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Focuses on a study which discussed the role of angiotensin IV in inducing tyrosine phosphorylation of focal adhesion kinase and paxillin in proximal tubule cells. Effects of angiotensin IV on cell growth; Materials and methods used; Results; Limitations of the study.

Background Angiotensin II exerts its actions through its specific receptors. However, expression of these receptors has not been determined in sweat glands. Objectives To clarify the expression and localization of the angiotensin receptors in normal human sweat glands and eccrine poroma. Methods Expression of angiotensin type 1 (AT1) and type 2 (AT2) receptors in normal human eccrine and apocrine sweat glands and 12 cases of eccrine poroma was studied using immunohistochemistry. Results In eccrine sweat glands, the acrosyringium and the inner surfaces and luminal cells of the intradermal duct showed positive staining with AT1. In apocrine sweat glands, the intraepithelial duct and luminal cells of the intradermal duct showed positive staining with AT1. In 12 cases of eccrine poroma, some of the tumour cells in the tumour strands and cells surrounding the luminal structures stained positively. There were no positive findings with AT2. Conclusions Studying AT1 distribution may be useful in understanding the pathophysiology of sweat glands and sweat gland tumours. [ABSTRACT FROM AUTHOR]

Objective: Angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism influence the circulating and cellular levels of ACE and has been shown to be a risk factor in a number of diseases including IgA nephropathy. We have investigated the association of ACE gene I/D polymorphism with the clinical presentation of idiopathic nephrotic syndrome (INS) in Kuwaiti children. Materials and methods: The genotypes for ACE gene I/D polymorphism were determined in 102 subjects (54 INS cases and 48 healthy controls) using a PCR method. Results: The distribution of DD, ID and II genotypes was 70%, 20% and 10% in INS cases compared with 52%, 46% and 2% in the controls. The mean age of onset of the disease was significantly lower in the INS cases with DD genotype (37 months) compared with cases with II genotype (65 months, p < 0.05). The clinical manifestation of the disease was considerably severe in cases with DD genotypes compared with cases having ID and II genotypes. The INS cases with DD genotype also showed a significantly higher incidence of steroid sensitivity and steroid dependence. Seventy-three per cent of the INS cases with minimal change lesion had a DD genotype. Also 70% of the cases which needed cytotoxic drugs had DD genotype. Conclusion: Our data suggest an association of the D-allele of the ACE gene I/D polymorphism with the clinical manifestation of INS in Kuwaiti Arab children. [ABSTRACT FROM AUTHOR]

Presents information on a study which examined the role of endothelin in mediating the renal hemodynamic and arterial pressure changes during chronic angiotensin II-induced hypertension. Methodology; Results of the study; Discussion.

Deals with a study which examined the physiological role of angiotensin II and tumor necrosis factor-alpha to the development of renal fibrosis. Materials and methods of the study; Results; Discussion of the results.

Examines the effect of angiotensin II (AII) on angipoietin 1 and 2 (Ang1 and 2) expression in cultured bovine retinal endothelial cells. Stimulation of Ang2 messenger RNA (mRNA) expression; Rate of Ang2 mRNA transcription; Role of AII in the enhancement of Ang2 protein synthesis.

Focuses on a study which evaluated angiotensin messenger RNA expression in the midcaudal arcuate nucleus of the rat brain during lactation. Methods; Results; Discussion.

Focuses on a study which evaluated whether the antiangiogenic effect of angiotensin-(1-7) in the mouse sponge model of angiogenesis might be receptor mediated and involved in the release of nitric oxide. Materials and methods; Results; Discussion.

Tests the hypothesis that lactation decreases angiotensinogen (AON) mRNA expression in the midcaudal arcuate nucleus of the rat brain. Distribution of AON mRNA in the forebrains of lactating and diestrous rat brains; Mechanism whereby lactation is associated with a reduction in AON mRNA in the midcaudal arcuate nucleus of the rat brain.

Studies brain angiotensin (AT) receptors and sympathoadrenal regulation during insulin-induced hypoglycemia. Efficacy of intracerebroventricular AT[sub 1]-receptor blockade; Plasma glucose-epinephrine relationship; Change in mean arterial pressure and heart rate during insulin-induced hypoglycemia.

