scholarly journals The α2‐Adrenoceptor Agonist, Dexmedetomidine, Elicits Pronounced Decreases in Arterial Blood Pressure and Renal Hemodynamics in Cyp1a1‐Ren2 Transgenic Rats with Angiotensin II‐Dependent Malignant Hypertension

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Christina K. Thorngren ◽  
Matthew E. Patterson ◽  
Porcha D. Davis ◽  
Kenneth D. Mitchell
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Renal Hemodynamics ◽  
Malignant Hypertension ◽  
Transgenic Rats ◽  
Arterial Blood ◽  
Α2 Adrenoceptor ◽  
Adrenoceptor Agonist

Cyclooxygenase-2 inhibition normalizes arterial blood pressure in CYP1A1-REN2 transgenic rats with inducible ANG II-dependent malignant hypertension

2006 ◽  
Vol 291 (3) ◽  
pp. F612-F618 ◽  
Author(s):  
Allison L. Opay ◽  
Cynthia R. Mouton ◽  
John J. Mullins ◽  
Kenneth D. Mitchell
Keyword(s):  
Blood Pressure ◽  
Renal Plasma Flow ◽  
Renal Hemodynamics ◽  
Malignant Hypertension ◽  
Hypertensive Rats ◽  
Transgenic Rats ◽  
Arterial Blood ◽  
Cox Inhibitor ◽  
Cox 2 ◽  
Cox 1

The present study was performed to determine the effects of cyclooxygenase (COX)-1 and COX-2 inhibition on blood pressure and renal hemodynamics in transgenic rats with inducible malignant hypertension [strain name: TGR(Cyp1a1Ren2)]. Male Cyp1a1-Ren2 rats ( n = 7) were fed a normal diet containing the aryl hydrocarbon, indole-3-carbinol (I3C; 0.3%), for 6–9 days to induce malignant hypertension. Mean arterial pressure (MAP) and renal hemodynamics were measured in pentobarbital sodium-anesthetized Cyp1a1-Ren2 rats during control conditions, following administration of the COX-2 inhibitor nimesulide (3 mg/kg iv), and following administration of the nonspecific COX inhibitor meclofenamate (5 mg/kg iv). Rats induced with I3C had higher MAP than noninduced rats ( n = 7; 188 ± 6 vs. 136 ± 4 mmHg, P < 0.01). There was no difference in renal plasma flow (RPF) or glomerular filtration rate (GFR) between induced and noninduced rats. Nimesulide elicited a larger decrease in MAP in hypertensive rats (188 ± 6 to 140 ± 8 mmHg, P < 0.01) than in normotensive rats (136 ± 4 to 113 ± 8 mmHg, P < 0.01). Additionally, nimesulide decreased GFR (0.9 ± 0.13 to 0.44 ± 0.05 ml·min−1·g−1, P < 0.05) and RPF (2.79 ± 0.27 to 1.35 ± 0.14 ml·min−1·g−1, P < 0.05) in hypertensive rats but did not alter GFR or RPF in normotensive rats. Meclofenamate further decreased MAP in hypertensive rats (to 115 ± 10 mmHg, P < 0.05) but did not decrease MAP in normotensive rats. Meclofenamate did not alter GFR or RPF in either group. These findings demonstrate that COX-1- and COX-2-derived prostanoids contribute importantly to the development of malignant hypertension in Cyp1a1-Ren2 transgenic rats. The data also indicate that COX-2-derived vasodilatory metabolites play an important role in the maintenance of RPF and GFR following induction of malignant hypertension in Cyp1a1-Ren2 transgenic rats.

