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.

The Intrinsic Brain Iso-Renin-Angiotensin System in the Rat: Its Possible Role in Central Mechanisms of Blood Pressure Regulation

1974 ◽  
Vol 48 (s2) ◽  
pp. 265s-268s ◽  
Author(s):  
D. Ganten ◽  
J. S. Hutchinson ◽  
P. Schelling
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rats ◽  
Renin Angiotensin System ◽  
Angiotensin Ii Receptor ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Renin Angiotensin

1. Angiotensin is produced by the intrinsic iso-renin-angiotensin system. 2. Angiotensin is secreted into the cerebrospinal fluid of nephrectomized rats. 3. Angiotensin in cerebrospinal fluid elevates systemic blood pressure. 4. Rats with hereditary diabetes insipidus are virtually non-responsive to intraventricular angiotensin. 5. Angiotensin II is elevated in the cerebrospinal fluid of spontaneously hypertensive rats. 6. An intraventricular perfusion of the angiotensin II receptor-blocking agent P 113 decreases blood pressure in spontaneously hypertensive rats.

Influence of dietary protein on glomerular angiotensin II-receptor binding in normotensive and spontaneously hypertensive rats

1992 ◽  
Vol 83 (1) ◽  
pp. 23-28 ◽  
Author(s):  
D. L. Vaughan ◽  
G. I. Russell
Keyword(s):  
Angiotensin Ii ◽  
Dietary Protein ◽  
Protein Intake ◽  
Renin Angiotensin System ◽  
Angiotensin Ii Receptor ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Renin Angiotensin ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto

1. The binding of angiotensin II to glomerular receptors was studied in spontaneously hypertensive and normotensive Wistar-Kyoto rats in response to 7, 16 and 32% isocaloric, isonatraemic protein diets. 2. Increased dietary protein elevated the systemic angiotensin II levels of both spontaneously hypertensive and Wistar-Kyoto rats [F0.05(2,26)=4.758, P<0.05; n=36], and this was not associated with changes in either systemic blood pressure or cortical renin activity. 3. Furthermore, no significant changes in the affinity or density of angiotensin II receptors were associated with changes of dietary protein intake in either strain. 4. These results indicate a dissociation between the systemic renin-angiotensin system and the tissue renin -angiotensin system in response to protein intake.

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.

Is angiotensin essential in drinking induced by water deprivation and caval ligation?

1981 ◽  
Vol 240 (1) ◽  
pp. R75-R80 ◽  
Author(s):  
M. C. Lee ◽  
T. N. Thrasher ◽  
D. J. Ramsay
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Water Intake ◽  
Water Deprivation ◽  
Essential Role ◽  
Vena Cava ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

The role of the renin-angiotensin system in drinking induced by water deprivation and caval ligation was assessed by infusion of saralasin into the lateral ventricles of rats. This technique was first validated by demonstrating its capability to specifically antagonize drinking to both systemic and central angiotensin II. However, neither the latency to drink nor the amount of water consumed following 24- or 30-h water deprivation was affected by saralasin. Furthermore, saralasin had no significant effect on the recovery of blood pressure or on the water intake following ligation of the abdominal vena cava. These observations suggest that the renin-angiotensin system alone does not play an essential role in the control of drinking following water deprivation or caval ligation in rats.

scholarly journals Black Soybean and Adzuki Bean Extracts Lower Blood Pressure by Modulating the Renin-Angiotensin System in Spontaneously Hypertensive Rats

Foods ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1571
Author(s):  
Eun-Woo Jeong ◽  
Se-Yeong Park ◽  
Yun-Sun Yang ◽  
Youjin Baek ◽  
Damin Yun ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rats ◽  
Renin Angiotensin System ◽  
Adzuki Bean ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Black Soybean ◽  
Renin Angiotensin