Studies the effect of repetitive intracerebroventrricular injections of angiotensin II on c-Fos and angiotensin AT[sub 1]-receptor expression in the rat brain. Decrease in c-Fos expression in median preoptic area, subfornical organ, paraventricular nucleus, and supraoptic nucleus; Coexpression of c-Fos and C-Jun with the AT[sub 1] receptor.

Tests the hypothesis that abnormal renal medullary response to angiotensin II in spontaneously hypertensive rats (SHR) is corrected by long-term treatment with the hypotensive agent enalapril. Effects of angiotensin II on renal blood flow in hypertensive rats; Relaxation responses of aortic rings.

Studies the mechanisms of angiotensin-(1-7)-induced inhibition of angiogenesis. Effects of the angiotensin-receptor antagonist losartan on the hemoglobin content of cannulated sponge discs; Possible mechanisms involved in the ANG-(1-7)-induced inhibition of angiogenesis; Involvement of AT[sub 1] and AT [sub 2] receptors in mediating the antiangiogenic effects of ANG (1-7).

Studies the role of angiotensin (ANG) II and endothelin-1 in exercise-induced diastolic dysfunction in heart failure. Effects of pacing-induced chronic heart failure; Influence of exercise on plasma levels of ANG II, plasma renin activity, and endothelin-1, before and after chronic heart failure.

Tests the hypothesis that angiotensin (ANG) II stimulates cardiac L-type calcium currents by a calcium and protein kinase C-dependent mechanism. Inhibition by losartan of the ANG II effects on intercellular calcium; Voltage dependence of steady-state activation and inactivation of intercellular calcium in the absence and presence of ANG II.

Studies the interaction between genetic variability of the renin-angiotension system and metabolic risk factors in premature myocardial infarction. Analysis of gene polymorphisms of angiotensin-I converting enzyme gene, angiotensinogen gene, and angiotensin-II type-1 receptor gene.

Examines whether the renal nerves modulate the effect of intraluminal angiotensin II on proximal tubule transport. Volume reabsorption; Indication that renal denervation abolished the luminal enalaprilat-sensitive component of proximal tubule transport.

Explains how nitric oxide (NO)/cyclic guanylic acid (cGMP) signaling modulates the regulation of sodium-potassium pump activity by angiotensin II in rat proximal tubules. Increase in intracellular cGMP concentration; Suggestion that NO/cGMP signaling pathway serves as a negative component in the regulation of sodium-potassium pump activity by angiotensin II.

Examines the effect of intracerebroventricular infusion of somatostatin or losartan, the angiotensin II type 1 receptor antagonist, on the sodium appetite and thirst of sodium-depleted sheep. Effect of intracerebroventricular infusion of hypertonic mannitol; Role for somatostatin and angiotensin II in the central mechanisms controlling sodium appetite.

Examines the role of angiotensin II (ANG II) in the glucocorticoid modulation of cardiovascular and autonomic nervous function in preterm lambs. Speculation that augmented cardiovascular function in glucocorticoid-treated premature lambs is dependent, in part, on a generalized sympathoexcitatory response and is mediated by central mechanisms.

Examines how angiotensin type 1 (AT[sub 1) receptor blockers prevent sympathetic hyperactivity and hypertension by chronic ouabain and hypertonic saline. Suggestion that peripheral administration of losartan as well as embusartan can cause sufficient central nervous effects to prevent the sympathetic hyperactivity and hypertension.

Presents information on a study which examined the effects of blockade of the renin-angiotensin system on the renal metabolism of arachidonic acid in rats. Methods used; Results; Discussion.

Presents information on a study which examined the effect of oral contraceptive usage on the renin angiotensin system in healthy, premenopausal women. Background on oral contraceptive medications; Methods used in the study; Results; Discussion.

Discusses the biphasic effect of angiotensin II (ANG II) on sodium ion transport in the kidney through its effects on sodium ion-potassium ion-adenosine triphosphatase (ATPase) activity. ANG II-induced cyclic guanosine monophosphate formation in rat proximal tubules; Approaches used to evaluate the role of nitric oxide signaling; Effect of SK&F 108566 on ANG II-stimulated sodium ion-potassium ion-ATPase activity.

Examines whether the renal nerves modulate the effect of intraluminal angiotensin II (ANG II) on proximal tubule transport. Physiology of ANG II; Effect of chronic renal denervation on the role of intraluminally generated ANG II on proximal tubule volume reabsorption; Effect of acute renal denervation on intraluminally generated ANG II mediated proximal tubule transport.

