

J Durand

Publications and source records attributed to J Durand.

At least 19 recordsLinked to original sources
PubMed1997

Compartmentalization of angiotensin II generation in the dog heart. Evidence for independent mechanisms in intravascular and interstitial spaces.

Angiotensin-converting enzyme inhibitors have beneficial effects that are presumably mediated by decreased angiotensin II (ANG II) production. In this study, we measure for the first time ANG I and ANG II levels in the interstitial fluid (ISF) space of the heart. ISF and aortic plasma ANG I and II levels were obtained at baseline, during intravenous infusion of ANG I (5 microM, 0.1 ml/min, 60 min), and during ANG I + the angiotensin-converting enzyme inhibitor captopril (cap) (2.5 mM, 0.1 ml/min, 60 min) in six anesthetized open-chested dogs. ISF samples were obtained using microdialysis probes inserted into the left ventricular myocardium (3-4 probes/dog). ANG I increased mean arterial pressure from 102+/-3 (SEM) to 124+/-3 mmHg (P < 0.01); addition of cap decreased MAP to 95+/-3 mmHg (P < 0.01). ANG I infusion increased aortic plasma ANG I and ANG II (pg/ml) (ANG I = 101+/-129 to 370+/-158 pg/ml, P < 0.01; and ANG II = 22+/-40 to 466+/-49, P < 0.01); addition of cap further increased ANG I (1,790+/-158, P < 0.01) and decreased ANG II (33+/-49, P < 0.01). ISF ANG I and ANG II levels (pg/ml) were > 100-fold higher than plasma levels, and did not change from baseline (8,122+/-528 and 6,333+/-677), during ANG I (8,269+/-502 and 6, 139+/-695) or ANG I + cap (8,753+/-502 and 5,884+/-695). The finding of very high ANG I and ANG II levels in the ISF vs. intravascular space that are not affected by IV ANG I or cap suggests that ANG II production and/or degradation in the heart is compartmentalized and mediated by different enzymatic mechanisms in the interstitial and intravascular spaces.

Angiotensin I↗
PubMed1997

Sexually dimorphic response of the balloon-injured rat carotid artery to hormone treatment.

BACKGROUND: Estrogen blunts the neointimal response to vascular injury in gonadectomized rats of both sexes; addition of a progestin blocks the estrogen effect. This study tested, in intact rats of both sexes, whether (1) exogenous estrogen has a vasoprotective effect in injured carotid arteries, (2) progestin (medroxyprogesterone acetate, MPA) blocks the vasoprotective effect of estrogen, and (3) any observed sexual dimorphism in the responses to estrogen and/or MPA can be accounted for by differences in serum 17 beta-estradiol levels. METHODS AND RESULTS: Intact male and female Sprague-Dawley rats were randomly divided into four subgroups treated with either (1) 17 beta-estradiol, (2) MPA, (3) 17 beta-estradiol + MPA, or (4) vehicle and were subjected to balloon injury of the right common carotid artery. Two weeks later, rats were killed by an overdose of pentobarbital, and the carotid arteries were evaluated for myointimal thickening. Neither estradiol nor MPA altered the neointimal response in males. In females, estradiol reduced and MPA enhanced the response, whereas addition of MPA to estradiol blocked the vasoprotective effects of estrogen. CONCLUSIONS: Intact male rats but not intact females are resistant to the vasoprotective effects of exogenous estrogen, despite attainment of physiological (for females) serum 17 beta-estradiol levels. MPA enhances the neointimal response in intact females, presumably by blocking the production and thus the vasoprotective effect of endogenous estrogen.

Angioplasty, Balloon↗
PubMed1997

Arachidonic acid-induced calcium signalling in human airway smooth muscle cells.

The spatiotemporal distribution of Ca2+ signals evoked by arachidonic acid (AA) was investigated in human bronchial smooth muscle cells (SMC), using the single cell video imaging technique and Fura-2 as a fluorescent dye. Baseline Ca2+ levels were markedly heterogeneous in one and the same cell; the local Ca2 concentration laid between 90 +/- 11 and 215 +/- 18 nM (n = 15). AA (2 mM) induced propagating Ca2+ waves, travelling at a mean velocity of 18 +/- 3 microns/sec (n = 7). Ca2+ signals originated at discrete trigger zones, whose kinetic properties differed from those of neighbouring regions. Ca2+ in the trigger zones rose in two phases, with rates of 9.5 +/- 0.8 and 88 +/- 6 nM/sec (n = 17). A single cell frequently exhibited more than one trigger zones. In some cells, the wave did not reach all regions; such inert zones separated functionally the cell in independently active regions. Some regions presented Ca2+ signals that did not spread to the rest of the cell, forming isolated foci. The spatiotemporal variability of Ca2+ signals evoked by AA could result from the heterogeneity of Ca2+ homeostatic processes.