PS 07-29 FLAVONE DERIVATIVE, CSH-3-124 DECREASES ARTERIAL BLOOD PRESSURE THROUGH INHIBITION OF ANGIOTENSIN II

2016 ◽  
Vol 34 (Supplement 1) ◽  
pp. e291
Author(s):  
Seon-Ah Jin ◽  
Hee jung Seo ◽  
Sun Kyeong Kim ◽  
Gyu Yong Song ◽  
Jin-Ok Jeong
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Arterial Blood ◽  
Flavone Derivative

scholarly journals REDUCTION OF ARTERIAL BLOOD PRESSURE OF HYPERTENSIVE PATIENTS AND ANIMALS WITH EXTRACTS OF KIDNEYS

1941 ◽  
Vol 73 (1) ◽  
pp. 7-41 ◽  
Author(s):  
Irvine H. Page ◽  
O. M. Helmer ◽  
K. G. Kohlstaedt ◽  
P. J. Fouts ◽  
G. F. Kempf
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Malignant Hypertension ◽  
Hypertensive Rats ◽  
Hypertensive Patients ◽  
Arterial Blood ◽  
Lower Blood ◽  
Mean Pressure ◽  
Activity Loss ◽  
Experimental Stage

1. Extracts of kidneys have been prepared containing a substance which lowers arterial blood pressure for prolonged periods in patients with essential and malignant hypertension, and in hypertensive dogs and rats. 2. Several different chemical procedures are proposed for the preparation of the extract. The best one has not been decided upon. 3. The quantity of original fresh whole kidney required to yield enough extract to lower blood pressure from hypertensive levels (200 mm. Hg mean pressure) to normal levels is roughly 600 to 900 gm. in dogs within 4 to 8 days. In hypertensive patients the yield from 700 to 1000 gm. daily for several weeks may be necessary. 4. Lowering of the blood pressure too rapidly in animals results in a shock syndrome which may be fatal. If overdosage is avoided, no appreciable rise in blood urea nitrogen occurs, nor do other signs of toxicity appear. 5. Lowering of blood pressure to nearly normal levels has been accomplished in 60 hypertensive dogs, and in some of these it has been allowed to rise and was again reduced as many as five times. Similar results have been obtained with hypertensive rats. 6. Six patients with essential hypertension have been treated resulting in prolonged reduction of blood pressure. Clinically the patients appear improved. 7. Five patients with malignant hypertension have been treated, with reduction of the blood pressure in all instances. One patient was treated despite urea clearance of 5 per cent of normal. His blood pressure was sharply reduced, but death in uremia occurred. The second patient also exhibited sharp reduction of pressure and died after treatment was discontinued. The other three are much improved after treatment, as indicated by increase in vision and mental activity, loss of dyspnea, improvement in the electrocardiogram, etc. 8. The length of time the blood pressure remains lowered varies greatly in both animals and man. The trend is usually upwards after discontinuing treatment for 4 to 6 days. 9. Increasing experience with this treatment suggests that it is of value in the management of hypertension, but it is yet in the experimental stage.

Role of arteria baroreceptor input on thirst and urinary responses to intracerebroventricular angiotensin II

1993 ◽  
Vol 265 (3) ◽  
pp. R591-R595 ◽  
Author(s):  
R. L. Thunhorst ◽  
S. J. Lewis ◽  
A. K. Johnson
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Water Intake ◽  
Enzyme Inhibitor ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Arterial Blood ◽  
Endogenous Formation

Intracerebroventricular (icv) infusion of angiotensin II (ANG II) in rats elicits greater water intake under hypotensive, compared with normotensive, conditions. The present experiments used sinoaortic baroreceptor-denervated (SAD) rats and sham-operated rats to examine if the modulatory effects of arterial blood pressure on water intake in response to icv ANG II are mediated by arterial baroreceptors. Mean arterial blood pressure (MAP) was raised or lowered by intravenous (i.v.) infusions of phenylephrine (1 or 10 micrograms.kg-1 x min-1) or minoxidil (25 micrograms.kg-1 x min-1), respectively. The angiotensin-converting enzyme inhibitor captopril (0.33 mg/min) was infused i.v. to prevent the endogenous formation of ANG II during testing. Urinary excretion of water and solutes was measured throughout. Water intake elicited by icv ANG II was inversely related to changes in MAP. Specifically, rats drank more water in response to icv ANG II when MAP was reduced by minoxidil but drank less water when MAP was elevated by phenylephrine. The influence of changing MAP on the icv ANG II-induced drinking responses was not affected by SAD. These results suggest that the modulatory effects of arterial blood pressure on icv ANG II-induced drinking can occur in the absence of sinoaortic baroreceptor input.

