Angiotensin receptors contribute to blood pressure homeostasis in salt-depleted SHR

2003 ◽  
Vol 284 (1) ◽  
pp. R164-R173 ◽  
Author(s):  
Shigefumi Nakamura ◽  
David B. Averill ◽  
Mark C. Chappell ◽  
Debra I. Diz ◽  
K. Bridget Brosnihan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Angiotensin Receptors ◽  
Receptor Subtypes ◽  
Ang Ii ◽  
Blood Pressure Lowering Effect ◽  
Blood Pressure Elevation ◽  
Spontaneously Hypertensive

This study evaluated the contribution of angiotensin peptides acting at various receptor subtypes to the arterial pressure and heart rate of adult 9-wk-old male conscious salt-depleted spontaneously hypertensive rats (SHR). Plasma ANG II and ANG I in salt-depleted SHR were elevated sevenfold compared with peptide levels measured in sodium-replete SHR, whereas plasma ANG-(1–7) was twofold greater in salt-depleted SHR compared with salt-replete SHR. Losartan (32.5 μmol/kg), PD-123319 (0.12 μmol · kg−1 · min−1), [d-Ala7]ANG-(1–7) (10 and 100 pmol/min), and a polyclonal ANG II antibody (0.08 mg/min) were infused intravenously alone or in combination. Combined blockade of AT2 and AT(1–7) receptors significantly increased the blood pressure of losartan-treated SHR (+15 ± 1 mmHg; P < 0.01); this change did not differ from the blood pressure elevation produced by the sole blockade of AT(1–7) receptors (15 ± 4 mmHg). On the other hand, sole blockade of AT2 receptors in losartan-treated SHR increased mean arterial pressure by 8 ± 1 mmHg ( P < 0.05 vs. 5% dextrose in water as vehicle), and this increase was less than the pressor response produced by blockade of AT(1–7) receptors alone or combined blockade of AT(1–7) and AT2 receptors. The ANG II antibody increased blood pressure to the greatest extent in salt-depleted SHR pretreated with only losartan (+11 ± 2 mmHg) and to the least extent in salt-depleted SHR previously treated with the combination of losartan, PD-123319, and [d-Ala7]ANG-(1–7) (+7 ± 1 mmHg; P < 0.01). Losartan significantly increased heart rate, whereas other combinations of receptor antagonists or the ANG II antibody did not alter heart rate. Our results demonstrate that ANG II and ANG-(1–7) act through non-AT1receptors to oppose the vasoconstrictor actions of ANG II in salt-depleted SHR. Combined blockade of AT2 and AT(1–7) receptors and ANG II neutralization by the ANG II antibody reversed as much as 67% of the blood pressure-lowering effect of losartan.

Increased Pressor Responsiveness to Enkephalin in Spontaneously Hypertensive Rats: The Role of Vasopressin

1980 ◽  
Vol 59 (s6) ◽  
pp. 235s-237s ◽  
Author(s):  
R. W. Rockhold ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Hypertensive Rats ◽  
Methionine Enkephalin ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection. 2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure. 3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats. 4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (d-Ala2)-methionine enkephalin. 5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.

Vasodepressor action of angiotensin in conscious chickens

1982 ◽  
Vol 243 (3) ◽  
pp. H456-H462 ◽  
Author(s):  
Y. Nakamura ◽  
H. Nishimura ◽  
M. C. Khosla
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Direct Action ◽  
Angiotensin Receptors ◽  
Ang Ii ◽  
Prostaglandin Synthetase ◽  
Vasopressin Antagonist ◽  
Native Chicken ◽  
Blood Pressure Responses ◽  
Depressor Action

In chronically cannulated conscious chickens, Gallus gallus, native chicken angiotensin II ([Asp1,Val5]ANG II) caused biphasic blood pressure responses, a depressor followed by a pressor response. The pressor response appears to be mediated primarily by catecholamines. The depressor responses increased with increasing doses and were accompanied by tachycardia. The onset of the depressor action of [Asp1,Val5]ANG II (2.49 +/- 0.22 s) was nearly as quick as that of acetylcholine or histamine. Replacement of aspartic acid in position 1 with sarcosine or asparagine reduced both depressor and pressor potencies, whereas there was no difference either in depressor or pressor potencies between [Asp1,Val5] and [Asp1,Ile5]ANG II. The depressor response to [Asp1,Val5]ANG II was not inhibited by atropine, a vasopressin antagonist, prostaglandin synthetase inhibitors, methysergide, or propranolol but was blocked markedly by [Sar1, Ile8]ANG II and partially by [Sar1,Thr8]ANG II. The results suggest that the vasodepressor action of ANG II is mediated by angiotensin receptors and may possibly be a direct action on the vascular smooth muscle.