Arachidonic Acid↗
PubMed1997

Hypoxia stimulates atrial natriuretic peptide gene expression in cultured atrial cardiocytes.

The current study tested the hypothesis that hypoxia stimulates atrial natriuretic peptide (ANP) gene expression and secretion in cultured atrial myocytes (AT-1 cells). AT-1 cells were obtained from a transplantable mouse atrial cardiomyocyte tumor lineage. Confluent AT-1 cells were exposed to hypoxia (1% oxygen) or normoxia (21% oxygen) as controls for 6 hours to 7 days. Medium ANP levels were measured by radioimmunoassay, and intracellular ANP gene transcripts were quantified by Northern and slot blot analyses. Exposure to hypoxia resulted in a significant increase in cellular ANP mRNA levels within 36 hours, which peaked (3.6-fold increase) at 2 days after hypoxic exposure, and produced a time-dependent increase in the release of ANP from AT-1 cells for 2 to 7 days. Transfection studies with recombinant DNA constructs that contained fragments of the -3003/+62 sequence of the ANP promoter and the luciferase reporter gene revealed that the regulatory sequences that mediate the hypoxia-induced increase in transcription are located within a region that extends from -638 to -518 bp to the transcriptional start site of the ANP gene. Gel mobility shift assays demonstrated that hypoxia-inducible nuclear proteins that bound to the 120-bp putative hypoxia-responsive elements of the ANP gene were produced during hypoxic exposure. We have thus defined a 120-bp region within the ANP gene promoter that contains hypoxia-responsive elements that might be responsible for the enhancement of ANP gene expression in atrial myocytes during hypoxic exposure.

Animals↗
PubMed1996

Medroxyprogesterone attenuates estrogen-mediated inhibition of neointima formation after balloon injury of the rat carotid artery.

BACKGROUND: Estrogen blunts the neointimal proliferative response to balloon injury of the carotid artery in intact female rats and gonadectomized rats of both sexes. This study tested whether, in gonadectomized rats of both sexes. (1) progestin (medroxyprogesterone acetate, MPA) alters neointima formation in injured carotid arteries, (2) addition of MPA alters the antiproliferative effects of estrogen, and (3) an interaction between MPA and estrogen can be accounted for by MPA-induced alterations in serum 17 beta-estradiol levels. METHODS AND RESULTS: Male and female Sprague-Dawley rats were subjected to gonadectomy, then were randomly divided into four subgroups and treated with either (1) 17 beta-estradiol, (2) MPA, (3) 17 beta-estradiol + MPA, or (4) vehicle, and balloon injury of the right common carotid artery was carried out. Two weeks later, rats were killed by overdose of pentobarbital, and the carotid arteries were subjected to morphometric analysis for evaluation of myointimal thickening. Estradiol inhibited myointimal proliferation after vascular injury in gonadectomized rats of both sexes (P < .05). MPA alone did not alter neointima formation, but addition of MPA to estradiol completely blocked the antiproliferative effects of estrogen without altering serum 17 beta-estradiol levels. CONCLUSIONS: These data indicate that exogenous progestin given alone does not alter the vascular injury response in the rat carotid injury model but that addition of a progestin blocks the antiproliferative effects of estrogen in this model. These effects are seen in gonadectomized rats of both sexes. These findings have direct implications for postmenopausal hormone replacement therapy in humans.

Animals↗
PubMed1996

Estrogen reduces myointimal proliferation after balloon injury of rat carotid artery.