Hypertension, causing cardiovascular disease, stroke, and heart failure, has been a rising health issue worldwide. Black soybeans and adzuki beans have been widely consumed throughout history due to various bioactive components. We evaluated the antihypertensive effects of black soybean and adzuki bean ethanol extracts on blood pressure, renin-angiotensin system (RAS), and aortic lesion in spontaneously hypertensive rats. A group of WKY (normal) and six groups of spontaneously hypertensive rats were administered with saline (SHR), 50 mg/kg of captopril (CAP), 250 and 500 mg/kg of black soybean extracts (BE250 and BE500), 250 and 500 mg/kg of adzuki bean extracts (AE250 and AE500) for eight weeks. BE250, BE500, AE250, and AE500 significantly (p < 0.05) reduced relative liver weight, AST, ALT, triglyceride, total cholesterol, systolic blood pressure, and angiotensin-converting-enzyme level compared to SHR. The angiotensin II level in AE500 and renin mRNA expression in BE500 and AE500 were significantly (p < 0.05) decreased compared to SHR. The lumen diameter was significantly (p < 0.05) reduced in only CAP. Furthermore, systolic and diastolic blood pressure and angiotensin II level in AE500 were lower than those of BE500. These results suggest that AE exhibit more antihypertensive potential than BE in spontaneously hypertensive rats.

scholarly journals The Impact of Four Different Classes of Anesthetics on the Mechanisms of Blood Pressure Regulation in Normotensive and Spontaneously Hypertensive Rats

2013 ◽  
pp. 471-478 ◽  
Author(s):  
M. BENCZE ◽  
M. BEHULIAK ◽  
J. ZICHA
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Renin Angiotensin System ◽  
No Synthase ◽  
Hypertensive Rats ◽  
Major Drawback ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
The Impact

Most anesthetics induce characteristic hemodynamic changes leading to blood pressure (BP) reduction but the role of renin-angiotensin system (RAS), sympathetic nervous system (SNS) and nitric oxide (NO) synthesis in this BP reduction is unknown. We therefore studied the influence of four widely used anesthetics – pentobarbital (P), isoflurane (ISO), ketamine-xylazine (KX) and chloralose-urethane (CU) – on the participation of these vasoactive systems in BP maintenance. BP effects elicited by the acute sequential blockade of RAS (captopril), SNS (pentolinium) and NO synthase (L-NAME) were compared in conscious and anesthetized Wistar or spontaneously hypertensive rats (SHR). Except for pentobarbital all studied anesthetics evidenced by diminished BP responses to pentolinium. The absolute pentolinium-induced BP changes were always greater in SHR than Wistar rats. KX anesthesia eliminated BP response to pentolinium and considerably enhanced BP response to NO synthase inhibition in SHR. In both rat strains the anesthesia with ISO or CU augmented BP response to captopril, decreased BP response to pentolinium and attenuated BP response to NO synthase inhibition. In conclusion, pentobarbital anesthesia had a modest influence on BP level and its maintenance by the above vasoactive systems. Isoflurane and chloralose-urethane anesthesia may be used in cardiovascular experiments if substantial BP decrease due to altered contribution of RAS, SNS and NO to BP regulation does not interfere with the respective research aim. Major BP reduction (namely in SHR) due to a complete SNS absence is a major drawback of ketamine-xylazine anesthesia.

scholarly journals Effect of AT1 receptor antagonism on vascular and circulating inflammatory mediators in SHR: role of NF-κB/IκB system

2005 ◽  
Vol 288 (1) ◽  
pp. H111-H115 ◽  
Author(s):  
David Sanz-Rosa ◽  
M. Pilar Oubiña ◽  
Eva Cediel ◽  
Natalia de las Heras ◽  
Onofre Vegazo ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Mrna Expression ◽  
Inflammatory Mediators ◽  
Plasma Levels ◽  
Inflammatory Markers ◽  
Angiotensin Ii Receptor ◽  
Tnf Α ◽  
Wistar Kyoto

