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Query: UMLS:C0004135 (
ATM
)
13,001
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Intracerebroventricular (ICV) angiotensin (AIl) administration stimulates central
AII
receptors to induce water consumption in rats. The aim of this study was to determine the role of brain
AT1
and AT2 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(-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
AT1
receptor antagonist, losartan (0.25 microg min(-1)) or the AT2 receptor blocker, PD 123319 (0.50 microg min(-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
AT1
and AT2 receptors to induce drinking, while in the normal sodium chloride fed rats the peptide activates the drinking response primarily by stimulation of central
AT1
receptors.
...
PMID:Central AT1 and AT2 receptors mediate chronic intracerebroventricular angiotensin II-induced drinking in rats fed high sodium chloride diet from weaning. 1135 Feb 80
The aim of this study was to analyze if the upregulation of angiotensin-converting enzyme and
AT1
receptors observed in a model of neointima formation results in increased contractions to angiotensin I (AI) and
AII
. Endothelial denudation was performed in left common carotid arteries of 3-month-old male Sprague-Dawley rats. Rats were killed at days 0, 4, 8 and 14 after injury and vascular reactivity was assessed in an organ bath. Responses were always compared with their contralateral vessels as a control. Contractile responses to 75 mM KCl were similar between groups. Noradrenaline (0.1 microM) induced significantly higher contractions at days 0 and 4. Relaxation to acetylcholine (Ach) (1 nM to 0.1 mM) was suppressed at day 0 and increased with time after injury. Relaxations to sodium nitroprusside (0.1 nM to 0.1 mM) were similar at all time points studied. Responses to AI and
AII
were increased at early steps of neointima formation and decreased with time after injury correlating with increased responses to Ach. Concentration-response curves to AI and
AII
had similar EC50 or Emax values at the same time points. These results indicate that in the rat i) neointima formation does not impair contractile responses to KCl nor relaxation to SNP, ii) a functional endothelium seems to regenerate with time after injury, and iii) the increase in ACE activity and
AT1
receptor number does not have functional consequences.
...
PMID:The upregulation of angiotensin-converting enzyme during neointima formation does not have functional consequences. 1169 65
In the present study we used the isolated rat aorta as a model to characterize the modulation of contractile effects of extra- and intracellularly administered angiotensin II by dithiothreitol (DTT) and hyperosmotic sucrose. DTT inactivation of
AT1
receptor as well as disruption of the clathrin-coated pits by hyperosmotic sucrose significantly inhibited the contraction induced by intracellularly administered
AII
. We suggest that these intracellular effects of angiotensin peptides are associated with
AT1
receptor activation/internalization and may thus be part of the mechanism of angiotensin peptides direct contractile effects in the vascular smooth muscle.
...
PMID:Contractile effects of intracellularly administered angiotensin II are partially dependent on membrane receptors internalization in isolated rat aorta. 1209 24
The marmoset adrenal is interesting as it is developmentally similar to humans and other primates, but in adulthood 17,20-lyase activity is very low. One possible explanation is an altered regulation of P450c17 expression by
AT1
-R. We investigated the expression and zonal distribution of the
AT1
-R in marmoset adrenal glands and adrenocortical cells in culture since it is known that
AT1
-R is a regulator of P450c17 expression and activity.
AT1
-R was expressed strongly in the ZG and to diminishing degrees through the remainder of the cortex. There was negative expression in a putative ZI. Dispersed adrenocortical cells retained
AT1
-R protein as detected by ICC. Cells cultured for several days and treated in serum-free media for 48 h maintained
AT1
-R expression, as measured by western. However, at that 48 h time point, treatment with Forsk,
AII
, TPA, or the combination of A+F or T+F did not appear to effect
AT1
-R expression. We conclude that marmoset adrenals express
AT1
-R similarly to humans and other higher mammals, adrenocortical cells retain
AT1
-R expression in culture, and consistent with other adrenal cell culture models,
AT1
-R expression is not lost in response to agonists long term.
...
PMID:Expression of AT1-R in marmoset whole adrenal glands and adrenocortical cells in culture. 1566 21
Angiotensin II antagonists (AIIAs) were introduced to treat hypertension about 10 years ago. During this period they were evaluated not only in terms of efficacy and safety but also in several large studies with clinical outcomes. They are efficacious in all clinical forms of hypertension and are effective also in all ethnic groups. Cardiovascular and renal protection in proteinuric diabetic nephropathy beyond blood pressure reduction was proved in major clinical studies: Losartan Intervention For Endpoint reduction in hypertension study (LIFE), Reduction of Endpoint in Non-Insulin dependent Diabetes Mellitus with the
AII
Antagonist Losartan (RENAAL) and Irbesartan Type 2 Diabetic Nephropathy Trial (IDNT). Their blood pressure independent protective effect is also mentioned by the blockade of
AT1
receptor. As a class AIIs have a tolerability profile similar to placebo.
...
PMID:Angiotensin II antagonists: clinical experience in the treatment of hypertension, prevention of cardiovascular outcomes and renal protection in diabetic nephropathy and proteinuria. 1676 99
AII
(angiotensin II) is a vasoactive peptide that plays an important role in the development of liver fibrosis mainly by regulating profibrotic cytokine expression such as TGF-beta (transforming growth factor-beta). Activated HSCs (hepatic stellate cells) are the major cell type responsible for ECM (extracellular matrix) deposition during liver fibrosis and are also a target for
AII
and TGF-beta actions. Here, we studied the effect of
AII
on the mRNA levels of TGF-beta isoforms in primary cultures of rat HSCs. Both quiescent and activated HSCs were stimulated with
AII
for different time periods, and mRNA levels of TGF-beta1, TGF-beta2 and TGF-beta3 isoforms were evaluated using RNaseI protection assay. The mRNA levels of all TGF-beta isoforms, particularly TGF-beta2and TGF-beta3, were increased after
AII
treatment in activated HSCs. In addition, activated HSCs were able to produce active TGF-beta protein after
AII
treatment. The mRNA expression of TGF-beta isoforms induced by
AII
required both ERK1/2 and Nox (NADPH oxidase) activation but not PKC (protein kinase C) participation. ERK1/2 activation induced by
AII
occurs via
AT1
receptors, but independently of either PKC and Nox activation or EGFR (epidermal growth factor receptor) transactivation. Interestingly,
AII
has a similar effect on TGF-beta expression in quiescent HSCs, although it has a smaller but significant effect on ERK1/2 activation in these cells.
...
PMID:Angiotensin II increases mRNA levels of all TGF-beta isoforms in quiescent and activated rat hepatic stellate cells. 2055 91
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