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PubMed1976

Angiotensin II and angiotensin III in rat blood.

Angiotensin II and its metabolites, [des-Asp-1]-angiotensin II (angiotensin III), [des-(Asp-1,Arg-2)]angiotensin II, and [des-(Asp-1,Arg-2,val-3)]angiotensin II, were measured in arterial and venous plasma from normal rats. Paper chromatography was used to separate the peptides which were measured with a radioimmunoassay method using an angiotensin II antiserum which had a 100% cross-reaction with each of these metabolites. A mean of 33% of the immunoreactive material in arterial plasma was angiotensin II, 58% angiotensin III, and 9% [des-(Asp-1,Arg-2)]angiotensin II/[des-(Asp-1,Arg-2,Val-3)]angiotensin II. A similar distribution was found in venous plasma. This and other evidence indicates that angiotensin-induced aldosterone secretion in the rat, unlike that in other mammalian species so far studied, may be mediated by angiotensin III.

Angiotensin II↗
PubMed1983

Intrarenal vascular effects of angiotensin II and angiotensin III in the dog.

The effects of intrarenal bolus injections of equal molar doses of angiotensin II and angiotensin III on renal blood flow were examined in seven pentobarbital anaesthetized dogs. Renal blood flow was measured with an electromagnetic flow probe. Angiotensin II produced a greater decrease in renal blood flow than angiotensin III at all bolus doses tested when the integral of the renal blood flow response was examined. In 10 other dogs, we compared the molar dose of intrarenal constant infusions of angiotensin II and angiotensin III required to decrease total renal blood flow by approximately 25%. The effect these peptides had on the distribution of renal cortical blood flow was determined with radioactive microspheres. In the constant infusion experiments, more moles of angiotensin III than angiotensin II were required to produce a given decrease in renal blood flow in each experiment. The average percent decrease in blood flow to each of the four cortical zones produced by angiotensin II was not different from that produced by angiotensin III. Our data demonstrate that angiotensin II is more potent than angiotensin III as a vasoconstrictor in the renal vasculature.

Angiotensin II↗
PubMed1975

Vascular and adrenocortical responses to a specific antagonist of angiotensin II.

Angiotensin II receptors in vascular smooth muscle and adrenal cortex have been characterized in the dog. The evidence was derived chiefly from experiments that assessed the ability of a structural analog of angiotensin II, [Sar1, Ile8] AII, to antagonize the effects of exogenously administered angiotensin II on arterial pressure and aldosterone secretion. [Sar1, Ile8] AII is a potent and specific blocker of the pressor response to angiotensinII; in the adrenal cortex, it is a much less effective inhibitor of aldosterone biosynthesis. These results indicate differences in the receptor sites for angiotensin II in vascular smooth muscle and adrenal cortex. Further, they raise the possibility that angiotensin II stimulates aldosterone secretion by mechanisms other than have already been proposed.

Adrenal Cortex↗
PubMed1976

Regional study of cerebral ventricle sensitive sites to angiotensin II.

Angiotensin II injected in small doses into the cerebral ventricles produces an increase in blood pressure and drinking behavior. The site of action for both of these effects was studied in 3 main experiments. (1) The response to several doses of angiotensin delivered to each ventricle was investigated with multiple ventricular cannulation. This revealed that the rostral ventricular system was involved in angiotensin II mediated responses. (2) CSF flow was limited by plugging specific anterior and posterior ventricular regions and then testing for angiotensin II induced drinking and pressor responses. This technique showed that the ventral anterior third ventricle must be reached by the peptide in order to produce either blood pressure or drinking effects. (3) In order to separate pressor components due to vasopressin release and sympathetic activation, hypophysectomized rats were also tested. The experiment showed that the pressor response to intraventricular angiotensin II is due to both sympathetic and pituitary hormonal components and both are dependent on sites sensitive to angiotensin in the anterior third ventricule. The ventral anterior third ventricle or periventricular tissue surrounding it seems to be essential for both blood pressure and drinking responses to intraventricular angiotensin II.

Angiotensin II↗
PubMed1998

Human adipose tissue expresses angiotensinogen and enzymes required for its conversion to angiotensin II.