Effect of Sodium Depletion on the Steroidogenic and Pressor Actions of Angiotensin in the Rat

1979 ◽  
Vol 56 (4) ◽  
pp. 325-333 ◽  
Author(s):  
W. B. Campbell ◽  
J. M. Schmitz ◽  
H. D. Itskovitz
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Sodium Depletion ◽  
Angiotensin I ◽  
Arterial Blood ◽  
Serum Aldosterone ◽  
Pressor Responses ◽  
Angiotensin Iii

1. To investigate the relative roles of angiotensin II (AII) and des-Asp1-angiotensin II (angiotensin III) in the control of blood pressure and aldosterone release, the effects of seven angiotensin agonists on mean arterial blood pressure and serum aldosterone concentrations were compared in normal and sodium-depleted, conscious rats. 2. In normal rats, angiotensin I, α-Asp1-angiotensin II, β-Asp1-angiotensin II, and angiotensin II-amide were equipotent in elevating mean arterial blood pressure. Angiotensin III, des-Asp1-angiotensin I, and poly-O-acetylserine-angiotensin II were 25%, 25%, and 41% as potent as angiotensin II, respectively. After sodium depletion, pressor responses to these angiotensin peptides were reduced approximately 60–80% when compared with control responses. In contrast, pressor responses to noradrenaline were not significantly affected by sodium depletion. 3. Angiotensin II, β-Asp1-angiotensin II, angiotensin II-amide, and angiotensin III were equipotent in increasing serum aldosterone concentrations in normal animals. Angiotensin I was 59% and des-Asp1-angiotensin I only 5% as potent as angiotensin II in their abilities to release aldosterone. After sodium depletion, control serum aldosterone concentrations increased as did the slope of the dose—response curve for each angiotensin peptide. Angiotensin II was the most potent steroidogenic peptide in sodium-depleted rats with angiotensin III and β-Asp1-angiotensin II being 27%, angiotensin I 7%, angiotensin II-amide 3%, and des-Asp1-angiotensin I 1% as potent as angiotensin II in releasing aldosterone. Poly-O-acetylserine-angiotensin II has less steroidogenic effect than angiotensin II or III in both normal and sodium-depleted animals. 4. Infusions of the angiotensin II antagonist, Sar1-Ile8-angiotensin II, and the angiotensin III antagonist, Ile7-angiotensin III, enhanced aldosterone release in normal rats without altering blood pressure. After sodium depletion, Sar1-Ile8-angiotensin II decreased blood pressure without affecting aldosterone release whereas Ile7-angiotensin III diminished aldosterone release without altering blood pressure. 5. These data suggest that angiotensin II, independent of its conversion into angiotensin III, is an important regulator of steroidogenesis in the rat in normal sodium states. In sodium depletion, the octapeptide retains significant steroidogenic activity; however, the contribution of angiotensin III to its steroidogenic effects is increased.

Support of arterial blood pressure by major pressor systems in conscious dogs

1988 ◽  
Vol 255 (3) ◽  
pp. H483-H491 ◽  
Author(s):  
P. H. Brand ◽  
P. J. Metting ◽  
S. L. Britton
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Steady State ◽  
Autonomic Nervous System ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Autonomic Function ◽  
Autonomic Ganglia ◽  
Arterial Blood

