Central angiotensin II-induced responses in spontaneously hypertensive rats

1977 ◽  
Vol 232 (4) ◽  
pp. H426-H433 ◽  
Author(s):  
W. E. Hoffman ◽  
M. I. Phillips ◽  
P. G. Schmid
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Pressure Effects ◽  
Spontaneous Hypertension ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Vascular Responsiveness ◽  
Vascular Sensitivity ◽  
Wistar Kyoto ◽  
The Brain

The brain isorenin angiotensin system has been implicated in the development of spontaneous hypertension by several investigators. The experiments reported here were designed to test the responsiveness of unanesthetized spontaneous hypertensive (SH) rats to intracerebroventricular angiotensin II injections compared to Wistar-Kyoto (WK) normotensive controls. The results indicate that there is no difference between SH and WK animals in drinking responses or antidiuretic hormone release to central angiotensin II injections; however, an increased pressor responsiveness to intraventricular angiotensin II in SH as compared to WK was observed. The results of intravenous infusions of pressor substances in these experiments and reports by other investigators suggest that the increased blood pressure effects to central angiotensin are due to three possible factors: 1) increased vascular responsiveness of SH to vasoconstrictor substances in general, 2) increased vascular sensitivity of SH rats to sympathetic outflow, and 3) decreased baroreceptor reflexes to acute increases in blood pressure. We suggest that the brain isorenin-angiotensin system may be involved in spontaneous hypertension by increased production of angiotensin II or by activation of a potentiated sympathetic system, but not by a generalized increased sensitivity of brain receptors to central angiotensin.

Role of angiotensin II and catecholamines in blood pressure variability responses to stress in SHR

1996 ◽  
Vol 270 (6) ◽  
pp. R1265-R1272 ◽  
Author(s):  
E. Gaudet ◽  
J. Blanc ◽  
J. L. Elghozi
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Acute Administration ◽  
Angiotensin Ii Receptor ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Air Jet ◽  
Wistar Kyoto

The contribution of the renin-angiotensin system (RAS) and the sympathetic nervous system (SNS) to blood pressure (BP) and heart rate (HR) variability responses to air-jet stress was assessed in spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. Activity of the encogenous RAS was suppressed by chronic treatment by a nonpeptide angiotensin II receptor antagonist (Iosartan). The role of alpha 1-adrenoceptor activity was evaluated in rats by acute administration of prazosin. In untreated animals, an air jet induced an increase in systolic BP (SBP; 9 +/- 2 mmHg for WKY and 8 +/- 2 mmHg for SHR) and in HR (56 +/- 19 beats/min for WKY and 76 +/- 8 beats/min for SHR), followed by an increase of the midfrequency (MF; 0.2-0.6 Hz) component of HR in WKY (183%) and by an increase of the MF component of SBP and diastolic BP in SHR (65%). Prazosin prevented BP rises as well as the MF component of BP and HR increases associated with air-jet stress. Chronic suppression of the RAS by losartan did not alter the BP response to the air jet in WKY and slightly reduced it in SHR but abolished all the BP and HR variability changes in both strains. These results indicate that the SNS but not RAS is essential for the BP rise induced by stress and demonstrate that RAS in conjunction with SNS is involved in BP and HR variability changes associated with stress.

Lack of Hypotensive Effect on Central Injection of Angiotensin Inhibitors in Spontaneously Hypertensive (SH) and Normotensive Rats

1976 ◽  
Vol 51 (s3) ◽  
pp. 385s-389s
Author(s):  
J. L. Elghozi ◽  
J. Altman ◽  
M. A. Devynck ◽  
J. F. Liard ◽  
J. P. Grunfeld ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rats ◽  
Hypotensive Effect ◽  
Spontaneous Hypertension ◽  
Cerebral Ventricles ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
The Brain

1. Injections of antagonists of angiotensin II into the cerebral ventricles of normotensive and spontaneously hypertensive rats were performed in order to assess the role of the isorenin—angiotensin system in the brain. 2. No hypotensive effect was obtained in either normotensive or hypertensive rats, suggesting that intracranial isoangiotensin has little role in the pathogenesis of spontaneous hypertension in the rat.