Angiotensin II regulates blood pressure and may affect adipogenesis and adipocyte metabolism. Angiotensin II is produced by cleavage of angiotensinogen by renin and angiotensin-converting enzyme in the circulation. In addition, angiotensin II may be produced in various tissues by enzymes of the renin-angiotensin system (RAS) or the nonrenin-angiotensin system (NRAS). We have analyzed the expression of angiotensinogen and enzymes required for its conversion to angiotensin II in human adipose tissue. Northern blot demonstrated angiotensinogen expression in adipose tissue from nine obese subjects. Western blot revealed a distinct band of expected size of the angiotensinogen protein (61 kDa) in isolated adipocytes. RT-PCR, followed by Southern blot, demonstrated renin expression in human adipose tissue. Angiotensin-converting enzyme messenger RNA was detected by RT-PCR, and the identity of the PCR products was verified by restriction enzyme cleavage. Transcripts for cathepsin D and cathepsin G, components of the NRAS, were detected by RT-PCR, verified by restriction enzyme cleavage. We conclude that human adipose tissue expresses angiotensinogen and enzymes of RAS and NRAS. This opens the possibility that angiotensinogen-derived peptides, produced in adipose tissue itself, may affect adipogenesis and play a role in the pathogenesis of obesity.

Adipose Tissue↗
PubMed2001

The differential effect of angiotensin II and angiotensin 1-7 on norepinephrine, epinephrine, and dopamine concentrations in rat hypothalamus: the involvement of angiotensin receptors.

Angiotensin 1-7 has been recently claimed the active member of the angiotensins' family. In the present study we compared the effect of angiotensin II and angiotensin 1-7 on the concentration of dopamine, serotonin, epinephrine, and norepinephrine and some of their metabolites in the rat hypothalamus, where the levels of angiotensins are particularly high. Intracerebroventricular injection of angiotensin II, but not angiotensin 1-7, time-dependently elevated the levels of both epinephrine (p < 0.05) and norepinephrine (p < 0.05) in the hypothalamus and both effects could be prevented by intracerebroventricular injection of either AT(1) (candesartan), AT(2) (PD123319) or AT(1-7) (A-779) receptor antagonist. Neither angiotensin II nor angiotensin 1-7 produced any changes in the level of dopamine, dihydroxyphenylacetic acid, homovanilic acid, serotonin, 5-hydroxyindoleacetic acid, or tryptophan at any time point in comparison with the control groups. However, AT(1) but not AT(2) receptor blockade, unmasked the stimulatory effect of angiotensin 1-7 on dopamine concentration in the hypothalamus. Thus, angiotensin II and its active metabolite angiotensin 1-7 regulate selectively, albeit differentially, adrenergic, noradrenergic and dopaminergic systems in the hypothalamus, the effects that involve AT(1), AT(2) and AT(1-7) angiotensin receptors.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1996

Variation of intrarenal angiotensin II and angiotensin II receptors by acute renal ischemia in the aged rat.

The properties of Ang II receptors in the aged kidney and their changes after acute renal ischemia are rarely known. The aim of this study was to examine the expression of Ang II receptor mRNA and characteristics of Ang II receptors in the aged kidney and to compare different responsiveness to 45 min of acute renal ischemia in young (3-4 months) and aged (23-24 months) rats. In the normal condition, AT1 mRNA expression was much lower in the aged than that in the young rats. Maximal binding (Bmax) was also lower in the aged (1315 +/- 48 vs. 2035 +/- 257 fmol/mg, p < 0.05). The dissociation constant (KD) of glomerular Ang II receptors, however, was significantly lower in the aged rats compared to the young (6.8 +/- 1.6 vs. 17.4 +/- 2.5 nM). After acute ischemia, the expression of AT1 mRNA decreased in the young rats but increased in the aged rats. Interestingly, Bmax of glomerular Ang II receptors was significantly increased in the aged ischemic rats (1852 +/- 94 vs. 1315 +/- 48 fmol/mg) with unchanged KD. These results show that: (a) the AT1 mRNA expression and the Ang II receptor binding site are decreased with the aging process in the rat kidney; (b) the acute renal ischemia effect on different age groups has a greatly discrepant pattern in respect of Ang II receptor modulation, which may provide a potential therapeutic future for the receptor antagonists in acute renal ischemia in the aged.