We investigated the role of angiotensin II in vascular and circulating inflammatory markers in spontaneously hypertensive rats (SHR). IL-1β, IL-6, and TNF-α aortic mRNA expression and plasma levels were measured in adult SHR untreated or treated with the angiotensin II receptor antagonist candesartan (2 mg·kg−1·day−1) or antihypertensive triple therapy (TT; in mg·kg−1·day−1: 20 hydralazine + 7 type 1 hydrochlorothiazide + 0.15 reserpine) for 10 wk. Likewise, aortic expression of NF-κB p50 subunit precursor p105 and its inhibitor (IκB) were measured. Age-matched Wistar-Kyoto rats (WKY) served as normotensive reference. High blood pressure levels were associated with increased ( P < 0.05) aortic mRNA expression of IL-1β, IL-6, and TNF-α. Hypertension was also accompanied by increased IL-1β and IL-6 plasma levels. No differences were observed in circulating TNF-α levels between SHR and WKY. SHR presented elevated aortic mRNA expression of the transcription factor NF-κB and reduction in its inhibitor, IκB. Candesartan decreased ( P < 0.05) blood pressure levels, aortic mRNA expression of IL-1β, IL-6, and TNF-α, and ( P < 0.05) IL-1β and IL-6 plasma concentration. However, although arterial pressure decrease was comparable for the treatments, TT only partially reduced the increments in inflammatory markers. In fact, candesartan-treated rats showed significantly lower levels of circulating and vascular inflammatory markers than TT-treated animals. The treatments increased IκB mRNA expression similarly. However, only candesartan reduced NF-κB mRNA expression. In summary, 1) SHR presented a vascular inflammatory process; 2) angiotensin II, and increased hemodynamic forces associated with hypertension, seems to be involved in stimulation of inflammatory mediators through NF-κB system activation; and 3) reduction of inflammatory mediators produced by candesartan in SHR could be partially due to both downregulation of NF-κB and upregulation of IκB.

Role of bradykinin in angiotensin-converting enzyme knockout mice

2003 ◽  
Vol 284 (6) ◽  
pp. H1969-H1977 ◽  
Author(s):  
Hong D. Xiao ◽  
Sebastien Fuchs ◽  
Justin M. Cole ◽  
Kevin M. Disher ◽  
Roy L. Sutliff ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Knockout Mice ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Low Blood Pressure ◽  
Urine Concentrating Ability

Angiotensin-converting enzyme (ACE) plays a central role in the renin-angiotensin system. Whereas ACE is responsible for the production of angiotensin II, it is also important in the elimination of bradykinin. Constitutively, the biological function of bradykinin is mediated through the bradykinin B2 receptor. ACE knockout mice have a complicated phenotype including very low blood pressure. To investigate the role of bradykinin in the expression of the ACE knockout phenotype, we bred B2 receptor knockout mice with ACE knockout mice, thus generating a line of mice deficient in both the B2 receptor and ACE. Surprisingly, these mice did not differ from ACE knockout mice in blood pressure, urine concentrating ability, renal pathology, and hematocrit. Thus abnormalities of bradykinin accumulation do not play an important role in the ACE knockout phenotype. Rather, this phenotype appears due to the defective production of angiotensin II.

scholarly journals The Renin-Angiotensin System Modulates Inflammatory Processes in Atherosclerosis: Evidence from Basic Research and Clinical Studies

2009 ◽  
Vol 2009 ◽  
pp. 1-13 ◽  
Author(s):  
Fabrizio Montecucco ◽  
Aldo Pende ◽  
François Mach
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Basic Research ◽  
Angiotensin Ii Receptor ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Renin Inhibitors ◽  
Arterial Blood ◽  
Inflammatory Processes

Recent evidence shows that the renin-angiotensin system is a crucial player in atherosclerotic processes. The regulation of arterial blood pressure was considered from its first description of the main mechanism involved. Vasoconstriction (mediated by angiotensin II) and salt and water retention (mainly due to aldosterone) were classically considered as pivotal proatherosclerotic activities. However, basic research and animal studies strongly support angiotensin II as a proinflammatory mediator, which directly induces atherosclerotic plaque development and heart remodeling. Furthermore, angiotensin II induces proatherosclerotic cytokine and chemokine secretion and increases endothelial dysfunction. Accordingly, the pharmacological inhibition of the renin-angiotensin system improves prognosis of patients with cardiovascular disease even in settings of normal baseline blood pressure. In the present review, we focused on angiotensin-convertingenzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), and renin inhibitors to update the direct activities of the renin-angiotensin system in inflammatory processes governing atherosclerosis.

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