Blood pressure responsiveness during the development of hypertension in the conscious spontaneously hypertensive rat

1985 ◽  
Vol 63 (10) ◽  
pp. 1258-1262 ◽  
Author(s):  
Corey B. Toal ◽  
Frans H. H. Leenen
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rat ◽  
Blood Pressure Response ◽  
Receptor Occupancy ◽  
Pressure Response ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Freely Moving ◽  
Wistar Kyoto

Blood pressure responsiveness to iv noradrenaline and angiotensin II was studied in conscious, freely moving, age-matched spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats from 4 to 16 weeks of age. At 4 and 6 weeks the SHR showed small, but nonsignificant increases in responsiveness compared with WKY to both noradrenaline and angiotensin II. At 8 weeks they exhibited similar responses to the WKY. Subsequently, at 12 and 16 weeks decreased responsiveness to noradrenaline (nonsignificant) and angiotensin II (p < 0.05 at 12 and 16 weeks) was observed in SHR versus WKY. At 16 weeks of age, hexamethonium caused potentiation of the blood pressure response to noradrenaline and angiotensin II, but to the same degree in the two strains. Captopril at this age did not elicit potentiation to noradrenaline or angiotensin II in either strain. These results indicate that there is no rise in blood pressure responsiveness to circulating pressor agents, parallel to the development of hypertension in SHR. Increased receptor occupancy or more active attenuating reflexes in SHR versus WKY appear not to be involved in the absence of hyperresponsiveness in intact consious SHR at 16 weeks of age.

scholarly journals Long-term exercise attenuates blood pressure responsiveness and modulates kidney angiotensin II signalling and urinary sodium excretion in SHR

2011 ◽  
Vol 12 (4) ◽  
pp. 394-403 ◽  
Author(s):  
Silmara Ciampone ◽  
Rafael Borges ◽  
Ize P de Lima ◽  
Flávia F Mesquita ◽  
Elizabeth C Cambiucci ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Exercise Training ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Receptor Expression ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

Observations have been made regarding the effects of long-term exercise training on blood pressure, renal sodium handling and renal renin–angiotensin–aldosterone (RAS) intracellular pathways in conscious, trained Okamoto–Aoki spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKy) normotensive rats, compared with appropriate age-matched sedentary SHR and WKy. To evaluate the influence of exercise training on renal function and RAS, receptors and intracellular angiotensin II (AngII) pathway compounds were used respectively, and lithium clearance and western blot methods were utilised. The current study demonstrated that increased blood pressure in SHR was blunted and significantly reduced by long-term swim training between the ages of 6 and 16 weeks. Additionally, the investigators observed an increased fractional urinary sodium excretion in trained SHR (SHRT) rats, compared with sedentary SHR (SHRS), despite a significantly decreased creatinine clearance (CCr). Furthermore, immunoblotting analysis demonstrated a decreased expression of AT1R in the entire kidney of TSHR rats, compared with SSHR. Conversely, the expression of the AT2R, in both sedentary and trained SHR, was unchanged. The present study may indicate that, in the kidney, long-term exercise exerts a modulating effect on AngII receptor expression. In fact, the present study indicates an association of increasing natriuresis, reciprocal changes in renal AngII receptors and intracellular pathway proteins with the fall in blood pressure levels observed in TSHR rats compared with age-matched SSHR rats.

scholarly journals Effects of Prehypertensive Losartan Treatment on Resistance Vessel Remodeling and Angiotensin II Type 1 Receptor Expression in Spontaneously Hypertensive Rats

2020 ◽  
Vol 33 (5) ◽  
pp. 471-471
Author(s):  
Ting-jun Wang ◽  
Wan-ru Chen ◽  
Xu Lin ◽  
Gui-li Lian ◽  
Chang-sheng Xu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Receptor Expression ◽  
Mesenteric Arteries ◽  
Resistance Vessel ◽  
Spontaneously Hypertensive ◽  
Vessel Remodeling ◽  
Wistar Kyoto ◽  
Losartan Treatment