The roles of the autonomic nervous system, vasopressin, and angiotensin II in support of blood pressure were evaluated in seven conscious, resting dogs while hydrated or dehydrated. Mean arterial blood pressure (MAP) was monitored, and the dogs were given hexamethonium to block autonomic ganglia. Thirty minutes later, they were given captopril, and after another 30 min, a vasopressin V1 antagonist, d(CH2)5TyrMeAVP, was given. The order okf administration of captopril and d(CH2)5TyrMeAVP was alternated in different experiments. Hexamethonium had no effect on steady-state MAP in either hydrated or dehydrated dogs. In hydrated dogs, the average MAP was 100 mmHg; d(CH2)5TyrMeAVP decreased MAP by approximately 12 mmHg, and captopril decreased MAP by 24 mmHg. The magnitude of the effect of these two inhibitors was independent of the order of their administration. Dehydration doubled the effect of d(CH2)5TyrMeAVP on MAP but had no effect on the response to captopril. The results suggest that 1) autonomic function is not essential for maintenance of arterial blood pressure in resting dogs; 2) during autonomic ganglionic blockade, arterial blood pressure is supported by both angiotensin II and vasopressin; and 3) dehydration increases the role of vasopressin in control of blood pressure.

Abstract 413: Renal Cyclooxygenase-2 Expression And Hemodynamic Role During Angiotensin II-dependent Hypertension

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Alexis A Gonzalez ◽  
Torrance Green ◽  
Camille R Bourgeois ◽  
Christina Luffman ◽  
Minolfa C Prieto ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Late Phase ◽  
Renal Hemodynamics ◽  
Cyclooxygenase 2 ◽  
Kidney Cortex ◽  
Dependent Manner ◽  
Sprague Dawley ◽  
Arterial Blood ◽  
Cox 2

Intrarenal cyclooxygenase-2 (COX-2) activity is increased during activation of the renin-angiotensin-system (RAS) increasing synthesis of prostaglandin E2 (PGE2) and buffering the vasoconstrictor and antinatriuretic effects of angiotensin II (AngII). While AngII upregulates intrarenal COX-2 expression, it remains unclear if this occurs in a time-dependent manner, thereby impacting renal hemodynamics differently during the early and late phases of the development of high blood pressure in AngII-induced hypertension. Male Sprague-Dawley rats were infused with AngII (0.4 μg/min/kg). Systolic blood pressure (SBP), COX-2 expression and PGE2 tissue content and urinary excretion were evaluated at day 3, 7 and 14 of the AngII infusions. In acute studies we evaluated the effects of COX-2 inhibition at day 5-7 and day 14 on renal hemodynamic parameters. Chronic AngII infusions increased SBP from day 7 through 14: 162 ± 5 mmHg; and 198 ± 15 mmHg versus controls: 114 ± 10 mmHg; P<0.05. COX-2 mRNA and protein levels were high in kidney cortex only at day 3 (mRNA: 241 ± 56%, protein: 160 ± 21%, P<0.05 versus controls). Medullary COX-2 mRNA and protein were increased on days 3 (mRNA: 176 ± 20%, protein: 185 ± 32%, P<0.05 versus controls), 7 (mRNA: 189 ± 23%, protein: 158 ± 15%, P<0.05 versus controls) and 14 (mRNA: 148 ± 15%, protein: 135 ± 13%, P<0.05 versus controls). Urinary and medullary PGE2 increased by day 3 and remained elevated during days 7 and 14. COX-2 inhibition decreased GFR and renal blood flow in AngII infused rats during both the early and late phases. Interestingly, COX-2 inhibition decreased mean arterial blood pressure at day 14 of AngII-infusion (COX-2 inhibition: 124 ± 9 versus 140 ± 7 mmHg, P<0.05) but not during the early normotensive phase (COX-2 inhibition: 110 ± 4 versus 115± 4 mmHg, P=NS). These results indicate that enhanced medullary COX-2 expression and PGE2 production during both the early and late phases attenuates the effects of AngII on renal hemodynamics. However COX-2 inhibition at day 14 reduced blood pressure, suggesting that a vasoconstrictor COX-2 metabolite contributes to the hypertension during the late phase.

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