scholarly journals Sex differences in blood pressure responsiveness to spontaneous K-complexes during stage II sleep

2020 ◽  
Author(s):  
Ian Mark Greenlund ◽  
Carl A. Smoot ◽  
Jason R. Carter
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Cardiac Cycle ◽  
Pressor Response ◽  
Systolic Arterial Pressure ◽  
Stage Ii ◽  
Men And Women ◽  
Blood Pressures ◽  
Blood Pressure Responses

K-complexes are a key marker of non-rapid eye movement sleep (NREM), specifically during stages II sleep. Recent evidence suggests the heart rate responses to a K-complexes may differ between men and women. The purpose of this study was to compare beat-to-beat blood pressure responses to K-complexes in men and women. We hypothesized that the pressor response following a spontaneous K-complex would be augmented in men compared to women. Ten men (Age: 23 ± 2 years, BMI: 28 ± 4 kg/m2) and ten women (Age: 23 ± 5 years, BMI: 25 ± 4 kg/m2) were equipped with overnight finger plethysmography and standard 10-lead polysomnography. Hemodynamic responses to a spontaneous K-complex during stable stage II sleep were quantified for 10 consecutive cardiac cycles, and measurements included systolic arterial pressure (SAP), diastolic arterial pressure (DAP), and heart rate. K-complex elicited greater pressor responses in men when blood pressures were expressed as SAP (cardiac cycle × sex: p = 0.007) and DAP (cardiac cycle × sex: p = 0.004). Heart rate trended to be different between men and women (cardiac cycle × sex: p = 0.078). These findings suggest a divergent pressor response between men and women following a spontaneous K-complex during normal stage II sleep. These findings could contribute to sex-specific differences in cardiovascular risk that exist between men and women.

Regression of myocardial hypertrophy and influence of adrenergic system

1983 ◽  
Vol 244 (1) ◽  
pp. H97-H101 ◽  
Author(s):  
S. Sen ◽  
R. C. Tarazi
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Regression Analysis ◽  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Myocardial Hypertrophy ◽  
Cardiac Response ◽  
Adrenergic System ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Studies of regression of myocardial hypertrophy in spontaneously hypertensive rats (SHR) suggest that the adrenergic system may play an important role in the reversal of hypertrophy. The effect of propranolol on reversal of hypertrophy, however, is still controversial. This study describes the effect of propranolol, given alone or in combination with hydralazine in different ratios for 4 wk, on blood pressure (BP), ventricular weight, and myocardial catecholamine (MC) concentrations. The data show that a certain ratio of propranolol to hydralazine (750:30) leads to moderate BP control (196-156 mmHg) without increased MC (634 vs. 552 ng/g) and moderately reduced hypertrophy. Reduction of BP alone with increased MC (hydralazine alone) or reduction of MC without BP control (propranolol alone) failed to reduce hypertrophy. A significant correlation between both ventricular weight and heart rate with MC (r = 0.6) was obtained by multiple regression analysis. This study suggests that adrenergic factors seem to play an important role in modulating structural cardiac response to variations in arterial pressure.

Dietary calcium modulates renal BBM angiotensin II binding and Na(+)-H+ antiporter activity in SHR

1991 ◽  
Vol 260 (5) ◽  
pp. F657-F662
Author(s):  
M. Levi ◽  
W. L. Henrich
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Brush Border Membrane ◽  
Spontaneously Hypertensive Rat ◽  
Ang Ii ◽  
Blood Pressure Lowering Effect ◽  
Spontaneously Hypertensive ◽  
Pressure Lowering ◽  
Number Of Binding Sites ◽  
Dissociation Constant Kd