Abstract Background To study the effects of prehypertensive losartan treatment on blood pressure, resistance vessel remodeling, and angiotensin II type 1 receptor (AT1R) expression in adult spontaneously hypertensive rats (SHRs). Methods Four-week-old SHR and Wistar-Kyoto rats were randomly divided into losartan-treated and untreated groups. Losartan was administrated by gavage from 4 to 10 weeks old. Blood pressure was monitored by the tail-cuff method till 26 weeks old. The third grade mesenteric arteries were then isolated. Vessel structure, relaxation reactivity, angiotensin II type 1 receptor expression, and angiotensin II levels were analyzed. Results Losartan treatment from 4 to 10 weeks of age significantly lowered systolic blood pressure from 10 to 26 weeks in SHR. At 26 weeks old, wall thickness to lumen radius and wall area to lumen area of mesenteric arteries were significantly lower in losartan-treated than untreated SHR (P &lt; 0.01). Maximum relaxation to acetylcholine and its pD2 were increased in losartan-treated compared to untreated SHR (P &lt; 0.01). Angiotensin II type 1 receptor mRNA and protein levels were significantly reduced in losartan-treated SHR (P &lt; 0.01). However, angiotensin II levels in plasma and mesenteric arteries of losartan-treated SHR were higher than those of untreated SHR (P &lt; 0.05). Losartan treatment lowered systolic blood pressure in Wistar-Kyoto at the age of 10 weeks (P &lt; 0.05), but had no significant effect on blood pressure after 14 weeks or mesenteric arteries at 26 weeks. Conclusions Blood pressure reduction induced by prehypertensive losartan treatment ameliorates resistance vessel remodeling and downregulates angiotensin II type 1 receptor expression in adult SHR.

Vasopressin in brain of spontaneously hypertensive rats

1982 ◽  
Vol 242 (4) ◽  
pp. H496-H499 ◽  
Author(s):  
W. Rascher ◽  
R. E. Lang ◽  
T. Unger ◽  
D. Ganten ◽  
F. Gross
Keyword(s):  
Blood Pressure ◽  
Plasma Concentration ◽  
Brain Stem ◽  
Spontaneously Hypertensive Rats ◽  
Age Groups ◽  
Plasma Osmolality ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
The Brain

In stroke-prone spontaneously hypertensive rats (SHRSP) and in normotensive Wistar-Kyoto rats (WKY), arginine vasopressin (AVP) was measured by means of a radioimmunoassay in the plasma, the pituitary gland, the hypothalamus, and the brain stem. In 6- and 14-wk-old SHRSP, the plasma concentration of AVP was lower than in age-matched WKY (P less than 0.01), whereas it was elevated at 28 wk of age (P less than 0.01). In the pituitary of 6-wk-old SHRSP, AVP was higher than in WKY (P less than 0.05), but no such difference was found in older rats. In the hypothalamus and the brain stem, AVP content was reduced in all age groups of SHRSP. Plasma osmolality was diminished in 28-wk-old SHRSP only (P less than 0.01), whereas hematocrit in all age groups was higher in SHRSP than in WKY. It is concluded that the secretion of AVP and possibly its synthesis in the hypothalamus are reduced in SHRSP. Whether the reduced AVP content in the brain stem is related to the sustained elevation of blood pressure has to be studied further.

Abstract P231: Offspring of Captopril Treated Spontaneously Hypertensive Rats Have Lower Angiotensin II Type 1 Receptor Expression Which is Associated With Lower Blood Pressure

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
J X Masjoan-Juncos ◽  
Tang-Dong Liao ◽  
Ginette Bordcoch ◽  
Cesar A Romero ◽  
Oscar A Carretero
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Posterior Wall ◽  
Receptor Expression ◽  
Shr Rats ◽  
Spontaneously Hypertensive ◽  
Intracerebroventricular Infusion ◽  
Lower Blood ◽  
The Brain

It has been reported that SHR rats receiving angiotensin converting enzyme (ACE) inhibitor Captopril decrease blood pressure (BP) in at least two generation after the treatment was stopped. A decreased response to an intracerebroventricular infusion angiotensin I and angiotensin II in treated animals and their offspring was reported; however there is no reported mechanism that explains the changes observed in the untreated offspring of the Captopril treated animals. We hypothesize that captopril reduces angiotensin II type 1 receptor (AT1R) expression in CNS of the offspring of SHR rats treated with captopril. Animal groups are as follows: control animals, captopril treated animals, offspring of the control animals, offspring of the treated animals where the mother was removed from the treatment immediately after giving birth and Offspring of treated animals where the mother was removed from the treatment at weaning. BP was measured by intra-arterial method and Tail cuff. AT1R expression was measured in brain tissue using the posterior wall of the forth ventricle, as well as the top half of the brain stem. BP was different between treated groups and their offspring vs. control (Table 1). AT1R expression was significantly reduced in both offspring groups of the treated animals, when compared to control (Table 1). Therefore we conclude that captopril reduces blood pressure in the offspring of captopril treated SHR rats and that associates with a decrease in AT1R expression in CNS. Further research is necessary to determine the possible epigenetic mechanisms involved in AT1R reduction.