Acute Disease↗
PubMed1979

[A comparison between the effects of angiotensin II and angiotensin III injected into the third cerebral ventricle on vasopressin secretion in conscious rats (author's transl)].

As the greater part of the immunoreactive angiotensin II in cerebrospinal fluid has been suggested to be angiotensin III, a comparison was made between the effects on vasopressin release of angiotensin II and angiotensin III administered into the third cerebral ventricle in conscious male rats. The blood samples were collected 90 seconds after the injection of angiotensin II or angiotensin III by means of decapitation. Plasma vasopressin (microU/ml) extracted and determined by radioimmunoassay were 2.3 +/- 0.8, 6.7 +/- 5.0, 14.0 +/- 2.2, 16.3 +/- 4.3 and 20.7 +/- 2.5 (mean +/- SEM), respectively following the injection of 0, 10, 25, 50 and 100ng of angiotensin II. The increases in plasma vasopressin produced by angiotensin II 25, 50 and 100ng were statistically significant (p less than 0.05). On the other hand, plasma vasopressin following the injection of 22.7 and 45.4ng of angiotensin III, which are equimolar to 25 and 50ng of angiotensin II each, were 14.9 +/- 2.7 and 16.3 +/- 5.6, respectively. No significant difference was found between the effect on plasma vasopressin of angiotensin II and that of angiotensin III at the dose level of 24.3 or 48.6 p. mol. These data indicate that angiotensin III is equipotent to angiotensin II in terms of vasopressin release when administered into the third cerebral ventricle. The possible role of angiotensin III in the brain on vasopressin secretion is discussed.

Angiotensin II↗
PubMed1977

A comparison between the prostaglandin releasing effects of angiotensin II and angiotensin III.

Angiotensin II and its natural fragment (des-aspartic acid)1-angiotensin II (angiotensin III) induced a dose-dependent contraction in the isolated rat stomach fundus strip and rat colon. 1-Acetyl-2-(8-chloro-10,11-dihydrodibenz(b,f)(1,4)oxazepine-10, carbonyl) hydrazine (SC 19220), a widely used competitive-blocker of prostaglandins and acetyl salicylic acid, a well-known inhibitor of prostaglandin biosynthesis, partially abolished the contraction induced by both peptides in the rat stomach fundus but not in the rat colon. The inhibition induced by SC 19220 and acetyl salicylic acid was found to be higher for angiotensin III than angiotensin II when the dose-response curves and equipotent concentrations of the peptides were compared before and after the drugs. These results were taken as evidence that some component of the contractile effects of angiotensin II and angiotensin III on the isolated rat stomach fundus involves the release of prostaglandins by the peptides and in this respect angiotensin III has higher potency than angiotensin II.

Angiotensin II↗
PubMed2002

Differential effects of angiotensin II and angiotensin-(1-7) at the nucleus tractus solitarii of transgenic rats with low brain angiotensinogen.

OBJECTIVES: In this study, we investigated the effects of angiotensin II and angiotensin-(1-7) at the nucleus tractus solitarii (nTS) in transgenic rats with a severe deficit in brain angiotensinogen production, TGR(ASrAOGEN) (TGR). METHODS: Angiotensin II (10 pmol), angiotensin-(1-7) (10 pmol) or NaCl (0.9%/50 nl) were microinjected into the nTS of urethane-anaesthetized TGR (n = 36) and Sprague Dawley (SD) (n = 34) rats. Mean arterial pressure (MAP) and heart rate were measured via a femoral artery catheter and the baroreflex control of heart rate was evaluated after increases in MAP induced by phenylephrine (baroreflex bradycardia). RESULTS: Angiotensin II microinjections into the nTS of the TGR induced a higher decrease in MAP and heart rate (-37 +/- 5 mmHg and -69 +/- 12 b.p.m., respectively) in comparison to SD rats (-18 +/- 1 mmHg and -43 +/- 5 b.p.m., respectively). In contrast, changes after angiotensin-(1-7) microinjections into the nTS of TGR (-6 +/- 1 mmHg and -13 +/- 4 b.p.m.) were significantly smaller than that induced in SD (-11 +/- 2 mmHg and -24 +/- 6 b.p.m.). The baseline baroreflex sensitivity to phenylephrine of TGR was accentuated in comparison to SD rats (0.70 +/- 0.06 versus 0.44 +/- 0.03 ms/mmHg). Angiotensin II microinjection into the nTS produced similar attenuation in the baroreflex bradycardia in both SD (0.28 +/- 0.07 versus 0.5 +/- 0.07 ms/mmHg, before injection) and TGR (0.44 +/- 0.1 versus 0.82 +/- 0.1 ms/mmHg, before injection). In contrast, angiotensin-(1-7) microinjection elicited a facilitation of the baroreflex bradycardia in SD (0.68 +/- 0.12 versus 0.41 +/- 0.03 ms/mmHg, before injection), while in TGR, angiotensin-(1-7) induced an attenuation of baroreflex bradycardia (0.34 +/- 0.07 ms/mmHg versus 0.55 +/- 0.05 ms/mmHg, before injection). CONCLUSIONS: These results indicate that a permanent inhibition of angiotensinogen synthesis in the brain can lead to an increase in the sensitivity of the baroreflex control of heart rate (baroreflex bradycardia) and an increase in angiotensin II responsiveness at the nTS. However, the nTS effect of angiotensin-(1-7) was significantly attenuated in these transgenic rats. These data further indicate that the decrease in brain angiotensins in the transgenic rats may be functionally relevant and support the concept of differential regulatory mechanisms for the effects of the two angiotensin peptides.