Provides information on a study which examined whether central administration of an angiotensin type 1 receptor blocker can prevent the sympathetic hyperactivity and hypertension effects of ouabain and sodium-rich artificial cerebrospinal fluid. Methods used in the study; Results and discussion.

Intracerebroventricular (ICV) angiotensin (AII) administration stimulates central AII receptors to induce water consumption in rats. The aim of this study was to determine the role of brain AT[sub 1] and AT[sub 2] receptors in mediating chronic ICV AII-induced drinking in rats raised on normal or high sodium chloride diets from weaning. Rats were weaned at 21 days of age and placed on normal or high sodium chloride diet for 10-12 weeks. At adulthood, the animals were instrumented with brain lateral ventricular cannulas and femoral arterial catheters. Low dose chronic central AII infusion (20 ng min[sup -1]) significantly (P < 0.05) increased water intake in both groups of rats when compared with their respective controls of 24 h artificial cerebrospinal fluid infusions. In a separate group of high sodium fed rats, coinfusion of AII with the AT[sub 1] receptor antagonist, losartan (0.25 micro g min[sup -1]) or the AT[sub 2] receptor blocker, PD 123319 (0.50 micro g min[sup -1]) blocked chronic ICV AII-induced drinking. Upon reinfusion of AII water intake increased above control. Following the cessation of AII infusions, water intake returned to values not significantly different from control (P > 0.05). In contrast, in the normal sodium fed rats losartan, but not PD 123319, blocked the AII-mediated water intake. The data demonstrate that in high sodium chloride fed rats AII stimulates both central AT[sub 1] and AT[sub 2] receptors to induce drinking, while in the normal sodium chloride fed rats the peptide activates the drinking response primarily by stimulation of central AT[sub 1] receptors. [ABSTRACT FROM AUTHOR]

The role of angiotensin subtype-1 (AT[sub 1]) and -2 (AT[sub 2]) receptors in mediating the effects of angiotensin II (ANG II) on several K[sup +] transporters was studied in rat distal colon using an Ussing chamber. Angiotensin II induced K[sup +] secretion at two different doses. Secretion occurred at 10[sup -8] and 10[sup -4, sub M], as a result of an increase in serosal-to-mucosal flux (J[sub s-m]). The ANG II-induced stimulation of J[sub s-m] at a low dose (10[sup -8] M) was abolished by PD123319 while losartan did not alter the low-dose ANG II-dependent increase in J[sub s-m]. In contrast, the increase in J[sub s-m] induced by a high-dose of ANG II (10[sup -4, sub M]) was blocked by losartan, whereas PD123319 partially reduced the stimulatory effect. In the presence of both blockers, high-dose ANG II induced an inhibition of basal J[sub s-m]. Low-dose ANG II activated the barium-sensitive K[sup +] channels, whereas the Na[sup +], K[sup +], 2Cl[sup -] cotransporter and the Na[sup +], K[sup +]-ATPase pump were unchanged. At the high dose, ANG II activated the barium-sensitive K[sup +] channels and the Na[sup +], K[sup +], 2Cl[sup -] cotransporter and inhibited the Na[sup +], K[sup +]-ATPase pump. These data indicate that ANG II stimulates serosal-to-mucosal K[sup +] flux in the rat distal colon at high and low doses via different receptors and K[sup +] transporters. [ABSTRACT FROM AUTHOR]

Focuses on a study which discussed TGR(ASrAOGEN)680, a transgenic rat line which exhibits decreased brain angiotensinogen content associated with a mild diabetes insipidus and lower blood pressure. Materials and methods of the study; Results; Discussion of the results.

Presents a study which compared the effects of vasoconstrictors nitric oxide and angiotensin II on the water uptake across the pelvic patch of Bufo marinus or toads. Materials and methods used; Cardiovascular effects of the vasoconstrictors; Pelvic patch studies.

Investigates whether a lesion of the subfornical organ (SFO) may reduce sodium depletion-induced salt appetite, which is largely dependent on angiotensin II. Reduction in mean arterial pressure; Water intakes during angiotensin II infusion into the SFO; Alteration of water intake with varying doses of minoxidil.