Dietary Ca is an important modulator of blood pressure in the spontaneously hypertensive rat (SHR). Since the kidney plays a key role in the pathogenesis of hypertension, the purpose of this study was to determine the potential renal mechanisms of the blood pressure-lowering effect of increasing dietary Ca content. In 21-day-old SHR fed 0.1 vs. 3.6% Ca diet for 14 days, increasing dietary Ca had no significant effects on basal [704 +/- 50 in 0.1% Ca vs. 784 +/- 61 ng angiotensin I (ANG I).mg-1.h-1 in 3.6% Ca, P = not significant (NS)], isoproterenol-stimulated (1,057 +/- 52 in 0.1% Ca vs. 1,104 +/- 59 ng ANG I.mg-1.h-1 in 3.6% Ca, P = NS), or angiotensin II (ANG II)-inhibited (370 +/- 50 in 0.1% Ca vs. 411 +/- 39 ng ANG I.mg-1.h-1 in 3.6% Ca, P = NS) renal superficial cortical slice renin release. In contrast, in apical brush-border membrane (BBM) vesicles isolated from the superficial cortex, increasing dietary Ca caused a significant decrease in ANG II binding, which was mediated by a decrease in the number of binding sites (Bmax, 376 +/- 14 in 0.1% Ca vs. 234 +/- 6 fmol ANG II/mg BBM protein in 3.6% Ca, P less than 0.01), and no change in the affinity [dissociation constant (Kd), 17.8 +/- 1.4 in 0.1% Ca vs. 13.4 +/- 2.8 nM ANG II in 3.6% Ca, P = NS].(ABSTRACT TRUNCATED AT 250 WORDS)

Control of blood pressure and hindlimb conductance during hemorrhage in conscious renal hypertensive rabbits

1995 ◽  
Vol 268 (6) ◽  
pp. H2302-H2310 ◽  
Author(s):  
G. Weichert ◽  
C. A. Courneya
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Similar Pattern ◽  
Ang Ii ◽  
Autonomic Nervous

We examined the response to hemorrhage in conscious normotensive and hypertensive rabbits under control conditions and during efferent blockade of 1) the hormones vasopressin (AVP) and angiotensin II (ANG II), 2) the autonomic nervous system, and 3) autonomic and hormonal inputs. We recorded mean arterial pressure, heart rate, and hindlimb conductance. The response to hemorrhage was unchanged with hormonal blockade alone. Blockade of the autonomic nervous system caused a faster rate of blood pressure decline, but the rate of decrease in hindlimb conductance was maintained at control levels. Blocking the autonomic nervous system and the hormones resulted in rapid blood pressure decline and an increase in hindlimb conductance. Although the three types of efferent blockade had a similar pattern of effects in normotensive and hypertensive rabbits, hypertensive rabbits exhibited less cardiovascular support during hemorrhage than normotensive rabbits. During hemorrhage, hypertensive rabbits had an attenuation of hindlimb vasoconstriction, a reduction in the heart rate-mean arterial pressure relationship, and reduced ability to maintain blood pressure compared with normotensive rabbits.

scholarly journals Renoprotective Effects of Small Interfering RNA Targeting Liver Angiotensinogen in Experimental Chronic Kidney Disease

Hypertension ◽  
2021 ◽  
Vol 77 (5) ◽  
pp. 1600-1612
Author(s):  
Dominique M. Bovée ◽  
Liwei Ren ◽  
Estrellita Uijl ◽  
Marian C. Clahsen-van Groningen ◽  
Richard van Veghel ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Mean Arterial Pressure ◽  
Kidney Disease ◽  
Arterial Pressure ◽  
Small Interfering Rna ◽  
Ang Ii ◽  
Blood Pressure Lowering Effect ◽  
Independent Manner ◽  
Interfering Rna

