scholarly journals Role of Endothelin and Isoprostanes in Slow Pressor Responses to Angiotensin II

Hypertension ◽  
2001 ◽  
Vol 37 (2) ◽  
pp. 505-510 ◽  
Author(s):  
Maria Clara Ortiz ◽  
Elisabeth Sanabria ◽  
Melissa C. Manriquez ◽  
Juan C. Romero ◽  
Luis A. Juncos
Keyword(s):  
Angiotensin Ii ◽  
Pressor Responses

scholarly journals Pressor responses to norepinephrine in rabbits with 3-day and 30-day renal artery stenosis. The role of angiotensin II.

1978 ◽  
Vol 43 (3) ◽  
pp. 437-446 ◽  
Author(s):  
S Ichikawa ◽  
J A Johnson ◽  
W L Fowler ◽  
C G Payne ◽  
K Kurz ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Artery Stenosis ◽  
Pressor Responses

Interaction between pregnancy-induced bioactive peptides and the placental proteases

1995 ◽  
Vol 7 (6) ◽  
pp. 1431 ◽  
Author(s):  
S Mizutani ◽  
K Goto ◽  
K Mizuno ◽  
A Itakura ◽  
O Kurauchi ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Umbilical Artery ◽  
Bioactive Peptides ◽  
Diastolic Pressure ◽  
Peptide Hormones ◽  
Maternal Serum ◽  
Doppler Technique ◽  
Vasoactive Peptides ◽  
Pressor Responses

Studies have shown that placental proteases metabolize vasoactive peptides, possibly derived from the fetus, and protect the exchange of peptide hormones across the placenta in order to maintain feto-placental homeostasis. Changes in maternal serum protease activities were useful for monitoring pre-eclampsia and predicting the onset of labour. The study showed that possible role of oxytocinase in the maintenance of gestation and the possible involvement of angiotensinase in the attenuated pressor responses to angiotensin II during pregnancy, respectively. In addition, the ratio of peak systolic over least diastolic pressure (S/D) of uterine or umbilical artery assessed by the Doppler technique was closely correlated with the concentrations of maternal serum proteases in pre-eclampsia, which suggested that placental proteases might control utero-placental circulation via the regulation of concentrations of vasoactive peptides in uteroplacental circulation.

The Role of Endogenous Opiates in the Area Postrema Pressor Pathway

1980 ◽  
Vol 59 (s6) ◽  
pp. 267s-269s ◽  
Author(s):  
Julianna E. Szilagyi ◽  
C. M. Ferrario
Keyword(s):  
Angiotensin Ii ◽  
Vertebral Artery ◽  
Area Postrema ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Endogenous Opiates ◽  
Pressor Responses ◽  
Vasomotor Activity ◽  
The Brain

1. Intra-vertebral artery-administered angiotensin II acts at the area postrema to facilitate central sympathetic vasomotor activity. Recent evidence suggests a possible role of the opiate system in the mechanism of action of angiotensin II at the level of the brain stem. 2. In these experiments, we show that the morphine antagonist naloxone reduces significantly the magnitude of the pressor response to vertebral artery-infused angiotensin II. 3. Morphine, in contrast, doubled the peak of the vertebral response to identical doses of the peptide. Neither naloxone nor morphine affected the pressor responses to intravenously administered angiotensin II. 4. The data suggest that the endogenous opiate system in the medulla modulates the cardiovascular effects of angiotensin II at the level of the area postrema.

scholarly journals The role of brain angiotensin II in the mechanism of the pressor responses to intracisternal injection of hypertonic NaCl in urethane anesthetized rats.

1982 ◽  
Vol 46 (5) ◽  
pp. 534-539 ◽  
Author(s):  
KAZUO TAKEDA ◽  
HAKUO TAKAHASHI ◽  
HIROSHI ASHIZAWA ◽  
ATSUSHI INOUE ◽  
RIEKO SHIKUMA ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Anesthetized Rats ◽  
Pressor Responses ◽  
Intracisternal Injection

Nitric oxide generation and hypoxic vasoconstriction in buffer-perfused rabbit lungs

1995 ◽  
Vol 78 (4) ◽  
pp. 1509-1515 ◽  
Author(s):  
F. Grimminger ◽  
R. Spriestersbach ◽  
N. Weissmann ◽  
D. Walmrath ◽  
W. Seeger
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Sharp Drop ◽  
Pulmonary Vasoconstriction ◽  
Exhaled No ◽  
Pressor Responses ◽  
Hypoxic Vasoconstriction ◽  
Alveolar Hypoxia