BACKGROUND: Vascular disease progresses more slowly in females with functional ovaries than in males. The mechanisms of this vasoprotective effect of female sex are incompletely understood. This study tested (1) whether there is a sex difference in the development of myointimal proliferation after balloon injury of the rat carotid artery in vivo, (2) whether this response is estrogen or androgen dependent, and (3) whether there is a sexual dimorphism in expression of the c-myc proto-oncogene in intact and/or damaged rat carotid arteries. METHODS AND RESULTS: Ten-week-old male and female Sprague-Dawley rats were either gonadectomized or studied intact. Gonadectomized rats of both sexes were implanted with estradiol, testosterone, or nothing (control) 3 days before vascular injury. Two weeks later, the rats were killed by overdose of pentobarbital, and the injured right and uninjured control left carotid arteries were fixed and subjected to morphometric analysis for evaluation of the degree of myointimal thickening. Separate groups of intact male and female rats were killed at 1 and 2 hours after vascular injury, and total RNA from injured and uninjured vessels was subjected to Northern blot analysis for assessment of steady state c-myc mRNA levels. Neointimal area and the ratio of neointimal to medial area were significantly less in intact female rats than in intact male rats (P < .05). Gonadectomy of female rats was associated with a greater increase in neointima formation after balloon injury than that observed in intact females (P < .05), but testosterone replacement did not further enhance this response. Estradiol treatment significantly inhibited myointimal proliferation after vascular injury in gonadectomized rats of both sexes (P < .05). Neither gonadectomy nor gonadectomy plus testosterone replacement altered the myointimal proliferative response to balloon injury in male rats. Steady state c-myc mRNA levels were detectable in undamaged carotid arteries in intact rats of both sexes and were significantly greater in males than in females; c-myc mRNA levels were increased in both sexes after carotid injury, but the response was significantly larger in magnitude and more rapid in males than in females. CONCLUSIONS: These data indicate that the sex difference in myointimal proliferation after vascular injury is estrogen dependent. C-myc gene expression is greater in the undamaged carotid artery of the male than in that of the female, and the responsiveness of this gene to balloon injury of the artery is more rapid and more robust in the male than in the female rat. These findings have direct implications for the prevention and treatment of vascular disease in humans.

Animals↗
PubMed1996

Incorporation of a fluorocarbon polymer implanted at the posterior surface of the rabbit cornea.

An implant of porous expanded polytetrafluoroethylene (PTFE) in the corneal stroma allows fast cell colonization and can become translucent. We studied the behavior of the same polymer implanted in the anterior chamber of the rabbit eye and sutured to the posterior surface of the cornea. The expanded tetrafluoroethylene was provided as 200-micron thick sheets in 3 pore diameters (20, 50 and 80 microns). Disks (5 mm) were implanted in the anterior chambers of 20 rabbits and sutured to the posterior surface of the cornea. Histological and ultrastructural studies were performed after 3 and 4 months. Quantimetry was done on TEM images to analyze the fibrillar structure of the intercellular matrix inside and around the implanted polymer. The material was well tolerated. In all cases there was mild central corneal edema, which disappeared after 1 month. Mild neovascularization occurred in five cases, decreasing after 1 month. The polymer became translucent after 8 days. Keratocytes from the corneal stroma colonized the implant via breaks in the Descemet's membrane along the sutures. Quantimetry showed three types of fibrils inside and beside the polymer. Corneal endothelial cells regenerated over the fibroblasts and the polymer. This fluorocarbon polymer implanted in the anterior chamber and sutured to the posterior surface of the cornea was well tolerated, and there was real incorporation, with keratocytes producing collagen fibrils inside the polymer and endothelial cells forming a posterior cell monolayer. This is promising for the development of a keratoprothesis with posterior fixation.

Animals↗
PubMed1996

Local mechanisms of phase-dependent postsynaptic modifications of NMDA-induced oscillations in the abducens motoneurons: a simulation study.