Small interfering RNA (siRNA) targeting liver angiotensinogen (AGT) lowers blood pressure, but its effectiveness in hypertensive chronic kidney disease is unknown. Considering that the kidney may generate its own AGT, we assessed the effectiveness of liver-targeted AGT siRNA in the 5/6th Nx (5/6th nephrectomy) rat—a hypertensive chronic kidney disease model. Five weeks after 5/6th Nx (baseline), rats were subjected to vehicle, AGT siRNA, AGT siRNA+losartan, losartan, or losartan+captopril. Baseline mean arterial pressure was 160±6 mm Hg. Over the course of 4 weeks, mean arterial pressure increased further by ≈15 mm Hg during vehicle treatment. This rise was prevented by AGT siRNA. Losartan reduced mean arterial pressure by 37±6 mm Hg and increased plasma Ang (angiotensin) II. Both AGT siRNA and captopril suppressed these effects of losartan, suggesting that its blood pressure–lowering effect relied on stimulation of vasodilator Ang II type 2 receptors by high Ang II levels. Proteinuria and cardiac hypertrophy increased with vehicle, and these increases were comparably abrogated by all treatments. No intervention improved glomerular filtration rate, while siRNA and losartan equally diminished glomerulosclerosis. AGT siRNA±losartan reduced plasma AGT by >95%, and this was accompanied by almost complete elimination of Ang II in kidney and heart, without decreasing renal AGT mRNA. Multiple linear regression confirmed both mean arterial pressure and renal Ang II as independent determinants of proteinuria. In conclusion, AGT siRNA exerts renoprotection in the 5/6th Nx model in a blood pressure–independent manner. This relies on the suppression of renal Ang II formation from liver-derived AGT. Consequently, AGT siRNA may prove beneficial in human chronic kidney disease.

Central angiotensin II-induced pressor responses and neural activity in utero and hypothalamic angiotensin receptors in preterm ovine fetus

2004 ◽  
Vol 286 (4) ◽  
pp. H1507-H1514 ◽  
Author(s):  
Zhice Xu ◽  
Lijun Shi ◽  
Jiaming Yao
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
In Utero ◽  
Angiotensin Receptors ◽  
Ang Ii ◽  
Central Administration ◽  
Pressor Responses ◽  
Ovine Fetus ◽  
Fos Expression ◽  
Sympathetic Pathway

The central renin-angiotensin system is important in the control of blood pressure in the adult. However, few data exist about the in utero development of central angiotensin-mediated pressor responses. Our recent studies have shown that the application of ANG II into the fetal brain can increase blood pressure at near term. The present study determined fetal blood pressure and heart rate in response to a central application of ANG II in the chronically prepared preterm ovine fetus, determined the action sites marked by c-Fos expression in the fetal central pathways after intracerebroventricular injection of ANG II in utero, and determined angiotensin subtype 1 receptors in the fetal hypothalamus. Central injection of ANG II significantly increased fetal mean arterial pressure (MAP). Adjusted fetal MAP against amniotic pressure was also increased by ANG II. Fetal heart rate was subsequently decreased after the central administration of ANG II and/or the increase of blood pressure. ANG II induced c-Fos expression in the central putative cardiovascular area, the paraventricular nuclei in the brain sympathetic pathway. Application of ANG II also caused intense Fos immunoreactivity in the tractus solitarius nuclei in the hindbrain. In addition, intense angiotensin subtype 1 receptors were expressed in the hypothalamus at preterm. These data demonstrate that central ANG II-related pressor centers start to function as early as at preterm and suggest that the central angiotensin-related sympathetic pathway is likely intact in the control of blood pressure in utero.

Cardiovascular actions of microinjections of angiotensin II in the brain stem of rats

1984 ◽  
Vol 246 (5) ◽  
pp. R811-R816 ◽  
Author(s):  
R. Casto ◽  
M. I. Phillips
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Brain Stem ◽  
Nucleus Tractus Solitarius ◽  
Area Postrema ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Ang Ii ◽  
The Brain

The blood pressure and heart rate responses to microinjection of angiotensin II (ANG II) into the brain stem of urethan-anesthetized rats were studied. Microinjection of ANG II into the area postrema (AP) resulted in significant elevation of blood pressure and significant reduction of heart rate. Microinjection into the region of the nucleus tractus solitarius (NTS) yielded a significant dose-dependent elevation in blood pressure and consistent increases in heart rate. The response to microinjection of ANG II into the region of the NTS was not due to leakage into the peripheral circulation, since intravenous administration of the ANG II antagonist, saralasin, did not attenuate the response. In fact, the cardiovascular response was increased after peripheral ANG II blockade, and the heart rate, which was consistently but not significantly elevated by NTS injection alone, was significantly elevated after saralasin pretreatment. Thermal ablation of the AP did not change the heart rate or the pressor response to microinjection of ANG II into the region of the NTS, indicating that the response was not mediated through the AP.

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