Tests the hypothesis that angiotensin II enhances beta-adrenergic receptor-mediated vasorelaxation in aortas from young but not old rats. Effect of angiotensin II on isoproterenol-stimulated vasorelaxation in young and old rats; Determination of angiotensin II receptor type involved in enhanced isoproterenol-stimulated vasorelaxation.

Focuses on a study which conducted experiments on how a lesion of the subfornical organ may reduce sodium depletion-induced salt appetite, which is largely dependent on angiotensin II. Methodology; Results of the study; Discussion of the results.

Presents a study which investigated whether chronic Angiotensin II receptor blockade was associated with modulation of cardiac Smad expression and activation in failing rat heart post-myocardial infarction. Materials and methods; Results; Discussion.

Presents a study which determined the effect of renin-angiotensin system inhibition on noradrenergic nerve terminal function in pacing-induced heart failure. Methods; Results; Discussion.

Presents a study which evaluated the role of angiotensin receptors in the rostral ventrolateral medulla in the cardiovascular response elicited by the bilateral injection of sarthran into this region. Methods; Results: Discussion.

Presents a study which investigated the effects of diastolic wall stress and angiotensin on the left ventricular (LV) hypertrophy induced by volume overload. Methods; Results; Discussion.

Presents a study which determined whether angiotensin II could reverse age-related, impaired beta-adrenergic receptor-mediated vasorelaxation. Characteristics of an aged cardiovascular system; Methodology; Results and discussion.

Presents a study which determined the temporal sequence for activation of the renin-angiotensin and sympathetic nervous system in response to cardiac pressure overload. Factors which offset the benefits of cardiac hypertrophy; Methodology; Results and discussion.

Presents a study which examined smooth muscle actin (SMA) expression regulation in cardiac fibroblasts. Examination of whether mechanical force and angiotensin II activity regulates SMA expression; Methodology; Results and discussion.

Focuses on a study which examined the activity and responsiveness of the renin-angiotensin system in the aging rat. Methods; Details on studies of chronic angiotensin-converting enzyme inhibitors; Assessment of the functional conversion of angiotensin (ANG) I to ANG II.

Tests the hypothesis that angiotensin II increases vasopressin-stimulated facilitated urea permeability in rat terminal inner medullary collecting duct (IMCD). Phosphorylation of urea transporter-1; Effect of staurosporine and angiotensin II on vasopressin-stimulated urea permeability.

Tests the hypothesis that renal nerve inhibition by central sodium chloride and angiotensin II is abolished by lesions of the lamina terminalis. Responses to intracerebroventricular infusion of hypertonic saline in intact and lesioned sheep; Changes in renal sympathetic nerve activity and mean arterial pressure.

Examines the location and expression of NAD(P)H oxidase-derived superoxide components in the mouse aorta, and investigates whether protein levels are increased by angiotensin II. Oxygen generation in mouse thoracic aortas; Bioactivity of endothelium-derived nitric oxide; Therapeutic success of endothelial nitrogen oxide synthase in restoring impaired vascular function.

Examines the role of angiotensin (ANG) IV-mediated vasorelaxation using an in situ model of endothelium-denuded pulmonary artery (PA) segments as well as PA endothelial cell (PAEC)-PA smooth muscle cell (PASMC) coculture system. Absence of ANG IV receptors in PASMC; Dose-dependent vasodilation caused by ANG IV.

Presents information on a study which investigated the effect of angiotensin II and atrial natriuretic peptide on intracellular hydrogen-ion concentration and calcium concentration in kidneys. Materials and methods; Results; Discussion.

Discusses a study which evaluated the ability of angiotensin II in regulating urea transport in the inner medullary collecting duct. Methods; Results; Discussion.

Presents information on a study which examined the location and expression of nicotinamide adenine dinucleotide(P)H oxidase components in the mouse aorta and investigated whether protein levels are increased by angiotensin II. Methodology of the study; Results and discussion on the study.

Focuses on a study which determined the role of endothelial intracellular calcium release in angiotensin IV-mediated pulmonary artery vasorelaxation. Effects of angiotensin IV activation of the endothelial cell isoform of nitric oxide synthase (ecNOS) in nitric oxide release; Catalytic activity of ecNOS; Materials and methods used; Results; Conclusions.

Presents information on a study which investigated whether angiotensin II is involved in the enhancement seen in dehydrated rats of the fever induced by bacterial endotoxin. Methods used in the study; Results and discussion.