Angiotensin I↗
PubMed1978

Correlation of the biological activity and solution conformation of [Asp1,Ile5]- and [Phe4,Tyr8]angiotensin II.

Angiotensin II is known to undergo a reversible conformational transition and a change in potency in rat uterus in vitro with pK approximately 6.5. We have shown by carbon-13 NMR that the conformational transition involves all-trans to partly cis isomerization of the His6-Pro7 peptide bond. Isomerization from all-trans at pH 6.8 to approximately 16% cis at pH 8.0 is therefore correlated with a 10-fold increase in biological activity for [Asp1,Ile5]-angiotensin II in rat uterus in vitro. Isomerization from all-trans at pH 6.8 to approximately 16% cis at pH 8.0 in the competitive inhibitor [Phe4,Tyr8]angiotensin II is correlated with exhibition of virtually no agonist activity at low pH to full agonist activity at high pH. An angiotensin II conformation with Pro7 in the cis form may therefore be the conformation with maximal binding or biological activity at the cellular receptor.

Angiotensin II↗
PubMed2004

Oxidative stress in hypertension and chronic kidney disease: role of angiotensin II.

Angiotensin II, via the type 1 (AT1) receptor, stimulates oxidative stress. The vasculature, interstitium, juxtaglomerular apparatus, and the distal nephron in the kidney express nicotinamide adenine dinucleotide phosphate (NADPH) oxidase that generates superoxide anion, which is an important component of angiotensin II-induced oxidative stress. The angiotensinogen gene is stimulated by NF-kappaB activation, which is sensitive to the redox ratio, providing a positive feedback loop that can upregulate angiotensin II production. Oxidative stress can accompany hypertension in many models, including the spontaneously hypertensive rat (SHR), angiotensin II-infused rats, renovascular hypertension, and the deoxycorticosterone acetate (DOCA) salt model of hypertension. AT1 receptor antagonists can abrogate the effects of angiotensin II on oxidative stress, thus providing an important mechanistic insight onto the renal protective effects of these agents in conditions associated with angiotensin II excess.

Angiotensin II↗
PubMed1994

Role of the NH2-terminal domain of angiotensin II (ANG II) and [Sar1]angiotensin II on conformation and activity. NMR evidence for aromatic ring clustering and peptide backbone folding compared with [des-1,2,3]angiotensin II.