1. In vivo experiments have shown that extracellular microelectrophoretic application of N-methyl-D-aspartate (NMDA) induced oscillatory plateau potentials with bursts of action potentials in rat abducens motoneurons. The period of these slow NMDA oscillations could be altered by single trigeminal non-NMDA excitatory input delivered at low frequency during the NMDA oscillations. 2. A resetting of the oscillations was observed depending on the phase of slow oscillatory cycle during which the trigeminal excitation occurred. 3. We investigated local mechanisms responsible for the phase-dependent modifications of NMDA oscillations, including contributions of voltage and concentration transients, in the mathematical model of the isopotential membrane compartment equipped with voltage-gated Na+, K+, and Ca2+ channels, with Ca2+-dependent K+ channels, and with ligand-gated NMDA and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor channels. The faithful model was constructed with the use of models described earlier, which were modified by increasing time constants of kinetic variables of all voltage-gated conductances and by including coupled dynamics of voltages and ion concentrations. The changes in ion concentrations were produced near the membrane by transmembrane currents and removal mechanisms (pumps, diffusion). 4. This work focuses on local arrangement of voltage- and ligand-gated conductances and on local ion concentration changes in two separate pools: the postsynaptic pool of AMPA receptors and the extrasynaptic pool. In terms of the electrotonic and diffusional length constants, these pools were electrotonically close but diffusionally remote. 5. It was found that the effect of resetting can be produced by a local interaction between plateau and spike-generating conductances and glutamate receptors. 6. In vivo phase-dependent interactions between NMDA oscillations and AMPA synaptic input were reproduced by the local model only when changes in intracellular sodium and extracellular potassium concentrations were taken into account and the mechanisms of ion removal from postsynaptic pools had slower kinetics than the fast pump system operating in the extracellular pool. 7. Postsynaptic changes in ion concentrations of Na+ and K+ in intra- and extracellular layers near the membrane shift of Nernst equilibrium potentials for these ions depending on the phase of activation of synaptic input. Thus Na+ and k+ components of all transmembrane currents involved in the pattern generation are differently affected by synaptic action during the oscillations. We conclude that slow postsynaptic changes in ion concentrations near the membrane play a key role in the resetting of the NMDA oscillations.

Abducens Nerve↗
PubMed1996

International migration and development in Mexican communities.

The theoretical and empirical literature generally regards international migration as producing a cycle of dependency and stunted development in sending communities. Most migrants' earnings are spent on consumption; few funds are channeled into productive investment. We argue that this view is misleading because it ignores the conditions under which productive investment is likely to be possible and profitable. We analyze the determinants of migrants' savings and remittance decisions, using variables defined at the individual, household, community, and macroeconomic levels. We identify the conditions under which U.S. earnings are repatriated to Mexico as remittances and savings, and indicate the factors leading to their productive investment.

Adult↗
PubMed1995

Sensitive method for quantitation of angiotensin-converting enzyme (ACE) activity in tissue.

A novel sensitive and specific method for the measurement of tissue angiotensin-converting enzyme (ACE) activity utilizing HPLC is described. ACE activity was determined in detergent-extracted canine hearts utilizing the synthetic ACE-specific substrate hippuryl histidyl leucine (HHL), both in the presence and the absence of the site-specific inhibitor captopril. Tissue ACE activity was quantitated from the moles of hippuric acid (HA) formed, in time-fixed assays, utilizing HPLC separation of HA from HHL and UV-spectrophotometry for quantitation of HA as in the standard Cushman and Cheung assay (Cushman DW and Cheung HS, Biochem Pharmacol 20: 1637-1648, 1971). Separation of HA from HHL was performed by reverse phase HPLC on a phenyl silica gel column with an eluent consisting of 20% acetonitrile in 0.1 M aqueous ammonium phosphate buffer, pH 6.8. After the standard liquid/liquid extraction procedure with ethyl acetate, HPLC analysis revealed the presence of unreacted substrate, HHL, in amounts comparable to the product of interest, HA, in the final assay; moreover, the amount of HA formed did not fall completely to zero in the presence of captopril. Regional studies of canine cardiac ACE activity utilizing the HPLC-based assay and the standard assay method showed a significantly higher ACE activity in the right ventricle compared with the left ventricle (2.37 +/- 0.7 vs 1.24 +/- 0.18 mU/g, P < 0.05 [N = 6], respectively) in the HPLC-based assay, but no difference in right and left ventricular ACE activities by the standard assay (0.25 +/- 0.08 vs 0.31 +/- 0.09 mU/g [N = 6], respectively). Kinetic studies utilizing the HPLC-based assay coupled with the use of captopril showed Km (1.34 +/- 0.08 mM) and Vmax (36.8 +/- 11.5 x 10(-10) M/min) values in agreement with those in the literature. Our results demonstrate that the application of HPLC to the standard Cushman and Cheung assay improves the sensitivity and specificity of the standard assay and enables the use of much smaller amounts (approximately 4 vs approximately 400 mg for the Cushman and Cheung assay) of tissue for ACE activity assay.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Distribution and spatial geometry of dopamine interplexiform cells in the retina. II. External arborizations in the adult rat and monkey.