Nitric oxide generation and hypoxic vasoconstriction in buffer-perfused rabbit lungs. J. Appl. Physiol. 78(4): 1509–1515, 1995.--We investigated the role of nitric oxide (NO) generation in hypoxic pulmonary vasoconstriction in buffer-perfused rabbit lungs. Exhaled NO was detected by chemiluminescence, and intravascular NO release was quantified as perfusate accumulation of nitrite, peroxynitrite, and nitrate (NOx). Under baseline conditions, exhaled NO was 45.3 +/- 4.1 parts per billion (1.8 +/- 0.2 nmol/min), and lung NOx release into the perfusate was 4.1 +/- 0.4 nmol/min. Alveolar hypoxia (alveolar PO2 of approximately 23 Torr) induced readily reproducible pressor responses preceded by a sharp drop in exhaled NO concentration. In contrast, perfusate NOx accumulation was not affected. Vasoconstrictor responses to U-46619 and angiotensin II were not accompanied by a decrease in NO exhalation. NG-monomethyl-L-arginine dose-dependently suppressed NO exhalation and amplified pressor responses to hypoxia > U-46619 and angiotensin II. In conclusion, portions of baseline NO generation originating from sites with ready access to the gaseous space sharply decrease in response to alveolar hypoxia, whereas the intravascular release of NO is unchanged. Such differential regulation of lung NO synthesis in response to hypoxia may suggest a complex role in the regulation or modulation of hypoxic pulmonary vasoconstriction.

scholarly journals Role of AT1 receptors and autonomic nervous system in mediating acute pressor responses to ANG II in anesthetized mice

1999 ◽  
Vol 277 (5) ◽  
pp. E838-E847 ◽  
Author(s):  
Trinity J. Bivalacqua ◽  
Ajay Dalal ◽  
Hunter C. Champion ◽  
Philip J. Kadowitz
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Angiotensin Ii ◽  
Peripheral Resistance ◽  
Inhibitory Effects ◽  
Hemodynamic Responses ◽  
Autonomic Nervous ◽  
Pressor Responses ◽  
Cd1 Mice

Hemodynamic responses to angiotensin II and the role of AT1 and AT2 receptors and the autonomic nervous system in mediating acute responses to angiotensin II were investigated in anesthetized CD1 mice. Injections of angiotensin II caused dose-related increases in systemic arterial pressure that were antagonized by candesartan. Pressor responses to angiotensin II were not altered by PD-123,319 in doses up to 25 mg/kg iv. At the lowest dose studied (20 μg/kg iv), the inhibitory effects of candesartan were competitive, whereas at the highest dose (100 μg/kg iv) the dose-response curve for angiotensin II was shifted to the right in a nonparallel manner with inhibitory effects that could not be surmounted. The inhibitory effects of candesartan were selective and were similar in animals pretreated with enalaprilat (1 mg/kg iv) to reduce endogenous angiotensin II production. Acute pressor responses to angiotensin II were not altered by propranolol (200 μg/kg iv), phentolamine (200 μg/kg iv), or atropine (1 mg/kg iv) but were enhanced by hexamethonium (5 mg/kg iv). Increases in total peripheral resistance induced by angiotensin II were inhibited by the AT1-receptor antagonist but were not altered by AT2-, α-, or β-receptor antagonists. These results suggest that acute pressor responses to angiotensin II are mediated by AT1 receptors, are buffered by the baroreceptors, and are not modulated by effects on AT2 receptors and that activation of the sympathetic nervous system plays little if any role in mediating rapid hemodynamic responses to the peptide in anesthetized CD1 mice.

Role of angiotensin II type 1 receptors in the subfornical organ in the pressor responses to central sodium in rats

2013 ◽  
Vol 1527 ◽  
pp. 79-86 ◽  
Author(s):  
Missale A. Tiruneh ◽  
Bing S. Huang ◽  
Frans H.H. Leenen
Keyword(s):  
Angiotensin Ii ◽  
Subfornical Organ ◽  
Pressor Responses

Antagonists of EDRF attenuate acetylcholine-induced vasodilation in isolated hamster lungs

1992 ◽  
Vol 72 (6) ◽  
pp. 2162-2167 ◽  
Author(s):  
C. M. Tseng ◽  
W. Mitzner
Keyword(s):  
Methylene Blue ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Krebs Solution ◽  
Inhibitory Effects ◽  
Relaxing Factor ◽  
Prostaglandin F2 Alpha ◽  
Pressor Responses

To evaluate the role of endothelium-dependent relaxing factor (EDRF) in acetylcholine- (ACh) induced vasodilation in the intact pulmonary circulation, we examined the effects of atropine and three EDRF antagonists that have been shown to be effective in vitro: nitro-L-arginine (NOARG), hemoglobin (Hb), and methylene blue (MB). We studied ACh-induced dilation after preconstriction with angiotensin II and prostaglandin F2 alpha (PGF2 alpha) in hamster lungs perfused with Krebs solution containing Ficoll (4 g/dl) and indomethacin (10 microM). In the constricted lungs with no blockers, infusion of ACh (1 microM) decreased the constriction by 67%, and this effect was completely abolished by atropine pretreatment (1 microM). Treatment of hamster lungs with each of the three EDRF blockers, NOARG (30 microM), Hb (10 microM), and MB (250 microM), augmented the pressor responses to angiotensin II and PGF2 alpha. However, NOARG and MB inhibited the ACh-induced dilation by 49 and 60%, respectively, without affecting vasodilatory responses to isoproterenol, an agent that relaxes vascular smooth muscle independent of EDRF synthesis. In contrast, Hb significantly inhibited both ACh- and isoproterenol-induced vasodilations. Because all these EDRF antagonists attenuated ACh-induced vasodilation in intact hamster lungs, we conclude that EDRF plays a role in this response. Nonselective inhibitory effects of Hb in hamster lungs, however, suggest that mechanisms other than inhibition of EDRF by this agent are also involved.

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