The role of the NH2 termini of angiotensin II (ANG II) and [Sar1]ANG II on conformation and activity were examined by proton NMR two-dimensional-J-correlated spectroscopy and one-dimensional nuclear Overhauser effect studies in the relatively nonpolar "receptor-simulating" environment provided by dimethyl sulfoxide-d6, using the biologically inactive COOH-terminal pentapeptide [des1,2,3]ANG II as control. Irradiation of C alpha H, C2H, and C4H proton resonances in ANG II and [Sar1]ANG II resulted in enhancements of Tyr and Phe ring proton resonances, indicating that the three aromatic rings cluster together. Very strong enhancements (17-22%) of the C alpha Y proton resonance in ANG II and [Sar1]ANG II upon irradiation of the C alpha H proton resonance, and vice versa, revealed that a Tyr-Ile-His bend is a predominant feature of the conformation of the two agonists. In contrast, saturation of the C alpha H and C alpha Y proton resonances in the control pentapeptide [des-1,2,3]ANG II did not produce, respectively, any C alpha Y or C alpha H proton nuclear Overhauser effect enhancement, illustrating the absence of a Tyr-Ile-His bend in the truncated ANG II peptide. The present findings indicate that the NH2-terminal domain of ANG II appears to have an essential role in generating the biologically active charge relay conformation of the hormone.

Algorithms↗
PubMed2003

Role of superoxide in modulating the renal effects of angiotensin II.

Angiotensin II is known to stimulate NADPH oxidase-dependent superoxide (O2-) generation, which may contribute to the acute renal vasoconstrictor and antinatriuretic actions of this peptide. To evaluate this hypothesis, the effects of a superoxide dismutase mimetic (tempol) or a NADPH inhibitor (apocynin) on the angiotensin renal actions were studied. Renal cortical nitric oxide (NO) was measured electrochemically in vivo. Tempol increased sodium excretion and NO levels. Apocynin raised renal blood flow, glomerular filtration rate, sodium excretion, and NO levels. These results indicate the presence of an endogenous NADPH oxidase-dependent O2- generation that may modulate renal function by scavenging NO. Angiotensin II infusion reduced renal blood flow, glomerular filtration, sodium excretion, and NO levels in a dose-dependent manner. The angiotensin receptor antagonist valsartan, tempol, or apocynin blunted the angiotensin effects on renal excretion and NO, suggesting that angiotensin receptors stimulation induces the NADPH oxidase-dependent O2- generation that might reduce NO bioavailability. This idea is supported by the finding that angiotensin increased O2- generation in renal homogenates, and this effect was prevented by valsartan, apocynin, or tempol. These results indicate that some of the acute renal effects of angiotensin II may be enhanced by an increased NADPH oxidase-derived O2- production that reduces renal NO bioavailability.

Acetophenones↗
PubMed2006

Enhanced sensitivity of Kv channels to hypoxia in the rabbit carotid body in heart failure: role of angiotensin II.

Angiotensin II (Ang II) plays an important role in the enhanced chemoreflex function that occurs in congestive heart failure (CHF), but the mechanism of this effect within the carotid body (CB) is not known. We investigated the sensitivity of Ca2+-independent, voltage-gated K+ (Kv) channels to hypoxia in CB glomus cells from CHF rabbits, and whether endogenous angiotensin II (Ang II) modulates this action. Using the conventional whole-cell patch clamp technique, we found that Kv currents (IK) under normoxic conditions were blunted in the CB glomus cells from CHF rabbits compared with sham rabbits. In addition, the inhibition of IK and the decrease of resting membrane potential (RMP) induced by hypoxia were greater in CHF versus sham glomus cells. Ang II, at 100 pM, had no direct effect on IK at constant normoxic PO2, but increased the sensitivity of IK and RMP to hypoxia in sham glomus cells. In CHF glomus cells, an AT1 receptor (AT1R) antagonist, L-158 809 (1 microM), alone did not affect IK at normoxia, but it decreased the sensitivity of IK and RMP to hypoxia. At higher concentrations, Ang II dose dependently (0.1-100 nM) reduced IK under constant normoxic conditions in sham and CHF glomus cells, with threshold concentrations of about 900 and 600 pM, respectively. Immunocytochemical and Western blot assessments demonstrated the down-expression of Kv3.4 but not Kv4.3 channels in CHF glomus cells. These results indicate that: (1) Ang II/AT1R signalling increases the sensitivity of Kv channels to hypoxia in CB glomus cells from CHF rabbits; (2) high concentrations of Ang II (> 1 nM) directly inhibit IK in CB glomus cells from sham and CHF rabbits; (3) changes in Kv channel protein expression (Kv3.4 versus Kv4.3) in the CB glomus cell may contribute to the suppression of IK and enhanced sensitivity of IK to hypoxia in CHF.

Angiotensin II↗