The morphology and distribution of dopaminergic interplexiform cells in adult rat and monkey retinas were analyzed to determine any correlation with the function of dopamine in the outer retinal layers. The retinas were processed as whole mounts for tyrosine hydroxylase immunohistochemistry. There was a network formed by the sclerally directed processes of interplexiform cells in the inner nuclear, outer plexiform, and outer nuclear layers running throughout the retina. Their density was higher in the superior retina than in the inferior retina of the rat and was especially high in the superior temporal quadrant. The external network in this quadrant was significantly less dense in the monkey than in the rat, as are the interplexiform cells. The somata of interplexiform and other dopaminergic cells were about the same size in both rats and monkeys. Computer-assisted reconstruction of external arborizations of individual cells showed that external processes lay very close to horizontal and photoreceptor cells and also to blood capillaries. Because they were long, thin, and highly varicose; branched at right angles; and often arose from an axon hillock, the external processes were identified as axons. Therefore, we define the dopaminergic interplexiform cells as multiaxonal neurons, with at least one outwardly directed axon that reaches the outer plexiform layer. The function of the network of external processes from the interplexiform dopaminergic cells is discussed in terms of modulating the release of dopamine to external layers.

Animals↗
PubMed1995

Use of denaturing gradient electrophoresis to determine the distributions of polymorphisms in entire genes in natural populations.

We show here that the method of genomic denaturing gradient electrophoresis (gDGGE) can be used to examine any gene that has been previously cloned and sequenced, and to detect and approximately localize within the gene the majority of its polymorphisms. By using pooled-DNA gDGGE, many different samples can be scanned on a single gel. Further, the patterns on the gels and results from sequencing of some of the alleles shows that a variety of different kinds of polymorphism, ranging from single base changes to more substantial allelic differences, can be distinguished. The extramacrochaetae (emc) gene of Drosophila melanogaster exhibits no polymorphism in its ORF that can be detected by this method, although a rearrangement polymorphism was detected in the 3' downstream region of the gene. The suppressor-of-hairless (Su(H)) gene of D. melanogaster, however, exhibits a variety of polymorphisms in its ORF. Some are small deletions or insertions in a glutamine-rich part of the gene product that would not have been detectable by ordinary screening methods. Many of the polymorphisms detected in this preliminary survey are likely to have an impact on the function of the Su(H) gene product.

Animals↗
PubMed1995

Control of inositol phosphate turnover in human airways during histamine stimulation.

The control of inositol phosphate (IP) turnover was investigated in intact human airway smooth muscle cells (SMC) during a brief exposure to a bronchoconstrictor agonist. The pool of membrane phosphatidylinositol 4,5-biphosphate was labelled by incubating SMC with myo-[3H]inositol and the [3H]IPs synthetized ([3H]1,4-IP2, [3H]1,3,4,-IP3, [3H]1,4,5,-IP3 and [3H]1,3,4,5-IP4) were separated by HPLC. We examined the role of protein kinase C (PKC) and of Ca2+ on IP turnover during a 5 sec application of histamine. Activation of PKC with the phorbol ester PMA (0.2 microM) decreased, whereas inhibition of PKC with 1 microM staurosporine increased the production of the 4 IPs examined in unstimulated and in histamine-stimulated SMC. Decreasing [Ca2+]i with 5 microM ionomycin in the absence of external Ca2+ diminished the IP production whereas in the presence of Ca2+, ionomycin exalted it and potentiated the response to histamine. Thapsigargin, 5 microM, which depletes the 1,4,5-IP3-sensitive Ca2+ stores, reduced the IP production due to histamine. The effects of PMA, staurosporine and thapsigargin were also tested on [Ca2+]i in fura-2-loaded single SMC. These results reveal that PKC exerts a negative and Ca2+ a positive feedback control on phospholipase C, that operate within 5 sec of agonist stimulation.

Alkaloids↗
PubMed1995

ETA-receptor antagonist prevents and reverses chronic hypoxia-induced pulmonary hypertension in rat.