Angiotensin II attenuates baroreflexes at nucleus tractus solitarius of rats

1986 ◽  
Vol 250 (2) ◽  
pp. R193-R198 ◽  
Author(s):  
R. Casto ◽  
M. I. Phillips
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Baroreflex Sensitivity ◽  
Nucleus Tractus Solitarius ◽  
Ang Ii ◽  
Spontaneously Hypertensive ◽  
Baroreceptor Reflexes ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
The Brain

Microinjection of angiotensin II (ANG II) into the nucleus tractus solitarius (NTS) has been shown to produce a dose-dependent increase in blood pressure and heart rate. We have tested the effect of subpressor infusions of ANG II (10 ng . kg-1 . min-1) in the NTS on reflex bradycardia after intravenous administration of the vasoconstrictor phenylephrine (1-12 micrograms) in normotensive urethan-anesthetized rats. ANG II within the brain is thought to contribute to the decreased baroreflex sensitivity in spontaneously hypertensive rats (SHR). The sensitivity of the baroreflex was significantly decreased by the infusion of ANG II (1.01 +/- 0.08) compared with control (2.41 +/- 0.51) in the normotensive animals. Baroreflex sensitivity was significantly decreased in SHR (0.40 +/- 0.21) compared with normotensive animals. We conclude that ANG II within the NTS can inhibit the function of baroreceptor reflexes in normotensive animals, suggesting that the endogenous peptide may perform an inhibitory role in the baroreflex arc, and this is further evidence that central ANG II is involved in blood pressure of SHR.

Indirect hypertensive actions of long-term intracarotid angiotensin II infusion during ovine pregnancy

1994 ◽  
Vol 72 (4) ◽  
pp. 311-316 ◽  
Author(s):  
S. C. Mukaddam-Daher ◽  
G. W. Aberdeen ◽  
S. C. Cha ◽  
J. Gutkowska ◽  
B. S. Nuwayhid ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Urine Volume ◽  
Plasma Renin ◽  
Sodium Balance ◽  
Angiotensin System ◽  
The Central Nervous System ◽  
The Brain ◽  
Internal Carotid Arteries

Angiotensin II (AngII) influences the regulation of mean arterial pressure (MAP) through numerous mechanisms, including an action of circulating AngII on the brain to alter autonomic activity. We have obtained evidence that the relative importance of this effect is increased during pregnancy. Consequently, these studies were undertaken to assess the effects of bilateral infusion of AngII (0.35 ng∙kg−1∙min−1∙artery−1) into the internal carotid arteries (ica) of sheep for 13 days. Six nonpregnant (NP) and six 105- to 125-day pregnant (PG) ewes were maintained in large metabolism cages, where MAP was continuously monitored. By day 10 of ica AngII infusion in NP ewes, MAP was increased from 83.9 ± 1.6 to 92.9 ± 2.8 mmHg (1 mmHg = 133.3 Pa) (p = 0.001). Twenty-four hour urine volume (UV, 2664 ± 341 to 1583 ± 228 mL; p = 0.005) and sodium excretion (UNaV, 190 ± 5 to 113 ± 19 mmol/day; p = 0.005) were decreased. 51Cr-tagged blood volume (BV) was increased on day 13 (3643 ± 187 to 4379 ± 446 mL; p = 0.05). In contrast, by only day 6 of ica AngII infusion in PG ewes, MAP increased from 79.1 ± 1.9 to 84.1 ± 1.4 mmHg (p = 0.03) in association with a BV expansion from 3999 ± 274 to 4207 ± 275 mL. These changes were preceded by decreases in UV (2813 ± 413 to 2198 ± 362 mL; p = 0.01) and UNaV (190 ± 15 to 118 ± 26 mmol/day; p = 0.01). By day 13, MAP had plateaued at 93.0 ± 1.2 mmHg. There were no changes in plasma AngII, plasma renin activity, arginine vasopressin, and atrial natriuretic factor during ica AngII infusion in either NP or PG ewes, suggesting that these effects are mediated via the central nervous system. Moreover, the data suggest that MAP is increased secondary to volume expansion associated with sodium and water retention. This effect appears to be more readily exhibited during pregnancy. Furthermore, this study demonstrates the importance of the rennin–angiotensin system in blood pressure homeostasis by actions other than direct vasoconstriction.Key words: angiotensin II, blood pressure, hypertension, sheep, pregnancy, sodium balance.

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