The selective endothelin-A (ETA)-receptor antagonist BQ-123 has been shown to prevent chronic hypoxia-induced pulmonary hypertension in the rat. Therefore in the current study we utilized BQ-123 to test the hypothesis that blockade of the ETA receptor can reverse as well as prevent the increase in mean pulmonary artery pressure, right ventricle-to-left ventricle plus septum ratio, and percent wall thickness in small (50-100 microns) pulmonary arteries observed in male Sprague-Dawley rats exposed to normobaric hypoxia (10% O2, 2 wk). Infusion of BQ-123 (0.4 mg.0.5 microliter-1.h-1 for 2 wk in 10% O2) begun after 2 wk of hypoxia significantly reversed the established pulmonary hypertension and prevented further progression of right ventricular hypertrophy during the third and fourth week of hypoxia. BQ-123 infusion instituted before exposure to hypoxia completely prevented the hypoxia-induced pulmonary hypertension, right ventricular hypertrophy, and pulmonary vascular remodeling. These findings suggest that, in the lung, hypoxia induced an increase synthesis of endothelin-1, which acts locally on ETA receptors to cause pulmonary hypertension, right heart hypertrophy, and pulmonary vascular remodeling, while ETA-receptor blockade can both prevent and reverse these processes.

Animals↗
PubMed1995

Endothelin-receptor antagonist bosentan prevents and reverses hypoxic pulmonary hypertension in rats.

The current study examined the effects of bosentan, an orally active antagonist of endothelin-A and -B receptors, on the development and maintenance of hypoxia (10% O2)-induced pulmonary hypertension and vascular remodeling in the rat. Pretreatment with bosentan (100 mg.kg-1.day-1, 1 gavage/day for 2 days) completely blocked the pulmonary vasoconstrictor response to acute hypoxia. Chronic bosentan treatment (100 mg.kg-1.day-1 po in the food) instituted 48 h before hypoxic exposure prevented the subsequent development of pulmonary hypertension, attenuated the associated right heart hypertrophy, and prevented the remodeling of small (50-100 microns) pulmonary arteries without altering systemic arterial pressure. Institution of bosentan treatment (for 4 wk) after 2 wk of hypoxia produced a significant reversal of established hypoxia-induced pulmonary hypertension (from 36 +/- 1 to 25 +/- 1 mmHg), right heart hypertrophy, and pulmonary vascular remodeling despite continuing hypoxic exposure. These findings support the hypothesis that endogenous endothelin-1 plays a major role in hypoxic pulmonary vasoconstriction and/or hypertension, right heart hypertrophy, and pulmonary vascular remodeling and suggest that endothelin-receptor blockade may be useful in the treatment of hypoxic pulmonary hypertension humans.

Animals↗
PubMed1995

Effects of dietary salt on angiotensin peptides in kidney.

This study used a novel simple method for the extraction, separation, identification, and quantitation of angiotensin-like immunoactivity from tissue to examine the effects of altering dietary NaCl intake on intrarenal angiotensin I, II, and III levels in salt-sensitive, spontaneously hypertensive rats, salt-resistant Wistar-Kyoto rats, and Sprague-Dawley rats. Seven-week-old male spontaneously hypertensive rats, Wistar-Kyoto rats, and Sprague-Dawley rats were assigned randomly to a diet containing either 8% (high) or 1% (basal) salt and were maintained on these diets for 3 wk. Rats were then decapitated without prior anesthesia, and kidneys were rapidly (< 30 s) removed, snap frozen in liquid nitrogen, and stored at -80 degrees C. Frozen tissue was extracted in 2 M acetic acid and then subjected to solid-phase extraction with the cation exchange resin AG 50W X4. Angiotensin peptides were separated by reversed-phase high-performance liquid chromatography on a phenyl silica gel column with an eluent consisting of 20% acetonitrile in 0.1 M ammonium phosphate buffer, pH 4.9, and quantitated by radioimmunoassay. The elution of standard peptides under isocratic conditions revealed clear resolution of angiotensin I, II, and III and the (1-7) and (3-8) peptides. Recoveries of both labeled and unlabeled angiotensin peptide standards from the extraction step were > 90%. Renal angiotensin II stores were significantly higher in spontaneously hypertensive rats than in Wistar-Kyoto or Sprague-Dawley rats, independent of diet. Renal angiotensin II and III were further suppressed during dietary salt supplementation in both salt-resistant strains but not in the spontaneously hypertensive rat. These findings are consistent with an enhanced (compared with Wistar-Kyoto and Sprague-Dawley rats) role for angiotensin II in the kidney of the salt-sensitive, spontaneously hypertensive rat, particularly under conditions of dietary salt supplementation.

Angiotensin I↗